Diseases & Conditions

Child Abuse

2008-01-29T20:18:00.000-08:00

It was not until the 19th century that children were granted the same legal status as domesticated animals with regard to protection against cruelty and/or neglect. In 1962, the term "battered child syndrome" became part of the medical vocabulary and by 1976 all of the states in the United States had adopted laws mandating the reporting of suspected child abuse.
What is the scope of the child abuse problem?From the early 1970's when a national data bank was created, the yearly number of reports of child abuse has risen progressively. Initially, 700,000 incidents of child abuse were reported annually. Now there are approximately 2 million cases reported every year. While "reports" of alleged child abuse are not always substantiated during the investigation process, most authorities believe that a large under reporting bias is inherent in the data. There is much more child abuse than gets reported.

What age child is abused?All ages. The frequency of documented child abuse increases with the age of the victim: children less than 2 years of age (6 per 1000) versus 15 to 17 years of age (14 per 1000). This statistic may reflect a true increase in mistreatment with the age of the child or it may at least in part reflect a rise in reporting. Obviously, very young children are incapable of verbally communicating the harm inflicted on them. Other factors such as fear, guilt, or confusion about the abuser's erratic behavior may also hinder younger children from informing on their abuser.
Are girls more often abused than boys?Yes. Girls are somewhat more likely to be abused. According to statistics published in 1996, about 52% of victims of maltreatment were female and 48% were male.
Is the pattern of abuse different for girls and boys?Yes. Some differences exist in the types of maltreatment experienced by female and male children. A review of data from 11 states in the U.S. reveals that 77% of sexual abuse victims were girls compared to 23% boys. Victims of emotional mistreatment were also more likely to be female (53%) than male (47%).
Conversely, a slightly greater proportion of victims of other types of maltreatment were male. Males comprised approximately 51% of neglect victims and 52% of both physical abuse and medical neglect victims.
Is there an association between poverty and child abuse?While children of families in all income levels suffer maltreatment, research suggests that family income is strongly related to incidence rates. Children from families with annual incomes below $15,000 per year are more than 25 times more likely than children from families with annual income above $30,000 to be harmed or endangered by abuse or neglect. Poverty clearly predisposes to child abuse.

Who abuses children?According to the statistics, the majority of perpetrators of child mistreatment (77%) are parents and another 11% are other relatives of the victim. People who are in other care taking relationships to the victim (e.g., child care providers, foster parents, and facility staff) account for only 2 percent of the offenders. About 10% of all perpetrators are classified as non-caretakers or unknown. In many states, child abusers by definition must be in a care taking role.
An estimated 81% of all offenders are under age 40. Overall, approximately 61% of perpetrators are female, although the gender of the abuser differs by the type of mistreatment. Neglect and medical neglect are most often attributed to female caretakers, while sexual abuse is most often associated with male offenders.
What is child abuse?The term child abuse encompasses four basic types of mistreatment: child neglect, physical abuse of a child, emotional abuse of a child, and sexual abuse of a child.
What does the term child neglect include?Child neglect is the most frequently reported form of child abuse (60% of all cases) and the most lethal.
Neglect is defined as the failure to provide for the shelter, safety, supervision, and nutritional needs of the child. Child neglect may be physical, educational, or emotional. The assessment of child neglect requires the consideration of cultural values and standards of care as well as the recognition that the failure to provide the necessities of life may be related to poverty.
Physical neglect includes the refusal or delay in seeking health care, abandonment, inadequate supervision, expulsion from the home, or refusal to allow a runaway to return home.
Educational neglect includes the allowance of chronic truancy, failure to enroll a child of mandatory school age in school, and failure to attend to a special educational need.
Emotional neglect involves a marked inattention to the child's needs for affection, refusal of or failure to provide needed psychological care, spousal abuse or parental substance abuse in the child's presence, and permission of drug or alcohol use by the child.

What actions are viewed as physical child abuse?Physical abuse is the second most frequently reported form of child abuse (25% of all cases).
This form of mistreatment is defined as willful (as opposed to accidental) physical injury inflicted upon the child. Physical abuse can be the result of punching, beating, kicking, biting, burning, shaking, or otherwise harming the child's body. The parent or caretaker may not have intended to hurt the child; rather, the injury may have resulted from excessive disciplinary efforts or physical punishment.
There exists a significant controversy regarding physical methods of discipline (e.g. spanking) and their relationship to more orthodox forms of physical abuse.
What constitutes emotional child abuse?Emotional abuse is the third most frequently reported form of child abuse (17% of all cases). This form is felt to be markedly under reported since it can be difficult to detect and document.
Emotional abuse includes acts or omissions by the parents or other caregivers that could cause serious behavioral, emotional, or mental disorders. Verbal assaults on the child or on other members of the family in the child's presence is a common form of emotional abuse. In some cases of emotional abuse, the acts of the parents or other caregivers alone, without any harm evident in the child's behavior or condition, are sufficient to warrant child protective services intervention. For example, the parents/caregivers may use extreme or bizarre forms of punishment, such as confinement of the child in a dark closet.
Emotional child abuse is also sometimes termed psychological child abuse, verbal child abuse, or mental injury of a child.
What is sexual child abuse?Sexual abuse is the least frequently reported form of child mistreatment (6% of all cases). Experts believe that sexual abuse may be the most under-reported type of abuse because of the secrecy or "conspiracy of silence" that so often characterizes these cases.
Sexual abuse includes fondling a child's genitals, intercourse, incest, rape, sodomy, exhibitionism, and commercial exploitation through prostitution or the production of pornographic materials.

How is alleged child abuse evaluated?A thorough nonjudgmental history of the immediate events as well as a review of potential similar experiences are often independently done by a physician, social worker, and/or the police department. The child may be interviewed separately from the parents as part of this information gathering process.
A complete physical exam of the child (which may include the taking of photographs to document physical/sexual abuse) is often followed by x-rays and/or laboratory tests to support the potential diagnosis of inflicted trauma and to rule out the possibility of medical conditions which could account for the physical findings noted during the examination.
How is child abuse treated?Steps which are often taken to correct child abuse are as follows:
The safety of the abused child and any other potential victim of abuse in the household is paramount. Removal of the victim and placement in protective custody in a group home or foster care are often necessary.
Effective counseling for the child, family, and the abuser is essential to deal with the associated emotional and psychological stress and trauma.
In the event of neglect, establishing realistic expectations of the child's needs and capabilities is required.
Parental high-risk behaviors such as substance/alcohol abuse must be addressed.
Pedophiles (people who have sexually abused children) often require intense psychological and pharmacological therapy prior to release into the community, because of the high rate of repeat offenders.
How can child abuse be prevented?This, too, is a very complex matter and includes these measures:
A support group structure is needed to reinforce parenting skills and closely monitor the child's well-being.
Visiting home nurse or social worker visits are also required to Observe and evaluate the progress of the child and his/her caretaking situation.
The support group structure and visiting home nurse or social worker visits are not mutually exclusive. Many studies have demonstrated that the two measures must be coupled together for the best possible outcome.
Children's school programs regarding "good touch...bad touch" can provide children with a forum in which to role-play and learn to avoid potentially harmful scenarios.
Parents should make sure that their child's daycare center is licensed and has an open door policy regarding parental visitation.

What more can be done to prevent child neglect?As children's advocates, we wish to remind parents about the importance of preventative child health care, including:
Proper use of car seats and seat belts;
Consistent use of helmets for bicycling and skateboarding;
Pool and water safety;
Firearm safety; and
Poisoning prevention.
Are persons who were abused as children more likely to become criminals later in life?According to a 1992 study sponsored by the National Institute of Justice (NIJ), maltreatment in childhood increases the likelihood of arrest as a juvenile by 53% and as an adult by 38%. Abuse as a child also increases the prospect of arrest for a violent crime by 38%.
For females, being abused or neglected in childhood raises the likelihood of arrest by 77%. A related 1994 NIJ study indicated that children who were sexually abused were 28 times more likely than a control group of non-abused children to be arrested for prostitution as an adult.
Child Abuse At A Glance
Child abuse is a significant and dangerous problem.
It is in fact a series of serious problems.
These problems include child neglect and abuse -- whether it be physical, emotional, or sexual.
Neglect is the most frequently reported form of child abuse and the most lethal.
Poor nutrition is a form of child abuse.
Failure to provide a child with appropriate schooling is a type of educational child abuse.
Children can be neglected and abused by parents, other caregivers, or society.
Poverty is a factor which contributes to child abuse.
Child abuse should be reported, investigated, and evaluated.
Prevention is the best strategy for the management of child abuse.

Boils(Skin Abscesses)

2008-01-29T20:16:00.000-08:00

What is a boil?
A boil, also referred to as a skin abscess, is a localized infection deep in the skin. A boil generally starts as a reddened, tender area. Over time, the area becomes firm and hard. Eventually, the center of the abscess softens and becomes filled with infection-fighting white blood cells that the body sends from the bloodstream to eradicate the infection. This collection of white blood cells, bacteria, and proteins is known as pus. Finally, the pus "forms a head," which can be surgically opened or spontaneously drain out through the surface of the skin.

What does a boil look like?
There are several different types of boils. Among these are:
Furuncle or carbuncle: This is an abscess in the skin caused by the bacterium Staphylococcus aureus. A furuncle can have one or more openings onto the skin and may be associated with a fever or chills.
Cystic acne: This is a type of abscess that is formed when oil ducts become clogged and infected. Cystic acne affects deeper skin tissue that the more superficial inflammation from common acne. Cystic acne is most common on the face and typically occurs in the teenage years.
Hidradenitis suppurativa: This is a condition in which there are multiple abscesses that form under the armpits and often in the groin area. These areas are a result of local inflammation of the sweat glands. This form of skin infection is difficult to treat with antibiotics alone and typically requires a surgical procedure to remove the involved sweat glands in order to stop the skin inflammation.
Pilonidal cyst: This is a unique kind of abscess that occurs in the crease of the buttocks. Pilonidal cysts often begin as tiny areas of infection in the base of the area of skin from which hair grows (the hair follicle). With irritation from direct pressure, over time the inflamed area enlarges to become a firm, painful, tender nodule making it difficult to sit without discomfort. These frequently form after long trips that involve prolonged sitting.

Why do boils occur?
There are many causes of boils. Some boils can be caused by an ingrown hair. Others can form as the result of a splinter or other foreign material that has become lodged in the skin. Others boils, such as those of acne, are caused by plugged sweat glands that become infected.
The skin is an essential part of our immune defense against materials and microbes that are foreign to our body. Any break in the skin, such as a cut or scrape, can develop into an abscess should it then become infected with bacteria.

Who is most likely to develop a boil?
Anyone can develop a boil. However, people with certain illnesses or medications that impair the body's immune system (the natural defense system against foreign materials or microbes) are more likely to develop boils. Among the illnesses that can be associated with impaired immune systems are diabetes and kidney failure. Diseases, such as hypogammaglobulinemia, that are associated with deficiencies in the normal immune system can increase the tendency to develop boils.
Many medications can suppress the normal immune system and increase the risk of developing boils. These medications include cortisone medications (prednisone and prednisolone) and medications used for cancer chemotherapy.

What is the treatment for a boil?
Most simple boils can be treated at home. Ideally, the treatment should begin as soon as a boil is noticed since early treatment may prevent later complications.
The primary treatment for most boils is heat application, usually with hot soaks or hot packs. Heat application increases the circulation to the area and allows the body to better fight off the infection by bringing antibodies and white blood cells to the site of infection.
As long as the boil is small and firm, opening the area and draining the boil is not helpful, even if the area is painful. However, once the boil becomes soft or "forms a head" (that is, a small pustule is noted in the boil), it can be ready to drain. Once drained, pain relief can be dramatic. Most small boils, such as those that form around hairs, drain on their own with soaking. On occasion, and especially with larger boils, the larger boil will need to be drained or "lanced" by a health-care practitioner. Frequently, these larger boils contain several pockets of pus that must be opened and drained.
Antibiotics are often used to eliminate the accompanying bacterial infection. Especially if there is an infection of the surrounding skin, the doctor often prescribes antibiotics. However, antibiotics are not needed in every situation. In fact, antibiotics have difficulty penetrating the outer wall of an abscess well and often will not cure an abscess without additional surgical drainage.

When should I seek medical attention?
Any boil or abscess in a patient with diabetes or a patient with an underlying illness that can be associated with a weakened immune system (such as cancer, rheumatoid arthritis, etc.) should be evaluated by a health-care practitioner. Additionally, many medicines, especially prednisone, that suppress the immune system (the natural infection-fighting system of the body) can complicate what would be an otherwise simple boil. Patients who are on such medications should consult their health-care practitioner if they develop boils. (If you are not sure about your medications' effects on the immune system, your pharmacist may be able to explain to you which medicines to be concerned about.)
Any boil that is associated with a fever should receive medical attention. A "pilonidal cyst," a boil that occurs between the buttocks, is a special case. These almost always require medical treatment including drainage and packing (putting gauze in the opened abscess to assure it continues to drain). Finally, any painful boil that is not rapidly improving should be seen by the health-care practitioner.

What can be done to prevent boils (abscesses)?
There are some measures that you can take to prevent boils from forming. The regular use of antibacterial soaps can help to prevent bacteria from building up on the skin. This can reduce the chance for the hair follicles to become infected and prevent the formation of boils. In some situations, your health-care practitioner may recommend special cleansers such as pHisoderm to even further reduce the bacteria on the skin. When the hair follicles on the back of the arms or around the thighs are continually inflamed, regular use of an abrasive brush (loofah brush) in the shower can be used break up oil plugs and build up around hair follicles.
Pilonidal cysts can be prevented by avoiding continued direct pressure or irritation of the buttock area when a local hair follicle becomes inflamed. At that point, regular soap and hot water cleaning and drying can be helpful.
For acne and hidradenitis suppurativa (see above), antibiotics may be required on a long-term basis to prevent recurrent abscess formation. As mentioned above, surgical resection of sweat glands in the involved skin may be necessary. Other medications, such as isotretinoin (Accutane), can be used for cystic acne and have been helpful in some patients with hidradenitis suppurativa. Recurrences are common in patients with hidradenitis suppurativa.
Finally, surgery may occasionally be needed, especially in pilonidal cysts that recur, but also for hidradenitis suppurativa. For pilonidal cysts, surgically removing the outer shell of the cyst is important to clear the boil. The procedure is typically performed in the operating room. For hidradenitis suppurativa, extensive involvement can require plastics surgical repair.
Boils At A Glance
A boil, or skin abscess, is a collection of pus that forms inside the body.
Antibiotics alone can be inadequate in treating abscesses.
The primary treatments for boils include hot packs and draining ("lancing") the abscess, but only when it is soft and ready to drain.
If you have a fever or long-term illness, such as cancer or diabetes, or are taking medications that suppress the immune system, you should contact your health-care practitioner if you develop a boil (abscess).
There are a number of methods that can be used to prevent the various forms of boils.

Abscessed Tooth

2008-01-29T20:14:00.000-08:00

An abscessed tooth is a painful infection at the root of a tooth or between the gum and a tooth. It's most commonly caused by severe tooth decay. Other causes of tooth abscess are trauma to the tooth, such as when it is broken or chipped, and gingivitis or gum disease.
These problems can cause openings in the tooth enamel, which allows bacteria to infect the center of the tooth (called the pulp). The infection may also spread from the root of the tooth to the bones supporting the tooth.

What are the symptoms of an abscessed tooth?
A toothache that is severe and continuous and results in gnawing or throbbing pain or sharp or shooting pain are common symptoms of an abscessed tooth. Other symptoms may include:

What does an abscessed tooth look like?
Fever
Pain when chewing
Sensitivity of the teeth to hot or cold
Bitter taste in the mouth
Foul smell to the breath
Swollen neck glands
General discomfort, uneasiness, or ill feeling
Redness and swelling of the gums
Swollen area of the upper or lower jaw
An open, draining sore on the side of the gum
If the root of the tooth dies as a result of infection, the toothache may stop. However, this doesn't mean the infection has healed; the infection remains active and continues to spread and destroy tissue. Therefore, if you experience any of the above listed symptoms, it is important to see a dentist even if the pain subsides.

How is an abscessed tooth diagnosed?
Your dentist will probe your teeth with a dental instrument. If you have an abscessed tooth, you will feel pain when the tooth is tapped by your dentist's probe. Your dentist will also ask you if your pain increases when you bite down or when you close your mouth tightly. In addition, your dentist may suspect an abscessed tooth because your gums may be swollen and red.
Your dentist may also take X-rays to look for erosion of the bone around the abscess.

How is an abscessed tooth treated?
Strategies to eliminate the infection, preserve the tooth, and prevent complications are the goals of treatment.
To eliminate infection, the abscess may need to be drained. Achieving drainage may be done through the tooth by a procedure known as a root canal. Root canal surgery may also be recommended to remove any diseased root tissue after the infection has subsided. Then, a crown may be placed over the tooth.
The tooth may also be extracted, allowing drainage through the socket.
Finally, a third way to drain the abscess would be by incision into the swollen gum tissue.
Antibiotics are prescribed to help fight the infection. To relieve the pain and discomfort associated with an abscessed tooth, warm salt-water rinses and over-the-counter pain-reducing medication like ibuprofen (Advil or Motrin) can be used.

Can an abscessed tooth be prevented?
Following good oral hygiene practices can reduce the risk of developing a tooth abscess. Also, if your teeth experience trauma (for example, become loosened or chipped), seek prompt dental attention.

Source: MedicineNet.com http://www.medicinenet.com/abscessed_tooth/article.htm

Cuts, Scrapes and Puncture Wounds

2008-01-29T20:13:00.000-08:00

What is the best way to care for a cut or scrape?
The first step in the care of cuts and scrapes is to stop the bleeding. Most wounds respond to gentle direct pressure with a clean cloth or bandage. Hold the pressure continuously for approximately 10-20 minutes. If this fails to stop the bleeding or if bleeding is rapid you should seek medical assistance.
The next step is to thoroughly clean the wound with soap and water. Remove any foreign material, such as dirt or bits of grass, that might be in the wound and which can lead to infection. You may use tweezers (clean them with alcohol first) to remove foreign material from the wound edges, but do not dig into the wound as this may push bacteria deeper into the wound. You may also gently scrub the wound with a washcloth to remove dirt and debris. Hydrogen peroxide and providone-iodine (Betadine) products may be used to clean the wound initially, but may inhibit wound healing if used long-term.
Cover the area with a bandage (such as gauze or a Band-Aid) to help prevent infection and dirt from getting in the wound. A first aid antibiotic ointment such as Bacitracin or Neosporin can be applied to help prevent infection and keep the wound moist.
Continued care to the wound is also important. Three times a day, wash the area gently with soap and water, apply an antibiotic ointment and cover with a bandage. Also, change the bandage immediately if it gets dirty or wet.

Who should seek medical care for a cut?
If you cannot control the bleeding from a cut, seek medical attention. Any cut that goes beyond the top layer of skin or is deep enough to see into might need stitches (sutures), and should be seen by a healthcare professional as soon as possible. Generally, the sooner sutures are put in, the lower the risk of infection. Ideally, wounds should be repaired within six hours of the injury.
People with suppressed immune systems (including diabetics, cancer patients on chemotherapy, people who take steroid medications, such as prednisone, or people with HIV) are more likely to develop a wound infection and should be seen by a healthcare professional.
Any wound that shows signs of infection should be seen by a healthcare professional (the "What are the signs of a wound infection" section).

What are the signs of a wound infection?
If the wound begins to drain yellow or greenish fluid (pus), or if the skin around the wound becomes red, warm, swollen, or increasingly painful; a wound infection may be present and medical care should be sought. Any red streaking of the skin around the wound may indicate an infection in the system that drains fluid from the tissues, called the lymph system. This infection (lymphangitis) can be serious, especially if it is accompanied by a fever. Prompt medical care should be sought if streaking redness from a wound is noticed.

How are puncture wounds different?
A puncture wound is caused by an object piercing the skin, creating a small hole. Some punctures can be very deep, depending on the source and cause.
Puncture wounds do not usually bleed much, however, treatment is necessary to prevent infection. A puncture wound can cause infection because it forces bacteria and debris deep into the tissue and the wound closes quickly forming an ideal place for bacteria to grow.
For example, if a nail penetrates deep into the foot, it can hit a bone and introduce bacteria into the bone. This risk is especially great if an object has gone through a pair of sneakers. The foam in sneakers can harbor a bacteria (Pseudomonas) that can lead to serious infection in the tissues.
First aid for puncture wounds includes cleaning the area thoroughly with soap and water. These wounds are very difficult to clean out. If the area is swollen, ice can be applied and the area punctured should be elevated. Apply antibiotic ointments (bacitracin or Polysporin) to prevent infection. Cover the wound with a bandage to keep out harmful bacteria and dirt.
Monitor at least daily (ideally three times a day) for signs of infection (the same signs as above in the cuts section). Change the bandage at least daily, or any time it becomes wet or dirty.
Additionally, people with suppressed immune systems or any particularly deep puncture wounds should be seen by a healthcare professional. If it is difficult to remove the puncturing object, it may have penetrated the bone and requires medical care.
Most puncture wounds do not become infected, but if redness, swelling or bleeding persists, see your healthcare professional.
Feet are a particular concern. Wear shoes to minimize the risk of a puncture wound from a nail or glass, especially if you have diabetes or loss of sensation in the feet for any reason.
Additional common causes of puncture wounds can include animal or human bites, or splinters from wood or other plant material, which carry a high risk of infection and should be treated by a physician.

Will I need a tetanus shot?
Most people in the United States have been immunized against tetanus (lockjaw). If you have been immunized, you will need a booster shot if you have not had one within 10 years (if it is a very dirty wound or occurs in a tetanus prone area-you need a booster within five years). If you have never had a tetanus shot, or if your series is incomplete (fewer than three shots), you might need tetanus immunoglobulin, a medication that can prevent lockjaw.
Cuts, Scrapes & Puncture Wounds At A Glance
Washing a cut or scrape with soap and water and keeping it clean and dry is all that is required to care for most wounds.
Cleaning the wound with hydrogen peroxide and iodine is acceptable initially but can delay healing and should be avoided long-term.
Apply antibiotic ointment and keep the wound covered.
Seek medical care within six hours if you think you might need stitches. Any delay can increase the rate of wound infection.
Any puncture wound through sneakers has a high risk of infection and should be seen by your healthcare professional.
Any redness, swelling, increased pain, fever or pus draining from the wound may indicate an infection that requires professional care.

Miscarriage(Spontaneous Abortion)

2008-01-29T20:11:00.000-08:00

What is a miscarriage?
A miscarriage (spontaneous abortion) is any pregnancy that ends spontaneously before the fetus can survive. The World Health Organization defines this unsurvivable state as an embryo or fetus weighing 500 grams or less, which typically corresponds to a fetal age (gestational age) of 20 to 22 weeks or less. Miscarriage occurs in about 15-20% of all recognized pregnancies, and usually occurs before the 13th week of pregnancy. The actual percentage of miscarriages is estimated to be as high as 50% of all pregnancies, since many miscarriages occur without the woman ever having known she was pregnant. Of those miscarriages that occur before the eighth week, 30% have no fetus associated with the sac or placenta. This condition is called blighted ovum, and many women are surprised to learn that there was never an embryo inside the sac.
Some miscarriages occur before women recognize that they are pregnant. About 15% of fertilized eggs are lost before the egg even has a chance to implant (embed itself) in the wall of the uterus. A woman would not generally identify this type of miscarriage. Another 15% of conceptions are lost before eight weeks' gestation. Once fetal heart function is detected in a given pregnancy, the chance of miscarriage is less than 5%.
A woman who may be showing the signs of a possible miscarriage (such as vaginal bleeding) may hear the term "threatened abortion" used to describe her situation.

What causes a miscarriage, and what are the tests for the different causes?
The cause of a miscarriage cannot always be determined. The most common known causes of miscarriage in the first third of pregnancy (1st trimester) are chromosomal abnormalities, collagen vascular disease (such as lupus), diabetes, other hormonal problems infection, and congenital (present at birth) abnormalities of the uterus. Chromosomal abnormalities of the fetus are the most common cause of early miscarriages, including blighted ovum (see above). Each of the causes will be described below.
Chromosomes are microscopic components of every cell in the body that carry all of the genetic material that determine hair color, eye color, and our overall appearance and makeup. These chromosomes duplicate themselves and divide many times during the process of development, and there are numerous points along the way where a problem can occur. Certain genetic abnormalities are known to be more prevalent in couples that experience repeated pregnancy losses. These genetic traits can be screened for by blood tests prior to attempting to become pregnant. Half of the fetal tissue from1st trimester miscarriages contain abnormal chromosomes. This number drops to 20% with 2nd trimester miscarriages. In other words, abnormal chromosomes are more common with 1st trimester than with 2nd trimester miscarriages. First trimester miscarriages are so very common that unless they occur more than once, they are not considered "abnormal" per se. They do not prompt further evaluation unless they occur more than once. In contrast, 2nd trimester miscarriages are more unusual, and therefore may trigger evaluation even after a first occurrence. It is therefore clear that causes of miscarriages seem to vary according to trimester.
Chromosomal abnormalities also become more common with aging, and women over age 35 have a higher rate of miscarriage than younger women. Advancing maternal age is the most significant risk factor for early miscarriage in otherwise healthy women.
Collagen vascular diseases are illnesses in which a person's own immune system attacks their own organs. These diseases can be potentially very serious, either during or between pregnancies. In these diseases, a woman makes antibodies to her own body's tissues. Examples of collagen vascular diseases associated with an increased risk of miscarriage are systemic lupus erythematosus, and antiphospholipid antibody syndrome. Blood tests can confirm the presence of abnormal antibodies and are used to diagnose these conditions.
Diabetes generally can be well-managed during pregnancy, if a woman and her doctor work closely together. However, if the diabetes is insufficiently controlled, not only is the risk of miscarriages higher, but the baby can have major birth defects. Other problems can also occur in relation to diabetes during pregnancy. Good control of blood sugars during pregnancy is very important.
Hormonal factors may be associated with an increased risk of miscarriage, including Cushing's Syndrome, thyroid disease, and polycystic ovary syndrome. It has also been suggested that inadequate function of the corpus luteum in the ovary (which produced progesterone necessary for maintenance of the very early stages of pregnancy) may lead to miscarriage. Termed luteal phase defect, this is a controversial issue, since several studies have not supported the theory of luteal phase defect as a cause of pregnancy loss.
Maternal infection with a large number of different organisms has been associated with an increased risk of miscarriage. Fetal or placental infection by the offending organism then leads to pregnancy loss. Examples of infections that have been associated with miscarriage include infections by Listeria monocytogenes, Toxoplasma gondii, parvovirus B19, rubella, herpes simplex, cytomegalovirus, and lymphocytic choriomeningitis virus. Abnormal anatomy of the uterus can also cause miscarriages. In some women there can be a tissue bridge (uterine septum), that acts like a partial wall dividing the uterine cavity into sections. The septum usually has a very poor blood supply, and is not well suited for placental attachment and growth. Therefore, an embryo implanting on the septum would be at increased risk of miscarriage.
Other structural abnormalities can result from benign growths in the uterus called fibroids. Fibroid tumors (leiomyomata) are benign growths of muscle cells in the uterus. While most fibroid tumors do not cause miscarriages, (in fact, they are a rare cause of infertility), some can interfere with the embryo implantation and the embryo's blood supply, thereby causing miscarriage.
Invasive surgical procedures in the uterus, such as amniocentesis and chorionic villus sampling, also slightly increase the risk of miscarriage.

What does NOT cause miscarriage?
It must be emphasized that exercise, working, and sexual intercourse do not increase the risk of pregnancy loss in routine (uncomplicated) pregnancies. However, in the unusual circumstance where a woman is felt by her physician to be at higher risk of spontaneous abortion, she may be advised to stop work and intercourse. Women with past history of premature delivery and other specific obstetrical conditions might fall under this category.

Are there lifestyle factors associated with miscarriage?
Smoking more than 10 cigarettes per day is associated with an increased risk of pregnancy loss, and some studies have even shown that the risk of miscarriage increases with paternal smoking. Other factors, such as alcohol use, fever, use of nonsteroidal anti-inflammatory drugs around the time of embryo implantation, and caffeine use have all been suggested to increase the risk of miscarriage, although more studies are needed to fully clarify any potential risks associated with these factors. Of course, alcohol is a known teratogen (a chemical that can damage the developing fetus), so pregnant women are advised to abstain from drinking alcoholic beverages.

What are the symptoms of a miscarriage?
Cramping and vaginal bleeding are the most common symptoms noticed with spontaneous abortion. The cramping and bleeding may be very mild, moderate, or severe. There is no particular pattern as to how long the symptoms will last.
Vaginal bleeding during early pregnancy is often referred to as a "threatened abortion." The term "threatened" abortion is used since miscarriage does not always follow vaginal bleeding in early pregnancy, even after repeated episodes or large amounts of bleeding. Studies have shown that 90-96% of pregnancies with fetal cardiac activity that result in vaginal bleeding at 7 to 11 weeks of gestation will result in an ongoing pregnancy.

What will the doctor look for during an examination with suspected miscarriage?
A woman's cervix might have some bloody discharge, but nothing else unusual will be characteristic of threatened abortion. Some women will have mild uterine tenderness during the manual examination of the uterus. The doctor may look to see if the cervix is dilated and will check to see if the uterus is enlarged to an extent appropriate for gestational age of the pregnancy.

How is threatened abortion evaluated?
Pelvic ultrasound is used to visualize fetal heartbeat and to determine whether a pregnancy is still viable. The ultrasound examination can also distinguish between intrauterine and ectopic pregnancies. The doctor may also order blood levels of serial human chorionic gonadotrophin (HCG) to help determine the viability of a pregnancy if the ultrasound examination is not conclusive. During the evaluation, the woman may be advised to rest and avoid sexual intercourse (activity).

What are common terms a woman might hear during evaluation for miscarriage?
Miscarriage (spontaneous abortion) is termination of pregnancy before the fetus is viable (able to survive).
Complete abortion describes spontaneous (not intentionally induced by medication or procedures) passage of all fetal and placental tissue. This is common prior to 12 weeks' gestation.
Incomplete abortion is when some, but not all, the fetal and placental tissue is expelled.
Products of conception refers to the combination of fetal and placental tissue.
Threatened abortion is when a miscarriage does not actually occur, but there is vaginal bleeding from the uterus. The cervix will not be dilated and does not show signs of imminent passage of fetal and placental tissue.
Missed abortion describes a fetal death in the uterus prior to viability, but the products of conception are not passed.
A septic (infectious) abortion is caused by bacterial infection and accompanied by fever, chills, pain, and a pus-containing discharge.

What treatment can a woman expect when she has had a miscarriage?
The central goal of the doctor in this situation will be to try to figure out whether the woman has passed all of the tissue from the fetus and placenta. If she has passed all the tissue, she may only require observation by medical personnel. On the other hand, a woman who has not passed all of the tissue (incomplete abortion) will usually need suction dilation and curettage of the uterus to remove any retained products of the pregnancy. This procedure is done with local anesthesia, and sometimes antibiotics may be prescribed for the woman.

When should a woman receive evaluation for underlying causes of pregnancy loss?
Currently, most practitioners will not initiate an extensive medical evaluation for a single pregnancy loss, since the chance of having a normal pregnancy subsequent to even two consecutive miscarriages is 80-90%. For women with recurrent pregnancy loss, an evaluation will focus on the pattern and history of the prior miscarriages. Three consecutive miscarriages would suggest a woman should receive further evaluation.
Thus, the following tests are considered for women with three consecutive miscarriages. Blood testing can be done to identify chromosomal abnormalities in the couple that could be transmitted to the fetus. The couple can each appear completely normal but still carry chromosomal defects, which, when combined, can be lethal to the embryo. This type of testing is called karyotyping, and it is performed on both members of the couple. A hysterosalpingogram (HSG) can identify anatomical abnormalities within the uterus. Antinuclear antibody, anticardiolipin antibody, VDRL, RPR, and lupus anticoagulant are some of the blood tests used to diagnose autoimmune diseases that can cause recurrent miscarriage. As described above, some of these illnesses will already by apparent to the woman and her doctor, but not all cases. Other antibody tests may be performed as well.

Can something be done to prevent future miscarriages?
The treatment of recurrent miscarriage depends on what is believed to be the underlying cause. This often is not as simple as it sounds. Careful evaluation may turn up several potential factors which alone or together may be responsible for the losses. If a chromosomal problem is found in one or both spouses, then counseling as to future risks is the only option for the couple, since there is currently no method to correct genetic problems.
If a structural problem is encountered with the uterus, surgical correction could be contemplated. It should be emphasized that just because a structural abnormality is found, it does not necessarily mean that it caused the miscarriage. Removal of a fibroid or uterine septum does not guarantee a future successful pregnancy, since the fibroid or uterine septum may not have been the cause of miscarriage in the first place.
Adequate control of diabetes and thyroid disease is critical in trying to prevent recurrent pregnancy loss in women with those conditions. For women with immunologic problems, certain medications are being studied that may be useful in achieving successful pregnancy outcomes. Blood thinners such as aspirin and heparin can, in some cases, prevent further pregnancy loss.
The use of progesterone to increase the blood levels of this hormone is sometimes used for patients with recurrent pregnancy loss, although large-scale controlled studies that confirm the utility of progesterone supplementation have not been carried out. However, many physicians report success with progesterone therapy. Progesterone may be given as vaginal suppositories, or in tablet or gel form. In dealing with recurrent pregnancy loss, it is important to realize that even though apparently obvious problems can be corrected, a miscarriage can still occur. This is not to say that attempts should not be taken to correct identified abnormalities that have been historically associated with miscarriage. However, no treatment can be guaranteed. Even with repeated miscarriages, there is still a very good chance of achieving a successful pregnancy. Early pregnancy and pre-pregnancy counseling can help identify risk factors and allow the practitioner to provide any special care that may be needed.
Miscarriage At A Glance
Spontaneous miscarriage is the loss of a pregnancy that ends spontaneously before the fetus can survive.
Exercise, working, and intercourse do NOT increase risk of miscarriage for women without underlying specific medical conditions that place them at risk.
Causes for miscarriage include genetic abnormalities, infection, medications, hormonal effects, structural abnormality of the uterus, and immune abnormalities.
After an isolated miscarriage, the chance of having a normal term pregnancy in the future is near 90%.
Treatment of recurrent miscarriage is directed toward the underlying cause.

Vaginal Bleeding(Menstruation)

2008-01-29T20:09:00.000-08:00

What is normal vaginal bleeding?
Normal vaginal bleeding is the periodic blood that flows as a discharge from the woman's uterus. Normal vaginal bleeding is also called menorrhea. The process by which menorrhea occurs is called menstruation.
Normal vaginal bleeding occurs as a result of cyclic hormonal changes. The ovaries are the main source of female hormones, which control the development of female body characteristics such as the breasts, body shape, and body hair. The hormones also regulate the menstrual cycle. The ovary, or female gonad, is one of a pair of reproductive glands in women. They are located in the pelvis, one on each side of the uterus. Each ovary is about the size and shape of an almond. The ovaries produce eggs (ova) and female hormones. During each monthly menstrual cycle, an egg is released from one ovary. The egg travels from the ovary through a Fallopian tube to the uterus. Unless pregnancy occurs, the cycle ends with the shedding of part of the inner lining of uterus, which is menstruation. Although it is actually the end of the physical cycle, the first day of menstrual bleeding is designated as "day 1" of the menstrual cycle in medical jargon.
The time of the cycle during which menstruation occurs is referred to as menses. The menses occurs at approximately 4 week intervals, representing the menstrual cycle.
Menarche is the time in a girl's life when menstruation first begins. Menopause is the time in a woman's life when the function of the ovaries ceases. The average age of menopause is 51 years old.

What is abnormal vaginal bleeding?
Abnormal vaginal bleeding is a flow of blood from the vagina that occurs either at the wrong time during the month or in inappropriate amounts. In order to determine whether bleeding is abnormal, and its cause, the doctor must answer 3 questions: Is the woman pregnant? What is the pattern of the bleeding? Is she ovulating?
Every woman who thinks she has an irregular menstrual bleeding pattern should think carefully about the specific characteristics of her vaginal bleeding in order to help her doctor evaluate her particular situation. Her doctor will require the details of her menstrual history. Each category of menstrual disturbance has a particular list of causes, necessary testing, and treatment. Each type of abnormality is discussed individually below.
1. Is the woman having abnormal vaginal bleeding during pregnancy?
Much of the abnormal vaginal bleeding during pregnancy occurs so early in the pregnancy that the woman doesn't realize she is pregnant. Therefore, irregular bleeding that is new may be a sign of very early pregnancy, even before a woman is aware of her condition.
2. What is the pattern of the abnormal vaginal bleeding?
The duration, interval, and amount of vaginal bleeding may suggest what type of abnormality is responsible for the bleeding.
An abnormal duration of menstrual bleeding can be either bleeding for too long of a period (hypermenorrhea), or too short of a period (hypomenorrhea).
The interval of the bleeding can be abnormal in several ways. A woman's menstrual periods can occur too frequently (polymenorrhea) or too seldom (oligomenorrhea). Additionally, the duration can vary excessively from cycle to cycle (metrorrhagia).
The amount (volume) of bleeding can also be abnormal. A woman can either have too much bleeding (menorrhagia) or too little volume (hypomenorrhea).
3. Is the woman ovulating?
Usually, the ovary releases an egg every month in a process called ovulation. Normal ovulation is necessary for regular menstrual periods. There are certain clues that a woman is ovulating normally including regular menstrual intervals, vaginal mucus discharge halfway between menstrual cycles, and monthly symptoms including breast tenderness, fluid retention, menstrual cramps, back pain, and mood changes. If necessary, doctors will order hormone blood tests (progesterone level), daily home body temperature testing, or rarely, a sampling of the lining of the uterus (endometrial sampling) to determine whether or not a woman is ovulating normally.
On the other hand, signs that a woman is not ovulating regularly include prolonged bleeding at irregular intervals after not having a menstrual period for several months, excessively low blood progesterone levels in the 2nd half of the menstrual cycle, and lack of the normal body temperature fluctuation during the time of expected ovulation. Sometimes, a doctor determines that a woman is not ovulating by sampling the lining of the uterus (endometrial sampling).

What conditions cause abnormal vaginal bleeding in women who are ovulating regularly?
Abnormal vaginal bleeding in women who are ovulating regularly, most commonly involve excessive, frequent, irregular, or decreased bleeding. Some of the common conditions that produce each of these symptoms are discussed below.
Excessively heavy menstrual bleeding (menorrhagia)
Excessively heavy menstrual bleeding, called menorrhagia, is menstrual bleeding of greater than 5 tablespoons per month. This condition occurs in about 10% of women. The most common pattern of menorrhagia is excessive bleeding that occurs in regular menstrual cycles and with normal ovulation.
There are several important reasons that menorrhagia should be evaluated by a doctor. First, menorrhagia can cause a woman substantial emotional distress and physical symptoms, such as severe cramping . Second, the blood loss can be so severe that it causes a dangerously lowered blood count (anemia), which can lead to medical complications and symptoms such as dizziness and fainting. Third, there can be dangerous causes of menorrhagia that require more urgent treatment.
Benign (noncancerous) causes of menorrhagia include:
uterine fibroids (benign tumors of smooth muscle tissue),
endometrial polyps (tiny benign growths that protrude into the womb),
adenomyosis,
intrauterine devices (IUD's) ,
underactive thyroid function (hypothyroidism),
an autoimmune disorder called systemic lupus erythematosus , and
blood clotting disorders.
Though not common, menorrhagia can be a sign of endometrial cancer. This situation is more frequent in women who are over the age of 40.
Although there are many causes of menorrhagia, in most women, the specific cause of menorrhagia is not found even after a full medical evaluation. These women are said to have dysfunctional uterine bleeding. Although no specific cause of the abnormal vaginal bleeding is found in women with dysfunctional uterine bleeding, there are treatments available to reduce the severity of the condition.
Sometimes, a woman has a condition that is well known to cause menorrhagia, but another condition may actually be the cause of her menorrhagia. For example, a woman with uterine fibroids may actually be experiencing menorrhagia because she has endometrial hyperplasia. Therefore, a woman should not assume that her heavy bleeding does not require further evaluation without consulting a doctor.
A woman with menorrhagia should visit a gynecologist in certain situations. As explained above, because more serious disorders are more common causes of menorrhagia in women who are over 40 as compared to those under age 40, women over age 40 are often referred to a gynecologist for further evaluation. If a woman persistently bleeds between her periods (intermenstrual bleeding) or medical treatment has not controlled the bleeding, she may then be referred to a gynecologist.
Irregular vaginal bleeding; menstrual periods that are too frequent (polymenorrhea)
Menstrual periods that are abnormally frequent (polymenorrhea) can be caused by certain sexually transmitted diseases (STDs) (such as chlamydia or gonorrhea) that cause inflammation in the uterus. This condition is called pelvic inflammatory disease. Endometriosis is a condition of unknown cause that can lead to pelvic pain and polymenorrhea. Sometimes, the cause of polymenorrhea is unclear, in which case the woman is said to have dysfunctional uterine bleeding.
Menstrual periods at irregular intervals (metrorrhagia)
Irregular menstrual periods (metrorrhagia) can be due to benign growths in the cervix, such as cervical polyps. The cause of these growths is usually not known. Metrorrhagia can also be caused by infections of the uterus (endometritis) and use of birth control pills (oral contraceptives). Sometimes after an evaluation, a woman's doctor might determine that her metrorrhagia does not have an identifiable cause and that further evaluation is not necessary at that time.
Decreased amount or duration of menstrual flow (hypomenorrhea)
An overactive thyroid function (hyperthyroidism) or certain kidney diseases can both cause hypomenorrhea. Oral contraceptive pills can also cause hypomenorrhea. It is important for women to know that lighter, shorter, or even absent menstrual periods as a result of taking oral contraceptive pills does not indicate that the contraceptive effect of the oral contraceptive pills is inadequate. In fact, many women enjoy this "side effect" of oral contraceptives.
Bleeding between menstrual periods (intermenstrual bleeding)
Women who are ovulating normally can experience light bleeding (sometimes referred to as “spotting”) between menstrual periods. Hormonal birth control methods (oral contraceptive pills or patches) as well as IUD use for contraception may sometimes lead to light bleeding between periods. Psychological stress, certain medications such as anticoagulant drugs, and fluctuations in hormone levels may all be causes of light bleeding between periods. Other conditions that cause abnormal menstrual bleeding, or bleeding in women who are not ovulating regularly (see below) can also be the cause of intermenstrual bleeding.

What conditions cause abnormal vaginal bleeding in women who are NOT ovulating regularly or vaginal bleeding after menopause?
Many conditions can interfere with the proper function of female hormones that are necessary for ovulation. For example, many conditions or circumstances may cause oligomenorrhea (reduction in the number of menstrual periods and/or amount of flow than usual) such as:
If a woman has chronic medical illnesses or is under significant medical or emotional stress, can begin to have a loss of her menstrual periods.
Malfunction of a particular part of the brain, called the hypothalamus, can cause oligomenorrhea.
Anorexia nervosa is an eating disorder associated with excessive thinness that causes many serious medical consequences as well as oligomenorrhea.
Polycystic ovarian syndrome (PCO) is a hormonal problem that causes women to have a variety of symptoms that include irregular or no menstrual periods, acne, obesity, infertility, and excessive hair growth; that are detectable with blood tests. For more, please read the Polycystic Ovarian Syndrome article.
The complete loss of ovulation is referred to as anovulation. Since ovulation allows the body to maintain an adequate supply of progesterone, anovulation is a condition in which a woman's hormonal balance is tipped toward too much estrogen and not enough progesterone. The excess estrogen is like a vitamin for the lining of the uterus. The result is that the lining of the uterus becomes too thick, which eventually leads to an increased risk of uterine pre-cancer or uterine cancer over many years. In order to replace progesterone and establish a proper hormonal balance, doctors will prescribe either progesterone to be taken at regular intervals, or an oral contraceptive that contains progesterone. Such treatment dramatically decreases the risk of uterine cancer in women who do not ovulate. Because uterine cancer results from many years of anovulation, any woman with prolonged anovulation needs to be treated to avoid developing uterine cancer.
Women who are postmenopausal should not experience vaginal bleeding. Any vaginal bleeding is considered abnormal in postmenopausal women. Women who are taking combined estrogen and progesterone hormone therapy (HRT) may experience some light, irregular vaginal bleeding during the first six months of treatment. Likewise, postmenopausal women who are taking a cyclic hormone regimen (oral estrogen and a progestin for 10-12 days per month) may experience some vaginal bleeding that is similar to a menstrual period for a few days each month.
Postmenopausal women who experience heavy or prolonged vaginal bleeding while on HRT should always see a doctor to rule-out more serious causes of vaginal bleeding. Less frequent but serious causes of vaginal bleeding in postmenopausal women include endometrial cancer or hyperplasia (overgrowth of the lining tissues of the uterus, which can be precancerous in some cases).

What causes vaginal bleeding during or after sexual intercourse?
Vaginal bleeding may occur during or after sexual intercourse for a number of reasons including:
Injuries to the vaginal wall or introitus (opening to the vagina) during intercourse
Infections (e.g. gonorrhea, chlamydia, yeast infections) are a cause of vaginal bleeding after intercourse.
Lowered estrogen levels in peri-menopausal or postmenopausal women may cause the lining of the vagina to become thinned and easily inflamed or infected, and these changes can be associated with vaginal bleeding after intercourse.
Anatomical lesions, such as tumors or polyps on the cervix or vaginal wall may lead to vaginal bleeding during or after intercourse.
Women who experience vaginal bleeding during or following sexual intercourse should always visit their doctor to determine the cause of the bleeding.

What causes abnormal vaginal bleeding during pregnancy?
Many women have some amount of vaginal bleeding during pregnancy. Some studies show that up to 30% of pregnant women will experience some degree of vaginal bleeding while they are pregnant. Vaginal bleeding during pregnancy is more common with twins and other multiple gestations than with singleton pregnancies (pregnancy with one fetus). Sometimes woman experience a very scant amount of bleeding in the first two weeks of pregnancy, usually around the time of the expected menstrual period. This slight bleeding is sometimes referred to as "implantation bleeding." Doctors do not know for certain what causes this bleeding, but it may occur as a result of the fertilized egg implanting in the uterine wall.
The amount of the bleeding, the stage of pregnancy, and any associated symptoms can all help determine the cause of vaginal bleeding in pregnancy. While vaginal bleeding in pregnancy does not signify a problem with the pregnancy, women who experience bleeding during pregnancy should always be evaluated by a doctor.
Causes of vaginal bleeding in pregnancy include miscarriage, an abnormal location of the placenta, ectopic pregnancy, cervical infection or polyp, and premature labor. Chronic medical conditions and medication use can also be related to vaginal bleeding during pregnancy.

What diagnostic tests are used to evaluate abnormal vaginal bleeding?
A woman who has irregular menstrual periods requires a physical examination with a special emphasis on the thyroid, breast, and pelvic area. During the pelvic examination, the physician attempts to detect cervical polyps or any unusual masses in the uterus. A Pap smear is also done to rule out cervical cancer. While the Pap smear is being obtained, samples might be taken from the cervix to test for the presence of infections such as chlamydia or gonorrhea.
A pregnancy test is routine if the woman is premenopausal. A blood count may be done to rule out a low blood count (anemia) resulting from excessive blood loss. If something in the patient's (or her family's) medical background or physical examination raises a doctor's suspicion, tests to rule-out certain blood clotting disorders may be done. Sometimes, a blood sample will be tested to evaluate thyroid function, liver function, or kidney function abnormalities. A blood test for progesterone levels or daily body temperature charting may be recommended to verify that the woman ovulates. If the doctor suspects that the ovaries are failing, such as with menopause, blood levels of follicle-stimulating hormone (FSH) may be tested. Additional blood hormone tests are done if the doctor suspects PCO or if excessive hair growth is present.
A pelvic ultrasound is often performed based on the woman's medical history and pelvic examination. If a woman does not adequately respond to medical treatment, if she is over age 40, or if she has persistent vaginal bleeding between her periods, a sampling of the lining of her uterus (termed endometrial sampling or endometrial biopsy) is analyzed. Endometrial sampling helps to rule out cancer or precancer in the uterus, or it can confirm a suspicion that a woman is not ovulating.

How is irregular vaginal bleeding treated?
Treatment for irregular vaginal bleeding depends on the underlying cause. After the cause is determined, the doctor decides if treatment is actually necessary. Sometimes, all that is needed is for dangerous causes to be ruled out and to determine that the irregular vaginal bleeding does not bother the woman enough to warrant medication or treatment. If thyroid, liver, kidney, or clotting problems are discovered, treatment is directed toward these conditions.
Medications for treatment of irregular vaginal bleeding depend on the cause. Examples are described below:
If the cause of the bleeding is lack of ovulation (anovulation), doctors may prescribe either progesterone to be taken at regular intervals, or an oral contraceptive, which contains progesterone, to achieve a proper hormonal balance. Such treatment dramatically decreases the risk of uterine cancer in women who do not ovulate.
If the cause of irregular vaginal bleeding is a precancerous change in the lining of the uterus, progesterone medications may be prescribed to reduce the buildup of precancerous uterine lining tissues in an attempt to avoid surgery.
When a woman has been without menses for less than 6 months and is bleeding irregularly, the cause may be menopausal transition. During this transition, a woman is sometimes offered an oral contraceptive to establish a more regular bleeding pattern, to provide contraception until she completes menopause, and to relieve hot flashes. A woman who is found to be menopausal as the cause of her irregular bleeding should also receive menopause counseling. (For more information about menopause treatment, see the Menopause article.)
If the cause of irregular vaginal bleeding is polyps or other benign growths, these are sometimes removed surgically to control bleeding because they cannot be treated with medication.
If the cause of bleeding is infection, antibiotics are necessary. Bleeding during pregnancy requires urgent evaluation by an obstetrician. Endometriosis can be treated with medications and/or surgery (such as laparoscopy). (For more information about the treatment of endometriosis, see the Endometriosis article.)
Sometimes, the cause of excessive bleeding is not apparent after completion of testing (dysfunctional uterine bleeding). In these cases, oral contraceptives can improve cycle control and lessen bleeding.
If bleeding is excessive and cannot be controlled by medication, a surgical procedure called dilation and curettage (D&C) may be necessary. In addition to alleviating the excessive bleeding, the D&C provides additional information that can rule out abnormalities of the lining of the uterus.
Occasionally, a hysterectomy is necessary when hormonal medications cannot control excessive bleeding. However, unless the cause is pre-cancerous or cancerous, this surgery should only be an option after other solutions have been tried.
Many new procedures are being developed to treat certain types of irregular vaginal bleeding. For example, studies are underway to evaluate techniques that selectively block the blood vessels involved in the bleeding. These newer methods may be less complicated options for some patients and as they are further evaluated they will likely become more widely available.
Vaginal Bleeding At A Glance
Normal vaginal bleeding is the periodic blood that flows as a discharge from the woman's uterus.
Normal vaginal bleeding is also called menorrhea. The process by which menorrhea occurs is called menstruation.
In order to determine whether bleeding is abnormal, and its cause, the doctor must answer 3 questions: Is the woman pregnant? What is the pattern of the bleeding? Is she ovulating?
Abnormal vaginal bleeding in women who are ovulating regularly most commonly involves excessive, frequent, irregular, or decreased bleeding.
There are many causes of abnormal vaginal bleeding that are associated with irregular ovulation.
A woman who has irregular menstrual periods requires a physical examination with a special emphasis on the thyroid, breast, and pelvic area.
Treatment for irregular vaginal bleeding depends on the underlying cause. After the cause is determined, the doctor decides if treatment is actually necessary.

Liver Blood Tests

2008-01-29T20:07:00.000-08:00

Introduction
An initial step in detecting liver damage is a simple blood test to determine the presence of certain liver enzymes in the blood. Under normal circumstances, these enzymes reside within the cells of the liver. But when the liver is injured, these enzymes are spilled into the blood stream.
Among the most sensitive and widely used of these liver enzymes are the aminotransferases. They include aspartate aminotransferase (AST or SGOT) and alanine aminotransferase (ALT or SGPT). These enzymes are normally contained within liver cells. If the liver is injured, the liver cells spill the enzymes into blood, raising the enzyme levels in the blood and signaling the liver damage.
What are the aminotransferases?The aminotransferases catalyze chemical reactions in the cells in which an amino group is transferred from a donor molecule to a recipient molecule. Hence, the names "aminotransferases".
Medical terms can sometimes be confusing, as is the case with these enzymes. Another name for aminotransferase is transaminase. The enzyme aspartate aminotransferase (AST) is also known as serum glutamic oxaloacetic transaminase (SGOT); and alanine aminotransferase (ALT) is also known as serum glutamic pyruvic transaminase (SGPT). To put matters briefly, AST = SGOT and ALT = SGPT.
Normally, where are the aminotransferases?AST (SGOT) is normally found in a diversity of tissues including liver, heart, muscle, kidney, and brain. It is released into serum when any one of these tissues is damaged. For example, its level in serum rises with heart attacks and with muscle disorders. It is therefore not a highly specific indicator of liver injury.
ALT (SGPT) is, by contrast, normally found largely in the liver. This is not to say that it is exclusively located in liver but that is where it is most concentrated. It is released into the bloodstream as the result of liver injury. It therefore serves as a fairly specific indicator of liver status.

What are normal levels of AST and ALT?The normal range of values for AST (SGOT) is from 5 to 40 units per liter of serum (the liquid part of the blood).
The normal range of values for ALT (SGPT) is from 7 to 56 units per liter of serum.
What do elevated AST and ALT mean?AST (SGOT) and ALT (SGPT) are sensitive indicators of liver damage from different types of disease. But it must be emphasized that higher-than-normal levels of these liver enzymes should not be automatically equated with liver disease. They may mean liver problems or they may not. The interpretation of elevated AST and ALT levels depends upon the whole clinical picture and so it is best done by doctors experienced in evaluating liver disease.
The precise levels of these enzymes do not correlate well with the extent of liver damage or the prognosis (outlook). Thus, the exact levels of AST (SGOT) and ALT (SGPT) cannot be used to determine the degree of liver disease or predict the future. For example, patients with acute viral hepatitis A may develop very high AST and ALT levels (sometimes in the thousands of units/liter range). But most patients with acute viral hepatitis A recover fully without residual liver disease. For a contrasting example, patients with chronic hepatitis C infection typically have only a little elevation in their AST and ALT levels. Some of these patients may have quietly developed chronic liver disease such as chronic hepatitis and cirrhosis (advanced scarring of the liver).
What liver diseases cause abnormal aminotransferase levels?The highest levels of AST and ALT are found with disorders that cause the death of numerous liver cells (extensive hepatic necrosis). This occurs in such conditions as acute viral hepatitis A or B, pronounced liver damage inflicted by toxins as from an overdose of acetaminophen (brand-name Tylenol), and prolonged collapse of the circulatory system (shock) when the liver is deprived of fresh blood bringing oxygen and nutrients. AST and ALT serum levels in these situations can range anywhere from ten times the upper limits of normal to thousands of units/liter.
Mild to moderate elevations of the liver enzymes are commonplace. They are often unexpectedly encountered on routine blood screening tests in otherwise healthy individuals. The AST and ALT levels in such cases are usually between twice the upper limits of normal and several hundred units/liter.
The most common cause of mild to moderate elevations of these liver enzymes is fatty liver. In the United States, the most frequent cause of fatty liver is alcohol abuse. Other causes of fatty liver include diabetes mellitus and obesity. Chronic hepatitis C is also becoming an important cause of mild to moderate liver enzyme elevations.

What medications cause abnormal aminotransferase levels?A host of medications can cause abnormal liver enzymes levels. Examples include:
Pain relief medications such as aspirin, acetaminophen (Tylenol), ibuprofen (Advil, Motrin), neproxen (Narosyn), diclofenac (Voltaren), and phenybutazone (Butazolidine)
Anti-seizure medications such as phenytoin (Dilantin), valproic acid, carbamazepine (Tegretol), and phenobarbital
Antibiotics such as the tetracyclines, sulfonamides, isoniazid (INH), sulfamethoxazole, trimethoprim, nitrofurantoin, etc.
Cholesterol lowering drugs such as the "statins" (Mevacor, Pravachol, Lipitor, etc.) and niacin
Cardiovascular drugs such as amiodarone (Cordarone), hydralazine, quinidine, etc.
Anti-depressant drugs of the tricyclic type
With drug-induced liver enzyme abnormalities, the enzymes usually normalize weeks to months after stopping the medications.
What are less common causes of abnormal aminotransferase levels?Less common causes of abnormal liver enzymes in the United States include chronic hepatitis B, hemachromatosis, Wilson's disease, alpha-1-antitrypsin deficiency, celiac sprue, Crohn's disease, ulcerative colitis, and autoimmune hepatitis. Though not as common as hepatitis C, hepatitis B can cause chronic liver disease with persistently abnormal liver enzymes.
Hemachromatosis is a genetic (inherited) disorder in which there is excessive absorption of dietary iron leading to accumulation of iron in the liver with resultant inflammation and scarring of the liver.
Wilson's disease is an inherited disorder with excessive accumulation of copper in diverse tissues including the liver and the brain. Copper in liver can lead to chronic liver inflammation, while copper in brain can cause psychiatric and motor disturbances.
Alpha-1-antitrypsin deficiency is an inherited disorder in which the lack of a glycoprotein (carbohydrate-protein complex) called alpha-1-antitrypsin lead to chronic lung disease (emphysema) and to liver disease.
Autoimmune hepatitis results from liver injury brought about by the body's own antibodies and defense systems attacking the liver.
Celiac sprue is a small intestinal illness where a patient has allergy to gluten and develops gas, bloating, diarrhea, and in advanced cases malnutrition. Patietns with celiac sprue can also develop mildly abnormal ALT and AST levels.
Crohn's disease and ulcerative colitis are diseases with chronic inflammation of the intestines. In these patients inflammation of the liver (hepatitis) or bile ducts (primary sclerosing cholangitis) also can occur, causing abnormal liver tests.
Rarely, abnormal liver enzymes can be a sign of cancer in the liver. Cancer arising from liver cells is called hepatocellularcarcinoma or hepatoma. Cancers spreading to the liver from other organs (such as colon, pancreas, stomach, etc) are called metastatic malignancies.

How are healthy people evaluated for mild to moderate rises in aminotransferase levels?Evaluation of healthy patients with abnormal liver enzymes needs to be individualized. A doctor may ask for blood test data from old records for comparison. If no old records are available, the doctor may repeat blood tests in weeks to months to see whether these abnormalities persist. The doctor will search for risk factors for hepatitis B and C including sexual exposures, history of blood transfusions, injectable drug use, and occupational exposure to blood products. A family history of liver disease may raise the possibility of inherited diseases such as hemachromatosis, Wilson's disease, or alpha-1- antitrypsin deficiency.
The pattern of liver enzyme abnormalities can provide useful clues to the cause of the liver disease. For example, the majority of patients with alcoholic liver disease have enzyme levels that are not as high as the levels reached with acute viral hepatitis and the AST tends to be above the ALT. Thus, in alcoholic liver disease, AST is usually under 300 units/liter while the ALT is usually under 100 units/ liter.
If alcohol or medication is responsible for the abnormal liver enzyme levels, stopping alcohol or the medication (under a doctor's supervision only) should bring the enzyme levels to normal or near normal levels in weeks to months. If obesity is suspected as the cause of fatty liver, weight reduction of 5% to 10% should also bring the liver enzyme levels to normal or near normal levels.
If abnormal liver enzymes persist despite abstinence from alcohol, weight reduction and stopping certain suspected drugs, blood tests can be performed to help diagnose treatable liver diseases. The blood can be tested for the presence of hepatitis B and C virus and their related antibodies. Blood levels of iron, iron saturation, and ferritin (another measure of the amount of iron stored in the body) are usually elevated in patients with hemachromatosis. Blood levels of a substance called ceruloplasmin are usually decreased inpatients with Wilson's disease. Blood levels of certain antibodies (anti- nuclear antibody or ANA, anti-smooth muscle antibody, and anti-liver and kidney microsome antibody) are elevated in patients with autoimmune hepatitis.
Ultrasound and CAT scan of the abdomen are sometimes used to exclude tumors in the liver or other conditions such as gallstones or tumors obstructing the ducts that drain the liver.
Liver biopsy is a procedure where a needle is inserted through the skin over the right upper abdomen to obtain a thin strand of liver tissue to be examined under a microscope. The procedure is oftentimes performed after ultrasound study has located the liver. Not everybody with abnormal liver enzymes needs a liver biopsy. The doctor will usually recommend this procedure if 1) the information obtained from the liver biopsy will likely be helpful in planning treatment, 2) the doctor needs to know the extent and severity of liver inflammation/damage, or 3) to evaluate the effectiveness of treatment.
Liver biopsy is most useful in confirming a diagnosis of a potentially treatable condition. These potentially treatable liver diseases include chronic hepatitis B and C, hemachromatosis, Wilson's disease, autoimmune hepatitis, and alpha-1-antitrypsin deficiency.

How about monitoring aminotransferase levels?What is usually most helpful is serial testing of AST (SGOT) and ALT (SGPT) over time to determine whether the levels are going up, staying stable, or going down. For example, patients undergoing treatment for chronic hepatitis C should be monitored with serial liver enzyme tests. Those responding to treatment will experience lowering of liver enzyme levels to normal or near normal levels. Those who develop relapse of hepatitis C after completion of treatment will usually develop abnormal liver enzyme levels again.
What about other liver enzymes?Aside from AST and ALT, there are other enzymes including alkaline phosphatase, 5'-nucleotidase ("5 prime" nucleotidase), and gamma-glutamyltranspeptidase (GGT) that are often tested for liver disease.
We have restricted this consideration of liver enzymes to AST and ALT because they are biochemically related to each other and, more importantly, they are the two most useful liver enzymes.

Ablation Therapy for Arrhythmias

2008-01-29T20:04:00.000-08:00

Heart Disease: Treating Arrhythmias with Ablation
Introduction to treating arrhythmias with ablation
Why do I need ablation therapy?
How should I prepare for catheter ablation?
What can I expect during catheter ablation?
What happens after catheter ablation?
How should I care for the wound site?

Introduction
Ablation is used to treat abnormal heart rhythms. It can be performed both surgically and non-surgically.
Non-surgical ablation is performed in a special lab called the electrophysiology (EP) laboratory. During this non-surgical procedure a catheter is inserted into your heart and then a special machine is used to direct energy to the heart muscle. This energy either "disconnects" or "isolates" the pathway of the abnormal rhythm (depending on the type of ablation). It can also be used to disconnect the electrical pathway between the upper chambers (atria) and the lower chambers (ventricles) of the heart.
For those that require heart surgery, ablation can be performed during coronary artery bypass or valve surgery.
In addition to re-establishing a normal heart rhythm in people with certain arrhythmias, ablation therapy can help control the heart rate in people with rapid arrhythmias, and prevent blood clots and strokes. The maze and surgical pulmonary vein isolation.
There are two types of surgery that can be used to treat the abnormal heart rhythm, atrial fibrillation. These procedures are often combined with other surgical therapies such as bypass surgery, valve repair, or valve replacement. They include:
The Maze procedure. The surgeon makes small cuts in the heart to interrupt the conduction of abnormal impulses and to direct normal sinus impulses to travel to the atrioventricular node (AV node) as they normally should. When the heart heals, scar tissue forms and the abnormal electrical impulses are blocked from traveling through the heart.
Surgical ablation. The surgeon creates controlled lesions on the heart and ultimately scar tissue to block the abnormal electrical impulses from being conducted through the heart and promote the normal conduction of impulses through the proper pathway. This procedure involves a single incision into the left atrium. One of three energy sources may be used to create the scars: radiofrequency, microwave or cryothermy (cold temperature).
The type of ablation performed depends upon the type of arrhythmia and the presence of other heart disease.

Why Do I Need Ablation Therapy?
Doctors recommend ablation therapy to treat:
Atrial fibrillation and atrial flutter
AV Nodal reentry tachycardia (AVNRT)
Accessory pathways
Ventricular tachycardia
How Should I Prepare for Catheter Ablation?
Ask your doctor which medications you should stop and when to stop them. Your doctor may ask you to stop certain medications (such as those that control your heart rate or aspirin products) one to five days before your procedure. If you are diabetic, ask your doctor how you should adjust your diabetic medications.
Do not eat or drink anything after midnight the evening before the procedure. If you must take medications, drink only with a small sip of water.
When you come to the hospital, wear comfortable clothes. You will change into a hospital gown for the procedure. Leave all jewelry and valuables at home.
What Can I Expect During Catheter Ablation?
The procedure will take place in a special room called the EP (electrophysiology) lab. Before the test begins, a nurse will help you get ready. You will lie on a bed and the nurse will start an IV (intravenous) line. This is so the doctors and nurses can give you medications and fluids through your vein during the procedure. You will be given a medication through your IV to help you relax. Depending on the type of ablation you have, you may or may not be awake during your procedure. If you are awake, you will be asked to report any symptoms, answer questions or follow instructions given to you by your doctor. If you are uncomfortable or need anything, please let your nurse know.
The nurse will connect you to several monitors.
After you become drowsy, your groin area will be shaved and you neck, upper chest, arm and groin will be cleansed with an antiseptic solution. Sterile drapes will be placed to cover you from your neck to your feet.
The doctor will numb the insertion site by injecting a medication. You will feel an initial burning sensation, and then it will become numb. Then, several catheters (special wires that can pace the heart and record its electrical activity) will be inserted into a large blood vessel(s) and or artery (in your groin, neck or arm) and advanced to your heart. If you are awake, it is important that you remain still and resist the temptation to raise your head to see what the doctor is doing while the catheters are being placed.
After the catheters are in place, the doctor will look at the monitor to assess your heart's conduction system.
Then, the doctor will perform the ablation procedure.
During traditional ablation, the doctor will use a pacemaker to give the heart electrical impulses to increase your heart rate. You may feel your heart beating faster or stronger when you are paced. If your arrhythmia occurs, the nurse will ask you how you are feeling. It is very important to tell the doctor or nurse the symptoms you feel. The doctor will then move the catheters around your heart to see which area(s) your arrhythmia is coming from. Once the doctor finds the area of your arrhythmia, energy is applied. You may feel some discomfort or a burning sensation in your chest, but you must stay quiet, keep very still and avoid taking deep breaths. If your pain is extreme, tell your nurse or doctor and they may give you more medication to help you.
During pulmonary vein ablation (for atrial fibrillation), the doctor delivers energy through a catheter to the area of the atria that connects to the pulmonary vein (ostia), producing a circular scar. The scar will then block any impulses firing from within the pulmonary vein, thus preventing atrial fibrillation from occurring. The process is repeated to all four pulmonary veins. In some cases, ablation may also be performed to other parts of the heart such as the subclavian veins and coronary sinus. The catheter is a special "cool tip" catheter. Fluid circulates through the catheter to help control the intensity of the temperature. Once the ablation is complete, the electrophysiologist will use monitoring devices to observe the electrical signals in the heart and evaluate if the signals are coming from areas around the pulmonary veins or are originating, as they should, from the sinus node.
The procedure usually takes about four to eight hours, but sometimes longer.

What Happens After Catheter Ablation?
The doctor will remove the catheters from your groin and apply pressure to the site to prevent bleeding. You will be on bed rest for one to six hours. Keep your legs as still as possible during this time to prevent bleeding.
After your procedure, you will be admitted to the hospital. You will be taken to your room and a special monitor, called telemetry, will be used to follow your heart rate and rhythm. Telemetry consists of a small box connected by wires to your chest with sticky electrode patches. The box causes your heart rhythm to be displayed on several monitors on the nursing unit. The nurses will be able to observe your heart rate and rhythm. In most cases, you will be able to go home the next day after the catheter ablation procedure.
You and your family will receive the results of the procedure after the procedure. Your doctor will also discuss when you can resume activities and how often you will need to visit your doctor.
Temporarily, many individuals experience heart palpitations on and off for a few weeks after the procedure. Sometimes you may also feel as if your abnormal heart rhythm is returning, but then it stops. These sensations are normal and you should not be alarmed. But, if you feel as if your abnormal heart rhythm has recurred, call your doctor.
You may be required to take medications to treat or control your abnormal rhythm after the procedure until the scars created in the heart heal. Healing after surgery takes 6-8 weeks.
If you have any other questions, please ask your doctor or nurse. Ask your health care provider how often you will need to go for follow-up appointments.
How Should I Care for the Wound Site?
You will have a small sterile dressing on your wound. It may be removed the next day. Keep the area clean and dry.
Call your doctor if you notice any redness, swelling or drainage at the incision site.

Tummy Tuck ( Abdominoplasty)

2008-01-29T20:02:00.000-08:00

Are sit-ups just not giving you the taut tummy you desire? If you've got a little too much flab or excess skin in your abdomen that won't diminish with diet or exercise, you may want to consider an abdominoplasty, popularly referred to as a "tummy tuck."
This procedure flattens your abdomen by removing extra fat and skin, and tightening muscles in your abdominal wall.
But be cautioned: This is a major surgery, so if you're considering it, take the time to educate yourself, thoroughly analyze your own situation and do not rush to make the final decision.
A tummy tuck should be the last resort for people who have exhausted all other measures, and the procedure should not be used as an alternative to weight loss.
Who Are the Best Candidates For a Tummy Tuck?
A tummy tuck is suitable for both men and women who are in good general health overall.
It should not be confused with a liposuction (the cosmetic surgery used to remove fat deposits), although your surgeon may elect to perform liposuction as part of a tummy tuck.
Women who have muscles and skin stretched by multiple pregnancies may find the procedure useful to tighten those muscles and reduce that skin. A tummy tuck is also an alternative for men or women who were obese at one point in their lives and still have excessive fat deposits or loose skin in the abdominal area.

Who Should Not Consider a Tummy Tuck?
If you're a woman who is still planning to have children, then you may want to postpone a tummy tuck until you're through bearing children. Here's why: During surgery, your vertical muscles are tightened. Future pregnancies can separate these muscles.
Are you still planning to lose a lot of weight? Then you do not want to consider a tummy tuck.
It's important to note that a tummy tuck can cause prominent, permanent scarring. If this is something you don't want, you may want to reconsider. Your doctor will discuss all these options with you when you go for the consultation.
How a Tummy Tuck is Done
Depending on your desired results, this surgery can take anywhere from one to five hours. The complexity of your particular situation also will determine whether you have it completed as an in-patient or outpatient procedure.
You will receive general anesthesia, which will put you to sleep during the operation. It's important to have someone with you who can drive you home. If you live alone, you also will need someone to stay with you at least the first night after the surgery.
There are two options for a tummy tuck. You and your surgeon will discuss your desired results, and he or she will determine the appropriate procedure during your consultation.
Complete abdominoplasty. Your abdomen will be cut from hipbone to hipbone in this procedure, the option for those patients who require the most correction. The incision will be made low, at about the same level as your pubic hair.
Your surgeon will then manipulate and contour the skin, tissue and muscle as needed. Your belly button will have a new opening if you undergo this procedure, because it's necessary to free your navel from surrounding tissue. Drainage tubes may be placed under your skin and these will be removed in a few days as your surgeon sees fit.
Partial or mini abdominoplasty. Mini-abdominoplasties are often performed on patients whose fat deposits are located below the navel and require shorter incisions.
During this procedure, your belly button most likely will not be moved. Your skin will be separated between the line of incision and your belly button. This type of surgery may also be performed with an endoscope (small camera on the end of a tube). The procedure may only take up to two hours, again, depending on your own personal situation and the complexity of your needs.

How to Prepare For Tummy Tuck Surgery
If you smoke, you will have to stop for a certain period as determined by your doctor. It is not enough to just cut down on smoking. You must stop completely for at least two weeks prior to surgery and for two weeks after. Smoking can increase the risk of complications and delay healing.
Make sure you eat well-balanced, complete meals and do not try to diet excessively before the surgery. Proper nutrition plays a key role in healing properly.
If you take certain medications, your surgeon may instruct you to stop taking these for a certain period before and after the surgery. Your surgeon will determine this as part of your pre-operative consultation.
Before undergoing the surgery, you'll need to get your home ready for your post-operative care. Your home recovery area should include:
Plenty of ice packs
Supply of loose, comfortable clothing that can be taken on and off very easily
Petroleum jelly for incision sites
Telephone within reaching distance
Hand-held shower head and bathroom chairYou know yourself best, so make sure you set up the safest, most comfortable recovery area before you undergo the surgery to meet your personal needs.
What Are the Complications and Side Effects of Tummy Tuck Surgery?
As expected, you will have pain and swelling in the days following surgery. Your doctor can prescribe a painkiller if needed and will instruct you on how to best handle the pain. Soreness may last for several weeks or months.
You may also experience numbness, bruising and overall tiredness for that same time period.
As with any surgery, there are risks. Remember, this surgery affects a very crucial part of your body. Though they're rare, complications can include infection, bleeding under the skin flap or blood clots. You may carry an increased risk of complications if you have poor circulation, diabetes or heart, lung or liver disease.
You may experience insufficient healing, which can cause more significant scarring or loss of skin. If you do heal poorly, you may require a second surgery.
As we mentioned before, the scars from a tummy tuck are fairly prominent and though they may fade slightly, they will never completely disappear. Your surgeon may recommend certain creams or ointments to use after you've completely healed to help with the scars.

Taking Care of Yourself After Surgery
Whether you're having a partial or complete tummy tuck, your incision site will be stitched and bandaged. It's very important that you follow all your surgeon's instructions on how to care for the bandage in the days following surgery. The bandage used will be a firm, elastic band that promotes proper healing. Your surgeon will also instruct you on how to best position yourself while sitting or lying down to help ease pain.
If you are an exceptionally physically active person, beware: You will have to severely limit strenuous exercise for at least six weeks. Your doctor will advise you on this as you go through the process. You may need to take up to one month off of work after the surgery to ensure proper recovery. Again, your doctor will help you determine this based on your personal situation.
Return to Living
Generally, most people love the new look after they've undergone this procedure. However, you may not feel like your normal self for months after the surgery. You've gone through a tremendous amount to make this happen, both emotionally and physically, and it's very important that you follow proper diet and exercise to maintain your new look.
Does Insurance Cover a Tummy Tuck?
Be warned: Insurance carriers generally do not cover elective, cosmetic surgery. But, your carrier may cover a certain percentage if you have a hernia that will be corrected through the procedure, or your anterior muscles are abnormally spread.
It's extremely important that you begin communicating with your insurance company early on, and that you discuss your insurance concerns with your surgeon. In most cases, your surgeon will write a letter to your insurance carrier, making the case for medical necessity, if it applies to you.
It's also very important to realize that insurance may only cover certain portions of the surgery, so make sure you get details. With any cosmetic surgery, this may affect future insurance coverage for you and your premiums may increase.

Abdominal Pain

2008-01-29T20:00:00.000-08:00

What is abdominal pain? Abdominal pain is pain that is felt in the abdomen. The abdomen is an anatomical area that is bounded by the lower margin of the ribs above, the pelvic bone (pubic ramus) below, and the flanks on each side. Although abdominal pain can arise from the tissues of the abdominal wall that surround the abdominal cavity (i.e., skin and abdominal wall muscles), the term abdominal pain generally is used to describe pain originating from organs within the abdominal cavity (i.e., beneath the skin and muscles). These organs include the stomach, small intestine, colon, liver, gallbladder, and pancreas. Occasionally, pain may be felt in the abdomen even though it is arising from organs that are close to but not within the abdominal cavity, for example, the lower lungs, the kidneys, and the uterus or ovaries. This latter type of pain is called "referred" pain because the pain, though originating outside the abdomen, is being referred to (felt) in the abdominal area.
What causes abdominal pain?Abdominal pain is caused by inflammation (e.g., appendicitis, diverticulitis, colitis ), by stretching or distention of an organ (e.g., obstruction of the intestine, blockage of a bile duct by gallstones, swelling of the liver with hepatitis), or by loss of the supply of blood to an organ (e.g., ischemic colitis). To complicate matters, however, abdominal pain also can occur without inflammation, distention or loss of blood supply. An important example of this latter type of pain is the irritable bowel syndrome (IBS). It is not clear what causes the abdominal pain in IBS, but it is believed to be due either to abnormal contractions of the intestinal muscles (e.g., spasm) or abnormally sensitive nerves within the intestines that give rise to painful sensations inappropriately (visceral hyper-sensitivity).

How is the cause of abdominal pain diagnosed?Doctors determine the cause of abdominal pain by relying on 1) characteristics of the pain, 2) findings on physical examination, 3) laboratory, radiological, and endoscopic testing, and 4) surgery.
Characteristics of the pain The following information, obtained by taking a patient's history, is important in helping doctors determine the cause of pain:
The way the pain begins. For example, abdominal pain that comes on suddenly suggests a sudden event, for example, the interruption of the supply of blood to the colon (ischemia) or obstruction of the bile duct by a gallstone (biliary colic).
The location of the pain. Appendicitis typically causes pain in the right lower abdomen, the usual location of the appendix. Diverticulitis typically causes pain in the left lower abdomen where most colonic diverticuli are located. Pain from the gallbladder (biliary colic or cholecystitis) typically is felt in the right upper abdomen where the gallbladder is located.
The pattern of the pain. Obstruction of the intestine initially causes waves of crampy abdominal pain due to contractions of the intestinal muscles and distention of the intestine. Obstruction of the bile ducts by gallstones typically causes steady (constant) upper abdominal pain that lasts between 30 minutes and several hours. Acute pancreatitis typically causes severe, unrelenting, steady pain in the upper abdomen and upper back. The pain of acute appendicitis initially may start near the umbilicus, but as the inflammation progresses, the pain moves to the right lower abdomen. The character of pain may change over time. For example, obstruction of the bile ducts sometimes progresses to inflammation of the gallbladder with or without infection (acute cholecystitis). When this happens, the characteristics of the pain change to those of inflammatory pain. (See below.)
The duration of the pain. The pain of IBS typically waxes and wanes over months or years and may last for decades. Biliary colic lasts no more than several hours. The pain of pancreatitis lasts one or more days.
What makes the pain worse. Pain due to inflammation (appendicitis, diverticulitis, cholecystitis, pancreatitis) typically is aggravated by sneezing, coughing or any jarring motion. Patients with inflammation as the cause of their pain prefer to lie still.
What relieves the pain. The pain of IBS and constipation often is relieved temporarily by bowel movements. Pain due to obstruction of the stomach or upper small intestine may be relieved temporarily by vomiting which reduces the distention that is caused by the obstruction. Eating or taking antacids may temporarily relieve the pain of ulcers of the stomach or duodenum because both food and antacids neutralize (counter) the acid that is responsible for irritating the ulcers and causing the pain.
Associated signs and symptoms. The presence of fever suggests inflammation. Diarrhea or rectal bleeding suggests an intestinal cause of the pain. The presence of fever and diarrhea suggest inflammation of the intestines that may be infectious or non-infectious (ulcerative colitis or Crohn's disease).
Physical examinationExamining the patient will provide the doctor with additional clues to the cause of abdominal pain. The doctor will determine:
The presence of sounds coming from the intestines that occur when there is obstruction of the intestines,
The presence of signs of inflammation (by special maneuvers during the examination),
The location of any tenderness
The presence of a mass within the abdomen that suggests a tumor or abscess (a collection of infected pus)
The presence of blood in the stool that may signify an intestinal problem such as an ulcer, colon cancer, colitis, or ischemia.
For example, finding tenderness and signs of inflammation in the left lower abdomen often means that diverticulitis is present, while finding a tender (inflamed) mass in the same area may mean that the inflammation has progressed and that an abscess has formed. Finding tenderness and signs of inflammation in the right lower abdomen often means that appendicitis is present, while finding a tender mass in the same area may mean that appendiceal inflammation has progressed and become an abscess. Inflammation in the right lower abdomen, with or without a mass, also may be found in Crohn's disease. (Crohn's disease most commonly affects the last part of the small intestine, usually located in the right lower abdomen.) A mass without signs of inflammation may mean that a cancer is present.
Tests While the history and physical examination are vitally important in determining the cause of abdominal pain, testing often is necessary to determine the cause. Laboratory tests. Laboratory tests such as the complete blood count (CBC), liver enzymes, pancreatic enzymes (amylase and lipase), and urinalysis are frequently performed in the evaluation of abdominal pain. An elevated white count suggests inflammation or infection (as with appendicitis, pancreatitis, diverticulitis, or colitis). Amylase and lipase (enzymes produced by the pancreas) commonly are elevated in pancreatitis. Liver enzymes may be elevated with gallstone attacks. Blood in the urine suggests kidney stones. When there is diarrhea, white blood cells in the stool suggest intestinal inflammation.
Plain x-rays of the abdomen. Plain abdominal x-rays of the abdomen also are referred to as a KUB (because they include the Kidney, Ureter, and Bladder). The KUB may show enlarged loops of intestines filled with copious amounts of fluid and air when there is intestinal obstruction. Patients with a perforated ulcer may have air escape from the stomach into the abdominal cavity. The escaped air often can be seen on a KUB on the underside of the diaphragm. Sometimes a KUB may reveal a calcified kidney stone that has passed into the ureter and resulted in referred abdominal pain
Radiographic studies. Abdominal ultrasound is useful in diagnosing gallstones, cholecystitis appendicitis, or ruptured ovarian cysts as the cause of the pain. Computerized tomography (CT) of the abdomen is useful in diagnosing pancreatitis, pancreatic cancer, appendicitis, and diverticulitis, as well as in diagnosing abscesses in the abdomen. Special CT scans of the abdominal blood vessels can detect diseases of the arteries that block the flow of blood to the abdominal organs. Magnetic resonance imaging (MRI) is useful in diagnosing gallstones that have passed out of the gallbladder and are obstructing the bile ducts. Barium x-rays of the stomach and the intestines (upper gastrointestinal series or UGI with a small bowel follow-through) can be helpful in diagnosing ulcers, inflammation, and blockage in the intestines. Computerized tomography (CT) of the small intestine can be helpful in diagnosing diseases in the small bowel such as Crohn's disease. Capsule enteroscopy, a small camera the size of a pill swallowed by the patient, can take pictures of the entire small bowel and transmit the pictures onto a portable receiver. The small bowel images can be downloaded from the receiver onto a computer to be inspected by a doctor later. Capsule enteroscopy can be helpful in diagnosing Crohn's disease, small bowel tumors, and bleeding lesions not seen on x-rays or CT scans
Endoscopic procedures. Esophagogastroduodenoscopy or EGD is useful for detecting ulcers, gastritis (inflammation of the stomach), or stomach cancer. Colonoscopy or flexible sigmoidoscopy is useful for diagnosing infectious colitis, ulcerative colitis, or colon cancer. Endoscopic ultrasound (EUS) is useful for diagnosing pancreatic cancer or gallstones if the standard ultrasound or CT or MRI scans fail to detect them.
Surgery. Sometimes, diagnosis requires examination of the abdominal cavity either by laparoscopy or surgery.

Special problem in irritable bowel syndrome (IBS) of diagnosing the cause of abdominal pain As previously discussed, the pain of IBS is due either to abnormal intestinal muscle contractions or visceral hypersensitivity. Generally, abnormal muscle contractions and visceral hypersensitivity are much more difficult to diagnose than other diseases causing abdominal pain, particularly since there are no typical abnormalities of the physical examination or the usual tests. The diagnosis is based on the history (typical symptoms) and the absence of other causes of abdominal pain.
Why can diagnosis of the cause of abdominal pain be difficult? Modern advances in technology have greatly improved the accuracy, speed, and ease of establishing the cause of abdominal pain, but significant challenges remain. There are many reasons why diagnosing the cause of abdominal pain can be difficult. They are:
Symptoms may be atypical. For example, the pain of appendicitis sometimes is located in the right upper abdomen, and the pain of diverticulitis on the right side. Elderly patients and patients taking corticosteroids may have little or no pain and tenderness when there is inflammation, for example, cholecystitis or diverticulitis. This occurs because corticosteroids reduce the inflammation.
Tests are not always abnormal. Ultrasound examinations can miss gallstones, particularly small ones. CT scans may fail to show pancreatic cancer, particularly small ones. The KUB can miss the signs of intestinal obstruction or stomach perforation. Ultrasounds and CT scans may fail to demonstrate appendicitis or even abscesses, particularly if the abscesses are small. The CBC and other blood tests may be normal despite severe infection or inflammation, particularly in patients receiving corticosteroids.
Diseases can mimic one another. IBS symptoms can mimic bowel obstruction, cancer, ulcer, gallbladder attacks or even appendicitis. Crohn's disease can mimic appendicitis. Infection of the right kidney can mimic acute cholecystitis. A ruptured right ovarian cyst can mimic appendicitis, while a ruptured left ovarian cyst can mimic diverticulitis. Kidney stones can mimic appendicitis or diverticulitis.
The characteristics of the pain may change. Examples discussed previously include the extension of the inflammation of pancreatitis to involve the entire abdomen and the progression of biliary colic to cholecystitis.

How can I help my doctor to determine the cause of my abdominal pain? Before the visit, prepare written lists of:
Medications you are currently taking, including herbs, vitamins, minerals, and food supplements.
Your allergies
The medications that you have tried for your abdominal pain.
Important medical illnesses that you have such as diabetes, heart disease, etc..
Previous surgeries such as appendectomy, hernia repairs, gallbladder removal, hysterectomy, etc..
Previous procedures such as colonoscopy, laparoscopy, CAT scan, ultrasound, upper or lower barium x-rays, etc..
Previous hospitalizations
Ill family members who have symptoms similar to yours.
Family members with gastrointestinal diseases (involving the esophagus, stomach, intestines, liver, pancreas, and gallbladder).
Be candid with your doctor about your prior and current alcohol consumption and smoking habits, any history of chemical dependence.
Be prepared to tell your doctor:
When the pain first started
If there were previous episodes of similar pain.
How frequently episodes of pain occur
If each episode of pain starts gradually or suddenly
The severity of the pain
What causes the pain and what makes the pain worse
What relieves the pain
The characteristics of the pain. Is the pain sharp or dull, burning or pressure like? Is the pain jabbing and fleeting, steady and unrelenting or crampy (coming and going)?
If the pain is associated with fever, chills, sweats, diarrhea, weight loss, constipation, rectal bleeding, loss of appetite, nausea or loss of energy?
After the visit, do not expect an instant cure or immediate diagnosis, and remember:
Multiple office visits and tests (blood tests, radiographic studies, or endoscopic procedures) are often necessary to establish the diagnosis and/or to exclude serious illnesses.
Doctors may start you on a medication before a firm diagnosis is made. Your response (or lack of response) to that medication sometimes may provide your doctor with valuable clues as to the cause of your abdominal pain. Therefore, it is important for you to take the medication that is prescribed.
Notify your doctor if your symptoms are getting worse, if medications are not working, or if you think you are having side effects from the medication.
Call your doctor for test results. Never assume that "the test must be fine since my doctor never called."
Do not self medicate (including herbs, supplements) without discussing with your doctor.
Even the best physician never bats 1000. Do not hesitate to openly discuss with your doctor referrals for second or third opinions if diagnosis cannot be firmly established and pain persists.
Self education is important, but make sure what you read came from credible sources.
Abdominal Pain At A Glance
Abdominal pain is pain that is felt in the abdomen.
Abdominal pain comes from organs within the abdomen or organs adjacent to the abdomen.
Abdominal pain is caused by inflammation, distention of an organ, or by loss of the blood supply to an organ. Abdominal pain in IBS may be caused by contraction of the intestinal muscles or hyper-sensitivity.
The cause of abdominal pain is diagnosed on the basis of the characteristics of the pain, physical examination, and testing. Occasionally, surgery is necessary for diagnosis.
The diagnosis of the cause of abdominal pain is challenging because characteristics of the pain may be atypical, tests are not always abnormal, diseases causing pain may mimic each other, and the characteristics of the pain may change over time

Abdominal Aortic Aneurysm

2008-01-29T19:56:00.000-08:00

What is an aneurysm?An aneurysm is an area of a localized widening (dilation) of a blood vessel. (The word "aneurysm" is borrowed from the Greek "aneurysma" meaning "a widening").
What is an aortic aneurysm?An aortic aneurysm involves the aorta, one of the large arteries that carries blood from the heart to the rest of the body. The aorta bulges at the site of the aneurysm like a weak spot on an old worn tire.
What are the thoracic and abdominal aorta?The aorta is first called the thoracic aorta as it leaves the heart, ascends, arches, and descends through the chest until it reaches the diaphragm (the partition between the thorax and abdomen). The aorta is then called the abdominal aorta after it has passed the diaphragm and continues down the abdomen. The abdominal aorta ends where it splits to form the two iliac arteries that go to the legs.
Where do aortic aneurysms tend to develop?Aortic aneurysms can develop anywhere along the length of the aorta. The majority, however, are located along the abdominal aorta. Most (about 90%) of abdominal aneurysms are located below the level of the renal arteries, the vessels that leave the aorta to go to the kidneys. About two-thirds of abdominal aneurysms are not limited to just the aorta but extend from the aorta into one or both of the iliac arteries.

What shape are most aortic aneurysms?Most aortic aneurysms are fusiform. They are shaped like a spindle ("fusus" means spindle in Latin) with widening all around the circumference of the aorta. (Saccular aneurysms just involve a portion of the aortic wall with a localized out pocketing).
What's inside an aortic aneurysm?The inside walls of aneurysms are often lined with a laminated blood clot that is layered like a piece of plywood.
Who is most likely to have an abdominal aortic aneurysm?Abdominal aortic aneurysms are most common after age 60. Males are 5 times more likely than females to be affected. This means men over 60 are at highest risk to develop an abdominal aortic aneurysm. Approximately 5% of men over age 60 develop an abdominal aortic aneurysm.
What is the most common cause of aortic aneurysms? The most common cause of aortic aneurysms is "hardening of the arteries" called arteriosclerosis. At least 80% of aortic aneurysms are from arteriosclerosis. The arteriosclerosis can weaken the aortic wall and the pressure of the blood being pumped through the aorta causes expansion at the site of weakness.
What are other causes of aortic aneurysms?
Other causes of aortic aneurysms include:
Cigarette smoking - cigarette smoking not only increases the risk of developing an abdominal aortic aneurysm, the chance of aneurysm rupture (a life threatening complication of abdominal aneurysm) is also more common among active smokers.
High blood pressure
High serum cholesterol
Diabetes mellitus
Genetic - There is a familial tendency to developing abdominal aortic aneurysms. Individuals with first-degree relatives having abdominal aortic aneurysms have a higher risk of developing abdominal aortic aneurysm than the general population. They also tend to develop the aneurysms at younger ages and have a higher tendency to suffer aneurysm rupture than individuals without family history.
There are also rare inheritable genetic diseases of connective tissue (tissue that make up the wall of the aorta) such as Ehlers-Danlos syndrome and Marfan's syndrome that can lead to the development of aortic aneurysms.
Post-traumatic: After physical trauma to the aorta.
Arteritis (inflammation of blood vessels) as occurs in Takayasu disease, giant cell arteritis, and relapsing polychondritis.
Mycotic (fungal) infection that may be associated with immunodeficiency, IV drug abuse, heart valve surgery.

What are the symptoms of an abdominal aortic aneurysm?
Most abdominal aortic aneurysms produce no symptoms (they are asymptomatic). They are often incidentally discovered when abdominal ultrasounds and/or CAT scan studies are ordered for other conditions. When they produce symptoms, the most common symptom is pain. The pain typically has a deep quality as if it is boring into the person. It is felt most prominently in the lower back region and lower abdomen. The pain is usually steady but may be relieved by changing position. The person may also become aware of an abnormally prominent abdominal pulsation.
Abdominal aortic aneurysm can remain asymptomatic or produce mild to moderate symptoms for years. However, a rapidly expanding abdominal aneurysm can cause sudden onset of severe, steady, and worsening lower back and lower abdominal pain. A rapidly expanding aneurysm is also at imminent risk of rupture. Actual rupture of an abdominal aneurysm can cause sudden onset of back and abdominal pain, sometimes associated with abdominal distension, a pulsating abdominal mass, and even shock (severe low blood pressure due to massive blood loss).
How is an abdominal aortic aneurysm diagnosed clinically?
Careful feeling of the abdomen by the doctor may reveal the abnormally wide pulsation of the abdominal aorta. This is characteristically felt on both sides of the aorta which is in the midline of the abdomen. Note that even large aneurysms can be very difficult to detect on physical examination in overweight people. Aneurysms on the verge of rupture and that are rapidly enlarging, are often tender.
What tests help in the diagnosis of an abdominal aortic aneurysm?
In about 90% of the cases, X-rays of the abdomen show calcium deposits in the aneurysm wall. But plain x-rays of the abdomen cannot determine the size and the extent of the aneurysm. Ultrasonography usually gives a clear picture of the size of an aneurysm. Ultrasound has about 98% accuracy in measuring the size of the aneurysm, and is safe and noninvasive. But ultrasound cannot accurately define the extent of the aneurysm and is inadequate for surgical repair planning. CT scanning of the abdomen, particularly with intravenous contrast dye, can be highly accurate in determining the size and extent of the aneurysm, and its relation to the renal arteries. But CAT scan requires the use of radiation and carries a risk of dye reaction (such as worsening of kidney function) when intravenous dye is used with CAT scanning. In patients with kidney diseases, the doctor may order a MRA (magnetic resonance angiography), which is a study of the aorta and the other arteries using MRI scanning. Both CAT scan and MRA are highly accurate in determining aneurysm size and extent, and are often sufficient in providing enough information in surgery planning. Only in selected special situations where abdominal aortography has to be performed before surgery. Aortography shows the origin of the major blood vessels arising from the aorta and reveals the size and extent of any aneurysm. But aortography is invasive and requires the insertion of a catheter through the groin into the aorta and use of contrast dye administered into the aorta.

What is the natural history of abdominal aortic aneurysms?
The natural history of abdominal aortic aneurysms depends on their size and the speed of expansion. Rupture of aneurysms is uncommon when they are less than 5.5 cm wide and are expanding slowly. Rupture is far more common in aneurysms that are over 5.5 cm wide and are expanding rapidly(>0.5 cm/year). Surgical repair is therefore usually recommended for aneurysms over 5.5 cm wide.
What are the complications with an abdominal aortic aneurysm?
Rupture is a feared problem. Rupture of an abdominal aneurysm is a catastrophe. It is highly lethal and is usually preceded by excruciating pain in the lower abdomen and back, with tenderness of the aneurysm. Rupture of an abdominal aneurysm causes profuse bleeding and leads to shock. Death may rapidly follow. Half of all persons with untreated abdominal aortic aneurysms die of rupture within 5 years. Abdominal aortic aneurysms are the 13th leading cause of death in the U.S.
Peripheral embolization of clot within the aneurysm can occur when a piece of clot comes loose and travels further out in the arterial system. This clot fragment can lodge in a smaller artery and block the flow of blood. Infection of aneurysms can occur from turbulent blood flow from the rough inner surface of the affected aorta.
How are abdominal aortic aneurysms repaired?
The goal of surgical treatment of abdominal aortic aneurysm is to prevent aneurysm rupture. Traditionally, repair of aortic aneurysms has been surgical. The surgery has usually consisted of opening the abdomen, removing (excising) the aneurysm, and sewing a synthetic (Dacron) tube in its place.
More recently, "minimally invasive" procedures have been devised using stent grafts that can be guided to the site of the aneurysm without the need to cut open the abdomen. The first stent graft was installed in 1991 by Dr. Juan Parodi in Argentina.
A stent graft developed by Dr. Thomas Fogarty at Stanford is a Dacron tube inside a collapsed metal-mesh cylinder. To install the stent, a small incision is made in the thigh to gain access to the femoral artery. The stent, about 6 inches (15 cm) long, is guided inside a long plastic capsule through the arteries to the lower aorta. Once the stent is in place, the holding capsule is removed. Activated by heat, the stent expands like a spring and becomes anchored to the artery wall. The by-passed aneurysm then is shielded from the blood flow and typically shrinks over time. According to a U.S. national multi-center study reported by Dr. Christopher Zari from Stanford in 1998, the "minimally invasive" installation of the stent graft carries a lower rate of complications and permits people to get back on their feet faster than traditional open surgery.

What is done if an abdominal aortic aneurysm threatens to rupture?
Threatened rupture of abdominal aneurysms is a surgical emergency. The operative risk for a ruptured aneurysm is about 50%. If kidney failure occurs after surgery, the prognosis (outlook) is particularly poor.
What is the medical management (non-surgical management) of abdominal aortic aneurysm?
For patients who are not surgical candidates (for example for patients with aneurysm smaller than 5 cm); medical treatment to prevent aneurysm expansion and rupture include:
Stopping cigarette smoking
Controlling high blood pressure
Lowering high blood cholesterol
Some doctors may consider medications called beta blockers, such as propanolol (Inderal), which has been shown in animal and some human studies to slow the rate of aneurysm expansion
Close monitoring of the aneurysm size with ultrasound or CAT scan every 6 to 12 months (sooner in high risk patients)
Abdominal Aortic Aneurysm At A Glance
An aneurysm is an abnormal area of localized widening of a blood vessel.
The aorta bulges at the site of an aneurysm like a weak spot on a worn tire.
Aortic aneurysms are typically spindle-shaped and involve the aorta below the arteries to the kidneys.
Five percent of men over 60 develop an abdominal aortic aneurysms.
The most common cause of an aneurysm is arteriosclerosis.
Abdominal aortic aneurysms often do not cause symptoms. If they do, they may cause deep boring pain in the lower back or abnormally prominent abdominal pulsation.
X-rays of the abdomen and other radiologic tests can be used in diagnosing an aneurysm.
Rupture of an aortic aneurysm is a catastrophe.
Repair of the aneurysm can be done by surgery or by installation of a stent graft.

Rheumatoid Arthritis

2008-01-26T04:44:00.000-08:00

What is rheumatoid arthritis?

Rheumatoid arthritis is an autoimmune disease that causes chronic inflammation of the joints. Rheumatoid arthritis can also cause inflammation of the tissue around the joints, as well as other organs in the body. Autoimmune diseases are illnesses that occur when the body tissues are mistakenly attacked by its own immune system. The immune system is a complex organization of cells and antibodies designed normally to "seek and destroy" invaders of the body, particularly infections. Patients with autoimmune diseases have antibodies in their blood that target their own body tissues, where they can be associated with inflammation. Because it can affect multiple other organs of the body, rheumatoid arthritis is referred to as a systemic illness and is sometimes called rheumatoid disease.

While rheumatoid arthritis is a chronic illness, meaning it can last for years, patients may experience long periods without symptoms. Typically, however, rheumatoid arthritis is a progressive illness that has the potential to cause joint destruction and functional disability.

A joint is where two bones meet to allow movement of body parts. Arthritis means joint inflammation. The joint inflammation of rheumatoid arthritis causes swelling, pain, stiffness, and redness in the joints. The inflammation of rheumatoid disease can also occur in tissues around the joints, such as the tendons, ligaments, and muscles.

In some patients with rheumatoid arthritis, chronic inflammation leads to the destruction of the cartilage, bone and ligaments causing deformity of the joints. Damage to the joints can occur early in the disease and be progressive. Moreover, studies have shown that the progressive damage to the joints does not necessarily correlate with the degree of pain, stiffness, or swelling present in the joints.

Rheumatoid arthritis is a common rheumatic disease, affecting more than two million people in the United States. The disease is three times more common in women as in men. It afflicts people of all races equally. The disease can begin at any age, but most often starts after age forty and before sixty. In some families, multiple members can be affected, suggesting a genetic basis for the disorder.

What causes rheumatoid arthritis?

The cause of rheumatoid arthritis is unknown. Even though infectious agents such as viruses, bacteria, and fungi have long been suspected, none has been proven as the cause. The cause of rheumatoid arthritis is a very active area of worldwide research. Some scientists believe that the tendency to develop rheumatoid arthritis may be genetically inherited. It is suspected that certain infections or factors in the environment might trigger the immune system to attack the body's own tissues, resulting in inflammation in various organs of the body such as the lungs or eyes.

Regardless of the exact trigger, the result is an immune system that is geared up to promote inflammation in the joints and occasionally other tissues of the body. Immune cells, called lymphocytes, are activated and chemical messengers (cytokines, such as tumor necrosis factor/TNF and interleukin-1/IL-1) are expressed in the inflamed areas.

Environmental factors also seem to play some role in causing rheumatoid arthritis. Recently, scientists have reported that smoking tobacco increases the risk of developing rheumatoid arthritis.

What are the symptoms of rheumatoid arthritis?

The symptoms of rheumatoid arthritis come and go, depending on the degree of tissue inflammation. When body tissues are inflamed, the disease is active. When tissue inflammation subsides, the disease is inactive (in remission). Remissions can occur spontaneously or with treatment, and can last weeks, months, or years. During remissions, symptoms of the disease disappear, and patients generally feel well. When the disease becomes active again (relapse), symptoms return. The return of disease activity and symptoms is called a flare. The course of rheumatoid arthritis varies from patient to patient, and periods of flares and remissions are typical.

When the disease is active, symptoms can include fatigue, lack of appetite, low grade fever, muscle and joint aches, and stiffness. Muscle and joint stiffness are usually most notable in the morning and after periods of inactivity. Arthritis is common during disease flares. Also during flares, joints frequently become red, swollen, painful, and tender. This occurs because the lining tissue of the joint (synovium) becomes inflamed, resulting in the production of excessive joint fluid (synovial fluid). The synovium also thickens with inflammation (synovitis).

In rheumatoid arthritis, multiple joints are usually inflamed in a symmetrical pattern (both sides of the body affected). The small joints of both the hands and wrists are often involved. Simple tasks of daily living, such as turning door knobs and opening jars can become difficult during flares. The small joints of the feet are also commonly involved. Occasionally, only one joint is inflamed. When only one joint is involved, the arthritis can mimic the joint inflammation caused by other forms of arthritis, such as gout or joint infection. Chronic inflammation can cause damage to body tissues, cartilage and bone. This leads to a loss of cartilage and erosion and weakness of the bones as well as the muscles, resulting in joint deformity, destruction, and loss of function. Rarely, rheumatoid arthritis can even affect the joint that is responsible for the tightening our vocal cords to change the tone of our voice, the cricoarytenoid joint. When this joint is inflamed, it can cause hoarseness of voice.

Since rheumatoid arthritis is a systemic disease, its inflammation can affect organs and areas of the body other than the joints. Inflammation of the glands of the eyes and mouth can cause dryness of these areas and is referred to as Sjogren's syndrome. Rheumatoid inflammation of the lung lining (pleuritis) causes chest pain with deep breathing or coughing. The lung tissue itself can also become inflamed and sometimes nodules of inflammation (rheumatoid nodules) develop within the lungs. Inflammation of the tissue (pericardium) surrounding the heart, called pericarditis, can cause a chest pain that typically changes in intensity when lying down or leaning forward. The rheumatoid disease can reduce the number of red blood cells (anemia), and white blood cells. Decreased white cells can be associated with an enlarged spleen (referred to as Felty's syndrome) and can increase the risk of infections. Firm lumps under the skin (rheumatoid nodules) can occur around the elbows and fingers where there is frequent pressure. Even though these nodules usually do not cause symptoms, occasionally they can become infected. A rare, serious complication, usually with long-standing rheumatoid disease, is blood vessel inflammation (vasculitis). Vasculitis can impair blood supply to tissues and lead to tissue death. This is most often initially visible as tiny black areas around the nail beds or as leg ulcers.

How is rheumatoid arthritis diagnosed?

The first step in the diagnosis of rheumatoid arthritis is a meeting between the doctor and the patient. The doctor reviews the history of symptoms, examines the joints for inflammation and deformity, the skin for rheumatoid nodules, and other parts of the body for inflammation. Certain blood and x-ray tests are often obtained. The diagnosis will be based on the pattern of symptoms, the distribution of the inflamed joints, and the blood and x-ray findings. Several visits may be necessary before the doctor can be certain of the diagnosis. A doctor with special training in arthritis and related diseases is called a rheumatologist.

The distribution of joint inflammation is important to the doctor in making a diagnosis. In rheumatoid arthritis, the small joints of the hands, wrists, feet, and knees are typically inflamed in a symmetrical distribution (affecting both sides of the body). When only one or two joints are inflamed, the diagnosis of rheumatoid arthritis becomes more difficult. The doctor may then perform other tests to exclude arthritis due to infection or gout. The detection of rheumatoid nodules (described above), most often around the elbows and fingers, can suggest the diagnosis.

Abnormal blood antibodies can be found in patients with rheumatoid arthritis. A blood antibody called "rheumatoid factor" can be found in 80% of patients. Citrulline antibody (also referred to as anti-citrulline antibody, anti-cyclic citrullinated peptide antibody, and anti-CCP) is present in most patients with rheumatoid arthritis. It is useful in the diagnosis of rheumatoid arthritis when evaluating patients with unexplained joint inflammation. A test for citrulline antibodies is most helpful in looking for the cause of previously undiagnosed inflammatory arthritis when the traditional blood test for rheumatoid arthritis, rheumatoid factor, is not present. Citrulline antibodies have been felt to represent the earlier stages of rheumatoid arthritis in this setting. Another antibody called "the antinuclear antibody" (ANA) is also frequently found in patients with rheumatoid arthritis.

A blood test called the sedimentation rate (sed rate) is a measure of how fast red blood cells fall to the bottom of a test tube. The sed rate is used as a crude measure of the inflammation of the joints. The sed rate is usually faster during disease flares, and slower during remissions. Another blood test that is used to measure the degree of inflammation present in the body is the C-reactive protein. The rheumatoid factor, ANA, sed rate, and C-reactive protein tests can also be abnormal in other systemic autoimmune and inflammatory conditions. Therefore, abnormalities in these blood tests alone are not sufficient for a firm diagnosis of rheumatoid arthritis.

Joint x-rays may be normal or only show swelling of soft tissues early in the disease. As the disease progresses x-rays can show bony erosions typical of rheumatoid arthritis in the joints. Joint x-rays can also be helpful in monitoring the progression of disease and joint damage over time. Bone scanning, a radioactive test procedure, can demonstrate the inflamed joints.

The doctor may elect to perform an office procedure called arthrocentesis. In this procedure, a sterile needle and syringe are used to drain joint fluid out of the joint for study in the laboratory. Analysis of the joint fluid, in the laboratory, can help to exclude other causes of arthritis, such as infection and gout. Arthrocentesis can also be helpful in relieving joint swelling and pain. Occasionally, cortisone medications are injected into the joint during the arthrocentesis in order to rapidly relieve joint inflammation and further reduce symptoms.

How is rheumatoid arthritis treated?

There is no known cure for rheumatoid arthritis. To date, the goal of treatment in rheumatoid arthritis is to reduce joint inflammation and pain, maximize joint function, and prevent joint destruction and deformity. Early medical intervention has been shown to be important in improving outcomes. Aggressive management can improve function, stop damage to joints as seen on x-rays, and prevent work disability. Optimal treatment for the disease involves a combination of medications, rest, joint strengthening exercises, joint protection, and patient (and family) education. Treatment is customized according to many factors such as disease activity, types of joints involved, general health, age, and patient occupation. Treatment is most successful when there is close cooperation between the doctor, patient, and family members.

Two classes of medications are used in treating rheumatoid arthritis: fast-acting "first-line drugs" and slow-acting "second-line drugs" (also referred to as Disease-Modifying Antirheumatic Drugs or DMARDs). The first-line drugs, such as aspirin and cortisone (corticosteroids), are used to reduce pain and inflammation. The slow-acting second-line drugs, such as gold, methotrexate and hydroxychloroquine (Plaquenil) promote disease remission and prevent progressive joint destruction, but they are not anti-inflammatory agents.

The degree of destructiveness of rheumatoid arthritis varies from patient to patient. Patients with uncommon, less destructive forms of the disease or disease that has quieted after years of activity ("burned out" rheumatoid arthritis) can be managed with rest, pain and anti-inflammatory medications alone. In general, however, patients improve function and minimize disability and joint destruction when treated earlier with second-line drugs (disease-modifying antirheumatic drugs), even within months of the diagnosis. Most patients require more aggressive second-line drugs, such as methotrexate, in addition to anti-inflammatory agents. Sometimes these second-line drugs are used in combination. In some patients with severe joint deformity, surgery may be necessary.

"First-line" drugs

Acetylsalicylate (Aspirin), naproxen (Naprosyn), ibuprofen (Advil, Medipren, Motrin), and etodolac (Lodine) are examples of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs are medications that can reduce tissue inflammation, pain and swelling. NSAIDs are not cortisone. Aspirin, in doses higher than that used in treating headaches and fever, is an effective antiinflammatory medication for rheumatoid arthritis. Aspirin has been used for joint problems since the ancient Egyptian era. The newer NSAIDs are just as effective as aspirin in reducing inflammation and pain, and require fewer dosages per day. Patients' responses to different NSAID medications vary. Therefore, it is not unusual for a doctor to try several NSAID drugs in order to identify the most effective agent with the fewest side effects. The most common side effects of aspirin and other NSAIDs include stomach upset, abdominal pain, ulcers, and even gastrointestinal bleeding. In order to reduce stomach side effects, NSAIDs are usually taken with food. Additional medications are frequently recommended to protect the stomach from the ulcer effects of NSAIDs. These medications include antacids, sucralfate (Carafate), proton-pump inhibitors (Prevacid, and others), and misoprostol (Cytotec).

Corticosteroid medications can be given orally or injected directly into tissues and joints. They are more potent than NSAIDs in reducing inflammation, and in restoring joint mobility and function. Corticosteroids are useful for short periods during severe flares of disease activity, or when the disease is not responding to NSAIDs. However, corticosteroids can have serious side effects, especially when given in high doses for long periods of time. These side effects include weight gain, facial puffiness, thinning of the skin and bone, easy bruising, cataracts, risk of infection, muscle wasting, and destruction of large joints, such as the hips. Corticosteroids also carry some increased risk of contracting infections. These side effects can be partially avoided by gradually tapering the doses of corticosteroids as the patient achieves improvement of the disease. Abruptly discontinuing corticosteroids can lead to flares of the disease or other symptoms of corticosteroid withdrawal, and is discouraged. Thinning of the bones due to osteoporosis may be prevented by calcium and vitamin D supplements. For further information on corticosteroids, please read the article on prednisone.

"Second-line" or "slow-acting" drugs
(Disease-modifying anti-rheumatic drugs or DMARDs)

While "first-line" medications (NSAIDs and corticosteroids) can relieve joint inflammation and pain, they do not necessarily prevent joint destruction or deformity. Rheumatoid arthritis requires medications other than NSAIDs and corticosteroids to stop progressive damage to cartilage, bone, and adjacent soft tissues. The medications needed for ideal management of the disease are also referred to as Disease-modifying Anti-rheumatic Drugs or DMARDs. They come in a variety of forms and are listed below. These "second-line" or "slow-acting" medicines may take weeks to months to become effective. They are used for long periods of time, even years, at varying doses. If effective, DMARDs can promote remission, thereby retarding the progression of joint destruction and deformity. Sometimes a number of second-line medications are used together as combination therapy. As with the first-line medications, the doctor may need to use different second-line medications before treatment is optimal.

Recent research suggests that patients who respond to a DMARD with control of the rheumatoid disease may actually decrease the known risk (small, but real) of lymphoma that exists from simply having rheumatoid arthritis.

Hydroxychloroquine (Plaquenil) is related to quinine, and is also used in the treatment of malaria. It is used over long periods for the treatment of rheumatoid arthritis. Possible side effects include upset stomach, skin rashes, muscle weakness, and vision changes. Even though vision changes are rare, patients taking Plaquenil should be monitored by an eye doctor (ophthalmologist).

Sulfasalazine (Azulfidine) is an oral medication traditionally used in the treatment of mild to moderately severe inflammatory bowel diseases, such as ulcerative colitis and Crohn's colitis. Azulfidine is used to treat rheumatoid arthritis in combination with antiinflammatory medications. Azulfidine is generally well tolerated. Common side effects include rash and upset stomach. Because Azulfidine is made up of sulfa and salicylate compounds, it should be avoided by patients with known sulfa allergies.

Methotrexate has gained popularity among doctors as an initial second-line drug because of both its effectiveness and relatively infrequent side effects. It also has an advantage in dose flexibility (dosages can be adjusted according to needs). Methotrexate is an immune suppression drug. It can affect the bone marrow and the liver, even rarely causing cirrhosis. All patients taking methotrexate require regular blood test monitoring of blood counts and liver function blood tests.

Gold salts have been used to treat rheumatoid arthritis throughout most of the past century. Gold thioglucose (Solganal) and gold thiomalate (Myochrysine) are given by injection, initially on a weekly basis for months to years. Oral gold, auranofin (Ridaura) was introduced in the 1980's. Side effects of gold (oral and injectable) include skin rash, mouth sores, kidney damage with leakage of protein in the urine, and bone marrow damage with anemia and low white cell count. Patients receiving gold treatment are regularly monitored with blood and urine tests. Oral gold can cause diarrhea. These gold drugs have lost such favor that many companies no longer manufacture them.

D-penicillamine (Depen, Cuprimine) can be helpful in selected patients with progressive forms of rheumatoid arthritis. Side effects are similar to those of gold. They include fever, chills, mouth sores, a metallic taste in the mouth, skin rash, kidney and bone marrow damage, stomach upset, and easy bruising. Patients on this medication require routine blood and urine tests. D-penicillamine can rarely cause symptoms of other autoimmune diseases.

Immunosuppressive medicines are powerful medications that suppress the body's immune system. A number of immunosuppressive drugs are used to treat rheumatoid arthritis. They include methotrexate (Rheumatrex, Trexall) as described above, azathioprine (Imuran), cyclophosphamide (Cytoxan), chlorambucil (Leukeran), and cyclosporine (Sandimmune). Because of potentially serious side effects, immunosuppressive medicines (other than methotrexate) are generally reserved for patients with very aggressive disease, or those with serious complications of rheumatoid inflammation, such as blood vessel inflammation (vasculitis). The exception is methotrexate, which is not frequently associated with serious side effects and can be carefully monitored with blood testing. Methotrexate has become a preferred second-line medication as a result.

Immunosuppressive medications can depress bone marrow function and cause anemia, a low white cell count and low platelets counts. A low white count can increase the risk of infections, while a low platelet count can increase the risk of bleeding. Methotrexate rarely can lead to liver cirrhosis and allergic reactions in the lung. Cyclosporin can cause kidney damage and high blood pressure. Because of potentially serious side effects, immunosuppressive medications are used in low doses, usually in combination with anti-inflammatory agents.

Newer treatments

Newer "second-line" drugs for the treatment of rheumatoid arthritis include leflunomide (Arava), and the "biologic" medications etanercept (Enbrel), infliximab (Remicade), anakinra (Kineret), and adalimumab (Humira).

Leflunomide (Arava) is available to relieve the symptoms and halt the progression of the disease. It seems to work by blocking the action of an important enzyme that has a role in immune activation. Arava can cause liver disease, diarrhea, hair loss, and/or rash in some patients. It should not be taken just before or during pregnancy because of possible birth defects.

Other medications that represent a novel approach to the treatment of rheumatoid arthritis and are the products of modern biotechnology. These are referred to as the biologic medications or biological response modifiers. In comparison with traditional DMARDs, the biologic medications have a much more rapid onset of action and can have powerful effects on stopping progressive joint damage. In general, their methods of action are also more directed, defined, and targeted.

Etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira) are biologic medications. These medications intercept a protein in the joints (tumor necrosis factor, or TNF) that causes inflammation before it can act on its natural receptor to "switch on " inflammation. This effectively blocks the TNF inflammation messenger from calling out to the cells of inflammation. Symptoms can be significantly, and often rapidly, improved in patients using these drugs. Etanercept (Enbrel) must be injected subcutaneously once or twice a week. Infliximab (Remicade) is given by infusion directly into a vein (intravenously). Adalimumab (Humira) is injected subcutaneously either every other week or weekly. Each of these medications will be evaluated by doctors in practice to determine what role they may have in treating various stages of rheumatoid arthritis. Research has shown that biological response modifiers also prevent the progressive joint destruction of rheumatoid arthritis. They are currently recommended for use after other second-line medications have not been effective. The biological response modifiers (TNF-inhibitors) are expensive treatments. They are also frequently used in combination with methotrexate and other DMARDs. Futhermore, it should be noted that the TNF-blocking biologics all are more effective when combined with methotrexate.

Anakinra (Kineret) is another biologic treatment that is used to treat moderate to severe rheumatoid arthritis. Anakinra (Kineret) works by binding to a cell messenger protein (IL-1, a proinflammation cytokine). Anakinra (Kineret) is injected under the skin daily. Anakinra (Kineret) can be used alone or with other DMARDs. The response rate of anakinra (Kineret) does not seem to be as high as with other biologic medications.

Rituxan (rituximab) is an antibody that was first used to treat lymphoma, a cancer of the lymph nodes. Rituxan can be effective in treating autoimmune diseases like rheumatoid arthritis because it depletes B-cells, which are important cells of inflammation and in producing abnormal antibodies that are common in these conditions. Rituxan is now available to treat moderate to severely active rheumatoid arthritis in patients who have failed the TNF-blocking biologics. Preliminary studies have shown that Rituxan was also found to be beneficial in treating severe rheumatoid arthritis complicated by blood vessel inflammation (vasculitis) and cryoglobulinemia.

Orencia (abatacept) is a recently developed biologic medication that blocks T-cell activation. Orencia (abatacept) is now available to treat adult patients who have failed a traditional DMARD or TNF-blocking biologic medication.

While biologic medications are often combined with traditional DMARDs in the treatment of rheumatoid arthritis, they are generally not used with other biologic medications because of unacceptible risk for serious infections.

The Prosorba column therapy involves pumping blood drawn from a vein in the arm into an apheresis machine, or cell separator. This machine separates the liquid part of the blood (the plasma) from the blood cells. The Prosorba column is a plastic cylinder about the size of a coffee mug that contains a sand-like substance coated with a special material called Protein A. Protein A is unique in that it binds unwanted antibodies from the blood that promote the arthritis. The Prosorba column works to counter the effect of these harmful antibodies. The Prosorba column is indicated to reduce the signs and symptoms of moderate to severe rheumatoid arthritis in adult patients with long standing disease who have failed or are intolerant to disease-modifying anti-rheumatic drugs (DMARDs). The exact role of this treatment is being evaluated by doctors and it is not commonly used currently.

Other treatments

There is no special diet for rheumatoid arthritis. One hundred years ago it was touted that "night-shade" foods, such as tomatos, would aggrevate rheumatoid arthritis. This is no longer accepted as true. Fish oil may have anti-inflammatory beneficial effects, but so far this has only been shown in laboratory experiments studying inflammatory cells. Likewise, the benefits of cartilage preparations remain unproven. Symptomatic pain relief can often be achieved with oral acetaminophen (Tylenol) or over-the-counter topical preparations, which are rubbed into the skin. Antibiotics, in particular the tetracycline drug minocycline (Minocin), have been tried for rheumatoid arthritis recently in clinical trials. Early results have demonstrated mild to moderate improvement in the symptoms of arthritis. Minocycline has been shown to impede important mediator enzymes of tissue destruction, called metalloproteinases, in the laboratory as well as in humans.

The areas of the body, other than the joints, that are affected by rheumatoid inflammation are treated individually. Sjogren's syndrome (described above, see symptoms) can be helped by artificial tears and humidifying rooms of the home or office. Medicated eye drops, cortisporine ophthalmic drops (Restasis), are also available to help the dry eyes in those affected. Regular eye check-ups and early antibiotic treatment for infection of the eyes are important. Inflammation of the tendons (tendinitis), bursae (bursitis) and rheumatoid nodules can be injected with cortisone. Inflammation of the lining of the heart and/or lungs may require high doses of oral cortisone.

Proper, regular exercise is important in maintaining joint mobility, and in strengthening the muscles around the joints. Swimming is particularly helpful because it allows exercise with minimal stress on the joints. Physical and occupational therapists are trained to provide specific exercise instructions and can offer splinting supports. For example, wrist and finger splints can be helpful in reducing inflammation and maintaining joint alignment. Devices, such as canes, toilet seat raisers, and jar grippers can assist daily living. Heat and cold applications are modalities that can ease symptoms before and after exercise.

Surgery may be recommended to restore joint mobility or repair damaged joints. Doctors who specialize in joint surgery are orthopedic surgeons. The types of joint surgery range from arthroscopy to partial and complete replacement of the joint. Arthroscopy is a surgical technique whereby a doctor inserts a tube-like instrument into the joint to see and repair abnormal tissues. For more information, please read the Arthroscopy article.

"Total joint replacement" is a surgical procedure whereby a destroyed joint is replaced with artificial materials. For example, the small joints of the hand can be replaced with plastic material. Large joints, such as the hips or knees, are replaced with metals. For more information, please read the Total Hip Replacement and Total Knee Replacement articles.

Finally, minimizing emotional stress can help improve the overall health of the patient with rheumatoid arthritis. Support and extracurricular groups afford patients time to discuss their problems with others and learn more about their illness.

Future treatments

Scientists throughout the world are studying many promising areas of new treatment approaches for rheumatoid arthritis. These areas include treatments that block the action of the special inflammation factors, such as tumor necrosis factor (TNFalpha) and interleukin-1 (IL-1), as described above. Many other drugs are being developed that act against certain critical white blood cells involved in rheumatoid inflammation. Also, new NSAIDs with mechanisms of action that are different from current drugs are on the horizon.

Better methods of more accurately defining which patients are more likely to develop more aggressive disease are becoming available. Recent antibody research has found that the presence of citrulline antibodies in the blood (see above in diagnosis) has been associated with a greater tendency toward more destructive forms of rheumatoid arthritis.

Studies involving various types of the connective tissue collagen are in progress and show encouraging signs of reducing rheumatoid disease activity. Finally, genetic research and engineering is likely to bring forth many new avenues of earlier diagnosis and accurate treatment in the near future. Gene profiling, also known as gene array analysis, is being identified as a helpful method of defining which people will respond to which medications. Studies are underway that are using gene array analysis to determine which patients will be at more risk for more aggressive disease. This is all occurring because of technology improvements. We are at the threshold of tremendous improvements in the way rheumatoid arthritis is managed.

Rheumatoid Arthritis At A Glance

Rheumatoid arthritis is an autoimmune disease that can cause chronic inflammation of the joints and other areas of the body.
Rheumatoid arthritis can affect persons of all ages.
The cause of rheumatoid arthritis is not known.
Rheumatoid arthritis is a chronic disease, characterized by periods of disease flares and remissions.
In rheumatoid arthritis, multiple joints are usually, but not always, affected in a symmetrical pattern.
Chronic inflammation of rheumatoid arthritis can cause permanent joint destruction and deformity.
Damage to joints can occur early and does not correlate with symptoms.
The "rheumatoid factor" is an antibody blood test that can be found in 80 % of patients with rheumatoid arthritis.
There is no known cure for rheumatoid arthritis.
The treatment of rheumatoid arthritis optimally involves a combination of patient education, rest and exercise, joint protection, medications, and occasionally surgery.
Early treatment of rheumatoid arthritis results in better outcomes.

Osteoporosis

2008-01-26T04:38:00.000-08:00

What is osteoporosis?

Osteoporosis is a condition characterized by the loss of the normal density of bone, resulting in fragile bone. Osteoporosis leads to literally abnormally porous bone that is more compressible like a sponge, than dense like a brick. This disorder of the skeleton weakens the bone causing an increase in the risk for breaking bones (bone fracture).

Normal bone is composed of protein, collagen, and calcium all of which give bone its strength. Bones that are affected by osteoporosis can break (fracture) with relatively minor injury that normally would not cause a bone fracture. The fracture can be either in the form of cracking (as in a hip fracture), or collapsing (as in a compression fracture of the vertebrae of the spine). The spine, hips, and wrists are common areas of bone fractures from osteoporosis, although osteoporosis-related fractures can also occur in almost any skeletal bone.

What are the symptoms of osteoporosis?

The osteoporosis condition can be present without any symptoms for decades, because osteoporosis doesn't cause symptoms unless bone fractures. Some osteoporosis fractures may escape detection until years later. Therefore, patients may not be aware of their osteoporosis until they suffer a painful fracture. Then the symptoms are related to the location of the fractures.

Fractures of the spine (vertebra) can cause severe "band-like" pain that radiates around from the back to the side of the body. Over the years, repeated spine fractures can cause chronic lower back pain as well as loss of height or curving of the spine, which gives the individual a hunched-back appearance of the upper back, often called a "dowager hump."

A fracture that occurs during the course of normal activity is called a minimal trauma fracture or stress fracture. For example, some patients with osteoporosis develop stress fractures of the feet while walking or stepping off a curb.

Hip fractures typically occur as a result of a fall. With osteoporosis, hip fractures can occur as a result of trivial accidents. Hip fractures may also be difficult to heal after surgical repair because of poor bone quality.

What are the consequences of osteoporosis?

Osteoporosis bone fractures are responsible for considerable pain, decreased quality of life, lost workdays, and disability. Up to 30% of patients suffering a hip fracture will require long term nursing home care. Elderly patients can further develop pneumonia and blood clots in the leg veins that can travel to the lungs (pulmonary embolism) due to prolonged bed rest after a hip fracture. Some 20% of women with a hip fracture will die in the subsequent year as an indirect result of the fracture. In addition, once a person has experienced a spine fracture due to osteoporosis, he or she is at very high risk of suffering another such fracture in the near future (next few years). About 20% of postmenopausal women who experience a vertebral fracture will suffer a new vertebral fracture of bone in the following year.

Why is osteoporosis an important public health issue?

In the United States, 44 million people have low bone density (either osteoporosis or osteopenia, see below). This amounts to 55% of the U.S. population 50 years-old and over.

In the U.S., more than 10 million people have osteoporosis and almost 34 million more have low bone density.

One in two white women will experience a bone fracture due to osteoporosis in her lifetime.

In the United States, direct health care costs from osteoporosis fractures amount to billion dollars, without even taking into account the indirect costs, such as lost work productivity.

Twenty percent of those who experience a hip fracture will die in the year following the fracture.

One-third of hip fracture patients are discharged to a nursing home within the year after fracture.

Only one-third of hip fracture patients regain their pre-fracture level of function.

With the aging of America, the number of people with osteoporosis related fractures will increase exponentially. The pain, suffering, and economic costs will be enormous.

What factors determine bone strength?

Bone mass (bone density) is the amount of bone present in the skeletal structure. Generally, the higher the bone density is, the stronger are the bones. Bone density is greatly influenced by genetic factors, which in turn are sometimes modified by environmental factors and medications. For example, men have a higher bone density than women. African Americans have a higher bone density than Caucasian or Asian Americans.

Normally, bone density accumulates during childhood and reaches a peak by around age 25. Bone density is then maintained for about ten years. After age 35, both men and women will normally lose 0.3% to 0.5% of their bone density per year as part of the aging process.

Estrogen is important in maintaining bone density in women. When estrogen levels drop after menopause, bone loss accelerates. During the first five to ten years after menopause, women can suffer up to two to four percent loss of bone density per year! This can result in the loss of up to 25 to 30% of their bone density during that time period. Accelerated bone loss after menopause is a major cause of osteoporosis in women.

What are the risk factors for developing osteoporosis?

Factors that will increase the risk of developing osteoporosis are:

Female gender;

Caucasian or Asian race;

Thin and small body frames;

Family history of osteoporosis (for example, having a mother with an osteoporotic hip fracture doubles your risk of hip fracture);

Personal history of fracture as an adult;

Cigarette smoking;

Excessive alcohol consumption;

Lack of exercise;

Diet low in calcium;

Poor nutrition and poor general health;

Malabsorption (nutrients are not properly absorbed from the gastrointestinal system) from conditions such as celiac sprue;

Low estrogen levels (such as occur in menopause or with early surgical removal of both ovaries);

Chemotherapy can cause early menopause due to its toxic effects on the ovaries;

Amenorrhea (loss of the menstrual period) in young women also causes low estrogen and osteoporosis; Amenorrhea can occur in women who undergo extremely vigorous training and in women with very low body fat (example: anorexia nervosa);

Chronic inflammation, due to diseases (such as rheumatoid arthritis and chronic liver diseases);

Immobility, such as after a stroke, or from any condition that interferes with walking;

Hyperthyroidism, a condition wherein too much thyroid hormone is produced by the thyroid gland (as in Grave's disease) or is caused by taking too much thyroid hormone medication;

Hyperparathyroidism, a disease wherein there is excessive parathyroid hormone production by the parathyroid gland (a small gland located near the thyroid gland). Normally, the parathyroid hormone maintains blood calcium levels by, in part, removing calcium from the bone. In untreated hyperparathyroidism, excessive parathyroid hormone causes too much calcium to be removed from the bone, which can lead to osteoporosis;

Vitamin D deficiency. Vitamin D helps the body absorb calcium. When vitamin D is lacking, the body cannot absorb adequate amounts of calcium to prevent osteoporosis. Vitamin D deficiency can result from lack of intestinal absorption of the vitamin such as occurs in celiac sprue and primary biliary cirrhosis;

Certain medications can cause osteoporosis. These include long-term use of heparin (a blood thinner), anti-seizure medications phenytoin (Dilantin) and phenobarbital, and long term use of oral corticosteroids (such as Prednisone).

How is osteoporosis diagnosed?

A routine x-ray can reveal osteoporosis of the bone, which appears much thinner and lighter than normal bones. Unfortunately, by the time x-rays can detect osteoporosis, at least 30% of the bone has already been lost. In addition, x-rays are not accurate indicators of bone density. The appearance of the bone on x-ray is often affected by variations in the degree of exposure of the x-ray film.

The National Osteoporosis Foundation, the American Medical Association, and other major medical organizations are recommending a dual energy x-ray absorptiometry scan (DXA, formerly known as DEXA) for diagnosing osteoporosis. DXA measures bone density in the hip and the spine. The test takes only 5 to 15 minutes to perform, uses very little radiation (less than one tenth to one hundredth the amount used on a standard chest x-ray), and is quite precise.

The bone density of the patient is then compared to the average peak bone density of young adults of same sex and race. This score is called the "T score," and it expresses the bone density in terms of the number of standard deviations (SD) below peak young adult bone mass.

Osteoporosis is defined as bone density T score of –2.5 SD or below.
Osteopenia (between normal and osteoporosis) is defined as bone density T score between –1 and –2.5 SD.

Who should have bone density testing?

The National Osteoporosis Foundation guidelines state that there are several groups of people who should consider DXA testing:

All postmenopausal women below age 65 who have risk factors for osteoporosis;

All women aged 65 and older;

Postmenopausal women with fractures, although this is not mandatory because treatment may well be started regardless of bone density;

Women with medical conditions associated with osteoporosis. These diseases number more than 50. A primary care physician can scan a patient's list of medical illnesses to verify that one of these conditions is not present;

Women whose decision to use medication might be aided by bone density testing.

The National Osteoporosis Foundation guidelines state that bone density testing does not need to be performed if a person has a known osteoporotic fracture because the condition will be treated with or without bone density results. In addition, bone density testing is not appropriate if the person undergoing the test is not willing to take any treatment based on the results. Therefore, if bone density testing is done, it should be performed on people willing to take some specific action based on the results.

How is osteoporosis treated and prevented?

The goal of osteoporosis treatment is the prevention of bone fractures by stopping bone loss and by increasing bone density and strength. Although early detection and timely treatment of osteoporosis can substantially decrease the risk of future fracture, none of the available treatments for osteoporosis are complete cures. In other words, it is difficult to completely rebuild bone that has been weakened by osteoporosis. Therefore, prevention of osteoporosis is as important as treatment. Osteoporosis treatment and prevention measures are:

Life style changes including quitting cigarette smoking, curtailing alcohol intake, exercising regularly, and consuming a balanced diet with adequate calcium and vitamin D;
Medications that stop bone loss and increase bone strength, such as alendronate (Fosamax), risedronate (Actonel), raloxifene (Evista), ibandronate (Boniva), calcitonin (Calcimar), and zoledronate (Reclast);
Medications that increase bone formation such as teriparatide (Forteo).

Lifestyle changes

Exercise, quitting cigarettes, and curtailing alcohol

Exercise has a wide variety of beneficial health effects. However, exercise does not bring about substantial increases in bone density. The benefit of exercise for osteoporosis has mostly to do with decreasing the risk of falls, probably because balance is improved and/or muscle strength is increased. Research has not yet determined what type of exercise is best for osteoporosis or for how long. Until research has answered these questions, most doctors recommend weight-bearing exercise, such as walking, preferably daily.

A word of caution about exercise: it is important to avoid exercises that can injure already weakened bones. In patients over 40 and those with heart disease, obesity, diabetes mellitus, and high blood pressure, exercise should be prescribed and monitored by their doctors. Finally, extreme levels of exercise (such as marathon running) may not be healthy for the bones. Marathon running in young women that leads to weight loss and loss of menstrual periods can actually cause osteoporosis.

Smoking one pack of cigarettes per day throughout adult life can itself lead to loss of 5% to 10% of bone mass. Smoking cigarettes decreases estrogen levels and can lead to bone loss in women before menopause. Smoking cigarettes can also lead to earlier menopause. In postmenopausal women, smoking is linked with increased risk of osteoporosis. Data on the effect of regular consumption of alcohol and caffeine on osteoporosis is not as clear as with exercise and cigarettes. In fact, research regarding alcohol and caffeine as risk factors for osteoporosis shows widely varying results, and is controversial. Certainly, these effects are not as powerful as other factors. Nevertheless, moderation of both alcohol and caffeine is prudent.

Calcium Supplements

Building strong and healthy bones requires an adequate dietary intake of calcium and exercise beginning in childhood and adolescence for both sexes. Most importantly, however, a high dietary calcium intake or taking calcium supplements alone is not sufficient in treating osteoporosis, and should not be viewed as an alternative to or substituted for more potent prescription osteoporosis medications. In the first several years after menopause, rapid bone loss can occur even if calcium supplements are taken.

The following calcium intake has been recommended by The National Institutes of Health Consensus Conference on Osteoporosis for all people, with or without osteoporosis:

800 mg/day for children ages 1 to 10
1000 mg/day for men, premenopausal women, and postmenopausal women also taking estrogen
1200 mg/day for teenagers and young adults ages 11 to 24
1500 mg/day for post menopausal women not taking estrogen
1200mg to 1500 mg/day for pregnant and nursing mothers
The total daily intake of calcium should not exceed 2000 mg

Daily calcium intake can be calculated by the following method:

Excluding dairy products, the average American diet contains approximately 250 mg of calcium;

There is approximately 300 mg of calcium in an 8-ounce glass of milk;

There is approximately 450 mg of calcium in 8 ounces of plain yogurt;

There is approximately 1300 mg of calcium in 1 cup of cottage cheese;

There is approximately 200 mg of calcium in 1 ounce of cheddar cheese;

There is approximately 90 mg of calcium in ½ cup of vanilla ice cream;

There is approximately 300 mg of calcium in 8 ounces of calcium-fortified orange juice.

Unfortunately, surveys have shown that average women in the United States are consuming less than 500 milligrams of calcium per day in their diet, less than the recommended amounts. Additional calcium can be obtained by drinking more milk and eating more yogurt or cottage cheese, or by taking calcium supplement tablets as well from calcium-fortified foods, such as orange juice.

The various calcium supplements contain different amounts of elemental calcium (the actual amount of calcium in the supplement). For example, Caltrate, Os-Cal and Tums are calcium carbonate salts. Each 1250 mg of calcium carbonate salt tablet (such as Caltrate 600 mg, Os-Cal 500 mg, or Tums 500 mg extra strength) contains 500 mg of elemental calcium. A person who needs 1000 mg/day of calcium supplement can take one tablet of Tums 500 mg extra strength (containing 500 mg of elemental calcium) twice daily with meals.

The calcium carbonate supplements are best taken in small divided doses with meals. The intestines may not be able to reliably absorb more than 500 mg of calcium all at once. Therefore, the best way to take 1000 mg of a calcium supplement is to divide it in two doses. Likewise, a dosage of 1500 mg should be divided into three doses.

Calcium supplements are safe and generally well tolerated. Side effects are indigestion and constipation. If constipation and indigestion occur with calcium carbonate supplements, calcium citrate (Citracal) can be used. Some patients have difficulty swallowing calcium tablets. In this situation, chewable candy-like calcium in the form of Viactiv brand is available. Certain medications can interfere with the absorption of calcium carbonate. Examples of such medications include proton-pump inhibitors [omeprazole (Prilosec), lansoprazole (Prevacid), lansoprazole (Protonix), and rabeprazole (Aciphex)], which are used in treating GERD (acid reflux) or peptic ulcers. In these cases, calcium citrate is preferred.

Many "natural" calcium carbonate preparations, such as oyster shells or bone meal, may contain high levels of lead or other harmful elements and should be avoided.

Vitamin D

An adequate calcium intake and adequate body stores of vitamin D are important foundations for maintaining bone density and strength. However, vitamin D and calcium alone are not sufficient treatment for osteoporosis. They are given in conjunction with other treatments. Vitamin D is important in several respects:

Vitamin D helps the absorption of calcium from the intestines.
A lack of vitamin D causes calcium-depleted bone (osteomalacia), which further weakens the bones and increases the risk of fractures.
Vitamin D, along with adequate calcium (1200 mg of elemental calcium), has been shown in some studies to increase bone density and decrease fractures in older postmenopausal, but not in premenopausal or perimenopausal women.

Vitamin D comes from the diet and the skin. Vitamin D production by the skin is dependent on exposure to sunlight. Active people living in sunny regions (Southern California, Hawaii, countries around the equator, etc.) can produce most of the vitamin D they need from their skin. Conversely, lack of exposure to sunlight, due to residence in northern latitudes or physical incapacitation, causes vitamin D deficiency. In less temperate regions such as Minnesota, Michigan, and New York, skin production of vitamin D is markedly diminished in the winter months, especially among the elderly. In that population, dietary vitamin D becomes important.

Unfortunately, vitamin D deficiency is quite common in the United States. In a study of hospitalized patients in a general medical ward, vitamin D deficiency was detected in 57% of the patients. An estimated 50% of elderly women consume far less vitamin D in their diet than is recommended.

The Food and Nutrition Board of the Institute of Medicine has recommended the following as an as adequate vitamin intake:

200 IU daily for men and women 19 to 50 years old,
400 IU daily for men and women 51 to 70 years old, and
600 IU daily for men and women 71 years and older.

But if a person already has osteoporosis, it is advisable to ensure 400 IU twice per day as usual daily intake, most commonly as a supplement alongside prescription osteoporosis medication.

An average multivitamin tablet contains 400 IU of vitamin D. Therefore, one to two multivitamins a day should provide the recommended amount of vitamin D. Alternatively, vitamin D can be obtained in combination with calcium in tablet forms, such as Caltrate 600 + D (600 mg of calcium and 200 IU of vitamin D) and others. Adequate calcium and vitamin D are critical for bone health.

Adequate levels of calcium and vitamin D are essential for optimal bone health, especially in addition to any prescription osteoporosis medication. Chronic excessive use of vitamin D, especially above 2000 units/day, can lead to toxic levels of vitamin D, elevated calcium levels in blood and urine, and may also cause kidney stones. Since various dietary supplements may also contain vitamin D, it is important to review vitamin D content in dietary supplements before taking additional vitamin D.

Hormone therapy (menopausal hormone therapy)

Menopausal hormone therapy (previously referred to as hormone replacement therapy or HRT) has been shown to prevent bone loss, increase bone density, and prevent bone fractures. It is useful in preventing osteoporosis in postmenopausal women. Estrogen is available orally (Premarin, Estrace, Estratest, and others) or as a skin patch (Estraderm, Vivelle, and others).

Estrogen is also available in combination with progesterone as pills and patches. Progesterone is routinely given along with estrogen to prevent uterine cancer that might result from estrogen use alone. Women who have had a hysterectomy (surgical removal of the uterus) may take estrogen alone. Nasally delivered estrogen and lower-dose combination pills of estrogen and progesterone are also being studied. However, due to adverse effects of menopausal hormone therapy, such as increased risks of heart attack, stroke, blood clots in the veins, and breast cancer; menopausal hormone therapy is no longer recommended for long-term use in the therapy of osteoporosis. Rather, menopausal hormone therapy is used short-term to relieve menopausal hot flashes.

Every woman needs to have an individualized discussion regarding estrogen replacement with her doctor because each woman will have a different balance of risk and benefit expected from hormone therapy. For more, please read the Hormone Therapy article.

Medications that prevent bone loss and breakdown

Currently, the most effective medications for osteoporosis that are approved by the FDA are anti-resorptive agents, which prevent bone breakdown. The bone is a living dynamic structure; it is constantly being removed (resorbed) and rebuilt. This process is an essential part of maintaining the normal calcium level in the blood and serves to repair tiny cracks in the bones that occur with normal daily activity. Osteoporosis results over time when the rate of bone resorption exceeds that of bone rebuilding. Anti-resorptive medications inhibit bone removal (resorption), thus tipping the balance in favor of bone rebuilding and increasing bone density. Menopausal estrogen hormone therapy is one example of an anti-resorptive agent. Others include alendronate (Fosamax), risedronate (Actonel), raloxifene (Evista), ibandronate (Boniva), calcitonin (Calcimar), and the recently approved zoledronate (Reclast).

Bisphosphates

Bisphosphonates decrease the risk of hip fracture, wrist fracture, and spine fracture in postmenopausal women osteoporosis.

To reduce side effects and to enhance absorption of the medicine, all bisphosphonates taken by mouth (orally) should be taken in the morning, on an empty stomach, thirty minutes before breakfast, and with at least 8 ounces (240 ml) of water (not juice). Taking the pill sitting or standing minimizes the chances of the pill being lodged in the esophagus. Patients should also remain upright for at least 30 minutes after taking the pill to avoid reflux of the pill into the esophagus. Newer intravenous bisphosphonates, such as ibandronate (Boniva) and zoledronate (Reclast) avoid these potential gastrointestinal problems.

Food, calcium, iron supplements, vitamins with minerals, or antacids containing calcium, magnesium, or aluminum can reduce the absorption of oral bisphosphonates, thereby resulting in loss of effectiveness. Therefore, oral bisphosphonates should be taken with plain water only in the morning before breakfast. Also, no food or drink should be taken for at least 30 minutes afterwards.

Alendronate (Fosamax)

Alendronate (Fosamax) is a biphosphonate anti-resorptive medication. Alendronate is approved for the prevention and treatment of postmenopausal osteoporosis as well as for osteoporosis that is caused by cortisone-related medications (glucocorticoid-induced osteoporosis). Alendronate has been shown to increase bone density and reduce fractures in the spine, hips, and arms. Alendronate is taken by mouth once-a-week to prevent and treat postmenopausal osteoporosis. Alendronate is the first osteoporosis medication also approved for increasing bone density in men with osteoporosis, either in a daily or a weekly dose schedule.

Alendronate is generally well tolerated with few side effects. One side effect of alendronate is irritation of the esophagus (the food pipe connecting the mouth to the stomach). Inflammation of the esophagus (esophagitis) and ulcers of the esophagus have been reported infrequently with alendronate use. For more, please read the Fosamax drug information article.

Risedronate (Actonel)

Risedronate (Actonel) is another bisphosphonate anti-resorptive medication. Like alendronate, this drug it is approved for the prevention and treatment of postmenopausal osteoporosis as well as for osteoporosis that is caused by cortisone-related medications (glucocorticoid-induced osteoporosis). Risedronate is chemically different from alendronate and has less likelihood of causing esophagus irritation. Risedronate is also more potent in preventing the resorption of bone than alendronate. For more, please read the Actonel drug information article.

Ibandronate (Boniva)

Ibandronate (Boniva) is an oral bisphosphonate for prevention and treatment of postmenopausal osteoporosis. It is available in both daily and monthly oral formulas as well as intravenously every three months. For more, please read the Boniva drug information article.

Zoledronate (Reclast)

Zoledronate (Reclast) is a unique yearly intravenous bisphosphonate anti-resorptive medication. This formulation seems to have very good bone strengthening ability by increasing bone density as well as significant fracture prevention both for spinal bone and bones away from the spine. Its convenience as given only once a year are obvious. As with all bisphosphonates, patients taking zoledronate (Reclast) must be loaded with adequate calcium and vitamin D prior to and after taking the medication for optimal results. Generally patients are given acetaminophen the day of the infusion and for several days afterward to prevent occasional minor muscle and joint aching. The infusion lasts approximately 20-30 minutes.

Selective estrogen receptor modulators (SERMs)

Raloxifene (Evista)

Raloxifene (Evista) belongs to a class of drugs called selective estrogen receptor modulators (SERMs). SERMs work like estrogen in some tissues but as an anti-estrogen in other tissues. The SERMs are developed to reap the benefits of estrogen while avoiding the potential side effects of estrogen. Thus, raloxifene can act like estrogen on bone, but as an anti-estrogen on the lining of the uterus.

The first SERM to reach the market was tamoxifen, which blocks the stimulative effect of estrogen on breast tissue. Tamoxifen has proven valuable in women who have had cancer in one breast in preventing cancer in the second breast. Raloxifene is the second SERM to be approved by the FDA. Raloxifene has been approved for the prevention and treatment of osteoporosis in postmenopausal women. In a three year study involving some 600 postmenopausal women, raloxifene was found to increase bone density and lower LDL cholesterol, while having no stimulative effect on the uterine lining (which means that it is unlikely to cause uterine cancer).

Because of its anti-estrogen effects, the most common side effects with raloxifene are hot flashes . Conversely, because of its estrogenic effects, raloxifene increases the risk of blood clots, including deep vein thrombosis (DVT) and pulmonary embolism (blood clots in the lung). The greatest increase in risk occurs during the first 4 months of use. Patients taking raloxifene should avoid prolonged periods of immobility during travel, when blood clots are more prone to occur. The risk of deep vein thrombosis with raloxifene is probably comparable to that of estrogen, about 2 to 3 times higher than the usual low occurrence rate. Raloxifene decreases the risk of spine fractures in postmenopausal women with osteoporosis, but the benefit in decreasing hip fracture risk is not yet known. (The only agents that are definitely proven to decrease hip fracture risk are bisphosphonates.) For more, please read the Evista drug information article.

Calcitonin (Calcimar, Miacalcin)

Calcitonin (Calcimar, Miacalcin) is a hormone that has been approved by the FDA in the United States for treating osteoporosis. Calcitonins come from several animal species, but salmon calcitonin is the one most widely used. Calcitonin can be administered as a shot under the skin (subcutaneously) or into the muscle (intramuscularly), or inhaled nasally (intranasally). Intranasal calcitonin is the most convenient of the three methods.

Calcitonin has been shown to prevent bone loss in postmenopausal women. In women with established osteoporosis, calcitonin has been shown to increase bone density and strength in the spine only.

Calcitonin is not as effective in increasing bone density and strengthening bone as estrogen and the other anti-resorptive agents. In addition, it is not as effective in reducing spine fracture risk, and has not been proven effective in reducing hip fracture risk. Therefore, calcitonin is not the first choice of treatment in women with established osteoporosis. Nevertheless, calcitonin is a helpful alternative osteoporosis treatment for patients who cannot tolerate other medications.

Common side effects of either injected or nasal spray calcitonin are nausea and flushing. Patients using Miacalcin Nasal Spray can develop nasal irritations, a runny nose, or nosebleeds. Injectable calcitonin can cause local skin redness at the site of injection, skin rash, and flushing. For more, please read the Calcitonin drug information article.

Teriparatide (Forteo)

Teriparatide (Forteo) is a synthetic version of the human hormone, parathyroid hormone, which helps to regulate calcium metabolism. It promotes the growth of new bone, while the other osteoporosis medications improve bone density by inhibiting bone resorption. Teriparatide (Forteo) is self-injected into the skin. Because long-term safety is not yet established, it is only FDA-approved for 24 months of use. It reduces spine fractures in women with known osteoporosis, but reduction of hip fracture risk is currently unproven. For more, please read the Forteo drug information article.

Choosing an osteoporosis medication

In choosing a medication for osteoporosis, a doctor will take into account all aspects of a patient's medical history and the severity of the osteoporosis.

If a postmenopausal woman has other menopausal symptoms such as hot flashes and vaginal dryness, menopausal hormone therapy will be the proper choice for these menopausal symptoms as well as for the prevention of osteoporosis. After the menopause symptoms have passed, some other non-estrogen prescription osteoporosis medication will be considered for the long-term.

If the prevention and treatment of osteoporosis is the only issue under consideration, then bisphosphonates such as alendronate, ibandronate, or risedronate are more effective than menopausal hormone therapy in preventing osteoporotic fractures, and less likely to be associated with substantial adverse effects. So far, bisphosphonates are the most effective category or prescription medications for treating postmenopausal osteoporosis.

A few specific serious esophageal conditions preclude the use of oral bisphosphonates. These are called esophageal stricture or achalasia. Caution is often advised for people with dysphagia, gastritis, duodenitis, or ulcers who take oral bisphosphonates. Any worsening symptom should be reported immediately, but the vast majority of people can tolerate bisphosphonates when the prescribing directions are followed carefully. Fortunately, gastroesophageal reflux disease (GERD) or heartburn, which are common, are not specific contraindications to the use of bisphosphonates. Prescribing directions should be followed carefully. Moreover, intravenous bisphosphonates, such as zoledronate (Reclast) may be given to those with gastrointestinal side effects from oral bisphosphonates.

In patients with GERD or who have symptoms of heartburn, risedronate may prove to cause less irritation to the esophagus than alendronate, but now intravenous bisphosphonates, such as zoledronate (Reclast) may be preferred.

Calcitonin is a weaker anti-resorptive medication than estrogenic bisphosphonates. It is reserved for those who cannot take or will not consider taking the other medications. Raloxifene is also a weaker medication [in improving bone density or preventing fractures) compared to estrogen or bisphosphonates (alendronate (Fosamax), ibandronate (Boniva), and risedronate (Actonel)]. Thus, in patients with moderate to severe osteoporosis, it is advisable to use the more potent anti-resorptive medications. The safety and effectiveness of more than three years of raloxifene use or more than 24 months of teriparatide use, have not been well-researched.

Estrogen replacement and raloxifene differ in their side effects and also in their effects on cholesterol panels. For example, raloxifene does not raise the "good HDL cholesterol," but estrogen replacement does. They both lower the "bad LDL cholesterol."

Prevention of osteoporosis due to long term corticosteroids

The long term use of corticosteroids (such as Prednisone, Cortisone, and Prednisolone) can lead to osteoporosis. Corticosteroids cause decreased calcium absorption from the intestines, increased loss of calcium from the kidneys, and increased calcium loss from the bones. To prevent bone loss while on long term corticosteroids, patients should:

Have an adequate calcium (1000 mg daily if premenopausal, 1500 mg daily if postmenopausal) and vitamin D intake. (Calcium alone or combined with vitamin D cannot be relied upon to prevent bone loss from corticosteroids unless other prescription medications are added.)
Discuss with the doctor the use of either alendronate or risedronate, both of which have been approved for the prevention and treatment of corticosteroid-induced osteoporosis.
Patients embarking on long term corticosteroids should discuss with their doctor DXA bone density scan prior to beginning therapy and careful monitoring for osteoporosis during therapy.

Monitoring osteoporosis therapy

The controversy of bone density testing in patients already taking osteoporosis medication

The American Medical Association and other reputable medical organizations have determined that repeat bone density testing (DXA scans) is NOT indicated in monitoring osteoporosis treatment or prevention on a routine basis. It is scientifically premature to measure bone density as a way of monitoring osteoporosis medications. Doctors simply do not know how to use these repeat bone density measurements during therapy. A few of the most important reasons are:

Bone density changes so slowly with treatment that the changes are smaller than the measurement error of the machine. In other words, repeat DXA scans cannot distinguish between a real increase in bone density due to treatment or a mere variation in measurement from the machine itself.

The real purpose of osteoporosis treatment is to decrease future bone fractures. There is no good correlation between increases in bone density with decreases in fracture risks with treatment. For example, alendronate has been shown to decrease fracture risk by 50%, but only to increase bone density by a few percent. In fact, most of the fracture reduction with raloxifene is not explained by raloxifene's effects on bone mineral density.

One density measurement taken during treatment will not help the doctor plan or modify treatment. For example, even if the DXA scan shows continued deterioration in bone density during treatment, there is not yet research data demonstrating that changing a medication, combining medications, or doubling medication doses will be safe and helpful in decreasing the future risk of fractures.

An important note, even if bone density deteriorates during treatment, it is quite likely that the patient would have lost even more bone density without treatment.

Recent research has shown that women who lose bone density after the first year of menopausal hormone therapy will gain bone density in the next two years, whereas women who gain in the first year will tend to lose density in the next two years of therapy. Therefore, bone density during treatment naturally fluctuates and this may not be relevant to the fracture protection of the medication.

For all of these reasons, as surprising as it may sound to many people (and even some doctors!), rechecking bone density is not at all like checking blood pressure during treatment of high blood pressure (hypertension). Routine bone density testing during treatment is unlikely to be helpful. In the future, however, if ongoing research brings new technology or new therapies, testing decisions will clearly change.

Prevention of hip fractures in elderly persons with osteoporosis

The FDA has approved hip protector garments for the prevention of hip fractures in elderly persons with known osteoporosis. Brand names available include Hipsaver and Safehip. These can be helpful for selected patients who are in the nursing home environment, although the real extent of protection against hip fractures that is gained with use of hip protectors is a matter of current controversy.

Osteoporosis At A Glance

Osteoporosis is a condition of increased susceptibility to fracture due to fragile bone.
Osteoporosis weakens bone, and increases risk of bone fracture.
Bone mass (bone density) decreases after age 35 years, and decreases more rapidly in women after menopause.
Key risk factors for osteoporosis include genetic factors, lack of exercise, lack of calcium and vitamin D, personal history of fracture as an adult, cigarette smoking, excessive alcohol consumption, low body weight, and family history of osteoporosis.
Patients with osteoporosis have no symptoms until bone fractures occur.
Diagnosis can be suggested by x-rays and confirmed by using tests to measure bone density.
Treatments for osteoporosis, in addition to prescription osteoporosis medications, include stopping use of alcohol and cigarettes, and assuring adequate exercise, calcium, and vitamin D.

Multiple Sclerosis

2008-01-26T04:33:00.000-08:00

What is multiple sclerosis?

Multiple sclerosis (MS) is a disease in which the nerves of the central nervous system (brain and spinal cord) degenerate. Myelin, which provides a covering or insulation for nerves, improves the conduction of impulses along the nerves and also is important for maintaining the health of the nerves. In multiple sclerosis, inflammation causes the myelin to eventually disappear. Consequently, the electrical impulses that travel along the nerves decelerate, that is, become slower. In addition, the nerves themselves are damaged. As more and more nerves are affected, a patient experiences a progressive interference with functions that are controlled by the nervous system such as vision, speech, walking, writing, and memory.

About 350,000 people in the U.S. have multiple sclerosis. Usually, a patient is diagnosed with multiple sclerosis between 20 and 50 years of age, but multiple sclerosis has been diagnosed in children and in the elderly. Multiple sclerosis is twice as likely to occur in Caucasians as in any other group. Women are twice as likely as men to be affected by multiple sclerosis earlier in life.

What causes multiple sclerosis?

The cause of multiple sclerosis is still unknown. In the last 20 years, researchers have focused on disorders of the immune system and genetics for explanations. The immune system is the body's defender and is highly organized and regulated. If triggered by an aggressor or foreign object, the immune system mounts a defensive action which identifies and attacks the invader and then withdraws. This process depends upon rapid communication among the immune cells and the production of cells that can destroy the intruder. In multiple sclerosis, researchers suspect that a foreign agent such as a virus alters the immune system so that the immune system perceives myelin as an intruder and attacks it. The attack by the immune system on the tissues that it is supposed to protect is called autoimmunity, and multiple sclerosis is believed to be a disease of autoimmunity. While some of the myelin may be repaired after the assault, some of the myelin disappears and nerves are stripped of this covering (become demyelinated). Scarring also occurs, and material is deposited into the scars and forms plaques.

Is multiple sclerosis inherited?

Although its role is unclear, genetics may play a role in multiple sclerosis. European gypsies, Eskimos and African Bantu essentially do not develop multiple sclerosis, while Native Indians of North and South America, Japanese and other Asian groups have a low incidence. The general population has less than a one-percent chance of ever contracting multiple sclerosis. The chance increases in families where a first–degree relative has the disease. Thus, a brother, sister, parent, or child of a person with multiple sclerosis stands a one-percent to three percent chance of developing multiple sclerosis. Similarly, an identical twin runs a nearly 30% chance of acquiring multiple sclerosis whereas a non–identical twin has only a 4% chance if the other twin has the disease. These statistics suggest that genetic factors play a major role in multiple sclerosis. However, other data suggest that environmental factors also play an important role.

What are the types of multiple sclerosis?

There are different clinical manifestations of multiple sclerosis. During an attack, a patient experiences a sudden deterioration in normal physical abilities that may range from mild to severe. This attack, sometimes referred to as an exacerbation of multiple sclerosis, typically lasts more than 24 hours and generally more than a few weeks (rarely more than four weeks).

About 65–80% of patients begin with Relapsing–Remitting (RR) MS, the most common type. In this type, patients experience a series of attacks followed by complete or partial disappearance of the symptoms (remission) until another attack occurs (relapse). It may be weeks to decades between relapses.

In Primary–Progressive (PP) MS, there is a continuous, gradual decline in a patient's physical abilities from the outset rather than relapses. About 10%–20% of patients begin with PP–MS.

Patients beginning with RR–MS can then enter a phase where relapses are rare but more disability accumulates, and are said to have the Secondary–Progressive (SP) type of multiple sclerosis. About 50% of RR–MS patients will develop SP–MS within 10 years. Progressive–Relapsing (PR) MS is a type of multiple sclerosis characterized by a steady decline in abilities accompanied by sporadic attacks. There are cases of of multiple sclerosis that are mild and can be recognized only retrospectively after many years and also rare cases of extremely rapid progression of multiple sclerosis symptoms (sometimes fatal) known as malignant or fulminant (Marburg variant) multiple sclerosis.

What are the symptoms of multiple sclerosis?

Symptoms of multiple sclerosis may be single or multiple and may range from mild to severe in intensity and short to long in duration. Complete or partial remission from symptoms occurs early in about 70% of multiple sclerosis patients.

Visual disturbances may be the first symptoms of multiple sclerosis, but they usually subside. A patient may notice blurred vision, red–green distortion (color desaturation), or sudden monocular blindness (blindness in one eye).
Muscle weakness with or without difficulties with coordination and balance may occur early.
Muscle spasms, fatigue, numbness, and prickling pain are common symptoms.
There may be a loss of sensation, speech impediment (typically a problem articulating words), tremors, or dizziness.

Fifty-percent of patients experience mental changes such as:

decreased concentration,
attention deficits,
some degree of memory loss,
inability to perform sequential tasks, or
impairment in judgment.

Other symptoms may include

depression,
manic depression,
paranoia, or
an uncontrollable urge to laugh and weep.

As the disease worsens, patients may experience sexual dysfunction or reduced bowel and bladder control. Heat appears to intensify multiple sclerosis symptoms for about 60% of patients. Pregnancy seems to reduce the number of attacks.

How is multiple sclerosis diagnosed?

Due to the broad range and subtleties of symptoms, multiple sclerosis may not be diagnosed for months to years after the onset of symptoms. Physicians, particularly neurologists, take detailed histories and perform complete physical and neurological examinations.

MRI (magnetic resonance imaging) scans with intravenous gadolinium helps to identify, describe, and in some instances date lesions in the brain (plaques).
An electro–physiological test, evoked potentials, examines the impulses traveling through the nerves to determine if the impulses are moving normally or too slowly.
Finally, examining the cerebro–spinal fluid that surrounds the brain and spinal cord may identify abnormal chemicals (antibodies) or cells that suggest the presence of multiple sclerosis.

Collectively, these three tests help the physician in confirming the diagnosis of multiple sclerosis. For a definite diagnosis of multiple sclerosis, dissemination in time (at least two separate symptomatic events or changes on MRI) and in anatomical space (for example, within the central nervous system) must be demonstrated.

How is multiple sclerosis treated?

There are many issues for the patient and physician to consider in treating multiple sclerosis. Goals may include reducing the number of attacks, improving recovery from attacks, and attempting to slow further progression of the disease (treatment with disease–modifying drugs). An additional goal is relief from complications due to the loss of function of affected organs (treatment with drugs aimed at specific symptoms). Most neurologists will consider treatment with disease–modifying drugs once the diagnosis of multiple sclerosis is established. Many will begin treatment at the time of the first multiple sclerosis attack, since clinical trials have suggested that patients in whom treatment is delayed may not benefit as much as patients who are treated early. Finally, utilizing support groups or counseling may be helpful for patients and their families whose lives may directly be affected by multiple sclerosis.

Once goals have been set, initial therapy may include medications to manage attacks, symptoms, or both. An understanding of the potential side effects of drugs is critical for the patient because sometimes side effects alone deter patients from drug therapy. Patients may choose to avoid drugs altogether or choose an alternative drug that may offer relief with fewer side effects. A continuous dialogue between the patient and physician about the medications is important in determining the needs for treatment.

Drugs known to affect the immune system have become the primary focus for managing multiple sclerosis. Initially, corticosteroids, such as prednisone (Deltasone, Liquid Pred, Deltasone, Orasone, Prednicen-M) or methylprednisolone (Medrol, Depo-Medrol), were widely used. However, since their effect on the immune system is non–specific and their use may cause numerous side effects, corticosteroids now tend to be used to manage only sudden, severe multiple sclerosis attacks.

Interferon

Since 1993, medications that alter the immune system, particularly interferons, have been used to manage multiple sclerosis. Interferons are protein messengers that cells of the immune system manufacture and use to communicate with one another. There are different types of interferons, such as alpha, beta, and gamma. All interferons have the ability to regulate the immune system and play an important role in protecting against viral infections. Each interferon functions differently, but the functions overlap. The beta interferons have been found useful in managing multiple sclerosis. Interferon beta–1b (Betaseron®) was the first interferon approved to manage RR–MS in 1993. In 1996, interferon beta–1a (Avonex®) gained FDA approval for RR–MS.

Overall, patients treated with interferons experience fewer relapses or a longer interval between relapses. Clinical trials have also shown effects on slowing the accumulation of disability. The most common side effect is a flu–like syndrome that includes fever, tiredness, weakness, chills, and muscle aches. This syndrome tends to occur less frequently as therapy continues. Other common side effects are injection site reactions, changes in blood cell counts, and abnormalities of liver tests. Regular liver tests and blood counts are recommended for patients receiving interferon beta–1b. With the concomitant use of analgesics and local skin measures, the tolerability to interferons has increased.

Clinical trials of interferon beta drugs in patients with the first attack of multiple sclerosis showed that in this early patient population, these drugs delay the onset of the second attack. Avonex® is administered intramuscularly once a week, Betaseron® is administered subcutaneously every other day, and Rebif® is administered subcutaneously three times per week.

Available interferon betas include:

IFN beta–1b (Betaseron®) that is used for the treatment of relapsing forms of multiple sclerosis, to reduce the frequency of clinical relapses. Patients with multiple sclerosis in whom efficacy has been demonstrated include patients who have experienced a first clinical episode and have MRI features consistent with multiple sclerosis.

IFN beta–1a (Rebif®) that is used for the treatment of patients with relapsing forms of multiple sclerosis to decrease the frequency of clinical relapses and delay the accumulation of physical disability. Efficacy of Rebif® in chronic progressive multiple sclerosis has not been established.

IFN beta–1a (Avonex®) that is used for the treatment of patients with relapsing forms of multiple sclerosis to slow the accumulation of physical disability and decrease the frequency of clinical relapses. Patients with multiple sclerosis in whom efficacy has been demonstrated include patients who have experienced a first clinical episode and have MRI features consistent with multiple sclerosis. Safety and efficacy in patients with chronic progressive multiple sclerosis has not been established.

Other medications

Glatiramer acetate

Glatiramer acetate (Copaxone) is another disease–modifying drug that is approved for reducing the frequency of relapses in RR–MS. Glatiramer acetate is a synthetic (man–made) amino acid mixture that may resemble a protein component of myelin. It is thought that the immune system reaction against myelin in multiple sclerosis may be blocked by glatiramer acetate. A reaction occurring immediately after the injection of glatiramer acetate is common, affecting one out of 10 patients. The reaction may involve flushing, chest pain or tightness, palpitations, anxiety, shortness of breath, tightness in the throat, or hives. The reaction usually resolves within 30 minutes and requires no treatment. Some patients may be at risk of developing lipoatrophy, inflammation and destruction of tissue beneath the skin at the site of injection. Glatiramer acetate is used for reducing the frequency of relapses in patients with relapsing–remitting multiple sclerosis.

Natalizumab

Natalizumab (Tysabri®) is a drug approved by the FDA to treat multiple sclerosis. Natalizumab is a monoclonal antibody against VLA–4, a molecule required for immune cells to adhere to other cells, penetrate the blood brain barrier and enter the brain. It is administered via monthly intravenous infusions. It carries a warning for a potentially fatal disease, progressive multifocal leukoencephalopathy (PML), a viral infection of the brain that usually leads to death or severe disability. For this reason only patients who have signed up for treatment under a controlled drug distribution program can get this treatment.

Natalizumab is used as monotherapy for the treatment of patients with relapsing forms of multiple sclerosis to delay the progression of physical disability and reduce the frequency of clinical relapses. The safety and efficacy of natalizumab beyond two years are unknown. Because natalizumab increases the risk of PML, it is generally recommended only for patients who have had an inadequate response to, or are unable to tolerate alternate multiple sclerosis therapies.

Mitoxantrone

Mitoxantrone (Novantrone®) is also approved by the FDA for the treatment of multiple sclerosis. Mitoxantrone is a chemotherapy drug that carries the risk of serious cardiac side effects or cancer. Because of these serious side effects, physicians tend to reserve its use for more advanced or worsening cases of multiple sclerosis.

Mitoxantrone is used for reducing neurologic disability and/or the frequency of clinical relapses in patients with secondary (chronic) progressive, progressive relapsing, or worsening relapsing–remitting multiple sclerosis (for example, patients whose neurologic status is significantly abnormal between relapses). Mitoxantrone is not used in the treatment of patients with primary progressive multiple sclerosis.

How are the manifestations of multiple sclerosis treated?

There are numerous medications that are used to manage complications associated with multiple sclerosis. The following table lists common complications, examples of drug and non–drug therapy, and comments about complications and/or management.

Table. Multiple sclerosis complications with examples of drug and non–drug management (this list is not exhaustive; some of the drugs listed below are used to treat multiple sclerosis symptoms even though they have not been FDA–approved for this particular purpose)

Complication	Drugs	Non–drug management and comments
Muscle spasticity	baclofen (Lioresal) tizanidine (Zanaflex) diazepam (Valium) clonazepam (Klonopin) dantrolene (Dantrium)	Physical therapy may also provide benefit. Most drugs are given by mouth. Some drugs are given via spinal pumps.
Weakness	None	Physical therapy and exercise mostly are used. Foot braces, canes or walkers are of benefit.
Eye problems (acute optic neuritis)	methylprednisolone (Solu–Medrol)	Solu–Medrol is given during the acute attack intravenously, sometimes followed by a corticosteroid by mouth.
Fatigue, emotional outbursts	Anti–depressants amantadine (Symmetrel) for fatigue; modafinil (Provigil) for fatigue	Decrease or avoid physical activity and heat exposure. Amitriptyline is used for sudden laughing/weeping.
Pain	aspirin Ibuprofen acetaminophen anti–convulsants anti–depressants	Aspirin, NSAIDs, acetaminophen, or physical therapy are used for muscle and back pain. Anti–convulsants, like carbamazepine (Tegretol) or gabapentin (Neurontin) are used for face or limb pain. Anti–depressants or electrical stimulation are used for prickling pain, intense tingling, and burning. Referral to pain specialist is recommended with severe pain.
Bladder dysfunction	Antibiotics Vitamin C oxybutynin (Ditropan)	Antibiotics are used to manage infections. Vitamin C and cranberry juice are used to prevent infections. Catheters are used to relieve urine retention. Oxybutynin (Ditropan, Ditropan LX, Oxytrol) or tolterodine (Detrol, Detrol LA)is used for bladder spasms.
Constipation		Increase fluids and fiber.
Sexual dysfunction	sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra), papaverine (Pavabid, Vasal) Vaginal gels	For males, erectile dysfunction drugs, papaverine, penile implant, or electrostimulation are used. For females, vaginal gels or a vibrating device are used.
Tremors		Often resistant to treatment. Sometimes drugs, or surgery are used if extreme.

What are the future directions for managing multiple sclerosis?

There is a great deal of ongoing research in multiple sclerosis, and there continues to be a focus on the immune system in investigational therapies. In addition, scientists are trying to develop techniques that allow brain cells to generate new myelin or that prevent neuronal death. Other promising approaches include the use of precursor (neuronal stem or progenitor) cells that could be implanted into the brain or spinal cord to repopulate areas of missing cells. Future therapy may involve methods designed to improve impulses traveling over the damaged nerves. Scientists also are exploring the effects of diet on multiple sclerosis.

Multiple Sclerosis At A Glance

Multiple sclerosis (MS) is a disease which progressively injures the nerves of the brain and spinal cord.
Injury to the nerves in multiple sclerosis may be reflected by alterations of virtually any sensory or motor (muscular) function in the body.
The cause of multiple sclerosis is unknown, but it has become widely accepted that genetic, immunological, and environmental factors play a role.
Current FDA–approved multiple sclerosis treatments include the beta–interferons (Betaseron®, Rebif® and Avonex®), glatiramer acetate (Copaxone®), mitoxantrone (Novantrone®) and natalizumab (Tysabri®). The selection of therapy should be made after the multiple sclerosis patient has been properly informed of drug efficacy, administration routes, risks of adverse events, and methods to enhance tolerability and compliance.

Fibromyalgia

2008-01-26T04:26:00.000-08:00

What is fibromyalgia?

Fibromyalgia is a chronic condition causing pain, stiffness, and tenderness of the muscles, tendons, and joints. Fibromyalgia is also characterized by restless sleep, awakening feeling tired, fatigue, anxiety, depression, and disturbances in bowel function. Fibromyalgia was formerly known as fibrositis.

While fibromyalgia is one of the most common diseases affecting the muscles, its cause is currently unknown. The painful tissues involved are not accompanied by tissue inflammation. Therefore, despite potentially disabling body pain, patients with fibromyalgia do not develop body damage or deformity. Fibromyalgia also does not cause damage to internal body organs. Therefore, fibromyalgia is different from many other rheumatic conditions (such as rheumatoid arthritis, systemic lupus, and polymyositis). In those diseases, tissue inflammation is the major cause of pain, stiffness and tenderness of the joints, tendons and muscles, and it can lead to joint deformity and damage to the internal organs or muscles.

What causes fibromyalgia?

The cause of fibromyalgia is not known. Patients experience pain in response to stimuli that are normally not perceived as painful. Researchers have found elevated levels of a nerve chemical signal, called substance P, and nerve growth factor in the spinal fluid of fibromyalgia patients. The brain nerve chemical serotonin is also relatively low in patients with fibromyalgia. Studies of pain in fibromyalgia have suggested that the central nervous system (brain) may be somehow supersensitive. Scientists note that there seems to be a diffuse disturbance of pain perception in patients with fibromyalgia.

Also, patients with fibromyalgia have impaired non-Rapid-Eye-Movement, or non-REM, sleep phase (which likely explains the common feature of waking up fatigued and unrefreshed in these patients). The onset of fibromyalgia has been associated with psychological distress, trauma, and infection.

Who does fibromyalgia affect?

Fibromyalgia affects predominantly women (over 80 percent) between the ages of 35 and 55. Rarely, fibromyalgia can also affect men, children, and the elderly. It can occur independently, or can be associated with another disease, such as systemic lupus or rheumatoid arthritis. The prevalence of fibromyalgia varies in different countries. In Sweden and Britain, 1 percent of the population is affected by fibromyalgia. In the United States, approximately 2 percent of the population have fibromyalgia.

What are symptoms of fibromyalgia?

The universal symptom of fibromyalgia is pain. As mentioned earlier, the pain in fibromyalgia is not caused by tissue inflammation. Instead, these patients seem to have an increased sensitivity to many different sensory stimuli, and an unusually low pain threshold. Minor sensory stimuli that ordinarily would not cause pain in individuals can cause disabling pain in patients with fibromyalgia. The body pain of fibromyalgia can be aggravated by noise, weather change, and emotional stress.

The pain of fibromyalgia is generally widespread, involving both sides of the body. Pain usually affects the neck, buttocks, shoulders, arms, the upper back, and the chest. "Tender points" are localized tender areas of the body that can bring on widespread pain and muscle spasm when touched. Tender points are commonly found around the elbows, shoulders, knees, hips, back of the head, and the sides of the breast bone.

Fatigue occurs in 90 percent of patients. Fatigue may be related to abnormal sleep patterns commonly observed in these patients. Normally, there are several levels of depth of sleep. Getting enough of the deeper levels of sleep may be more important in refreshing a person than the total number of hours of sleep. Patients with fibromyalgia lack the deep, restorative level of sleep, called "non-rapid-eye- movement" (non-REM) sleep. Consequently, patients with fibromyalgia often awaken in the morning without feeling fully rested. Some patients awaken with muscle aches or a sensation of muscle fatigue as if they had been "working out" all night!

Mental and/or emotional disturbances occur in over half of fibromyalgia patients. These symptoms include poor concentration, forgetfulness, mood changes, irritability, depression, and anxiety. Since a firm diagnosis of fibromyalgia is difficult, and no confirmatory laboratory tests are available, patients with fibromyalgia are often misdiagnosed as having depression as their primary underlying problem.

Other symptoms of fibromyalgia include migraine and tension headaches, numbness or tingling of different parts of the body, abdominal pain related to irritable bowel syndrome ("spastic colon"), and irritable bladder, causing painful and frequent urination. Like fibromyalgia, irritable bowel syndrome can cause chronic abdominal pain and other bowel disturbances without detectable inflammation of the stomach or the intestines. For further information, please see the read the Irritable Bowel Syndrome article.

Each patient with fibromyalgia is unique. Any of the above symptoms can occur intermittently and in different combinations.

How is fibromyalgia diagnosed?

There is no blood or x-ray test to help the doctor determine whether someone has fibromyalgia. Therefore, the diagnosis of fibromyalgia is made purely on clinical grounds based on the doctor's history and physical examination. In patients with widespread body pain, the diagnosis of fibromyalgia can be made by identifying point tenderness areas (typically, patients will have at least 11 of the 18 classic tender points), by finding no accompanying tissue swelling or inflammation, and by excluding other medical conditions that can mimic fibromyalgia. Many medical conditions can cause pain in different areas of the body, mimicking fibromyalgia. These conditions include:

low thyroid hormone level (hypothyroidism)
parathyroid disease (causing elevated blood calcium level)
muscle diseases causing muscle pain (such as polymyositis)
bone diseases causing bone pain (such as Paget's disease)
elevated blood calcium (hypercalcemia)
infectious diseases (such as hepatitis, Epstein Barr virus, AIDS)
cancer

Even though there is no blood test for fibromyalgia, blood tests are important to exclude other medical conditions. Therefore, thyroid hormone and calcium blood levels are obtained to exclude hypercalcemia, hyperparathyroidism and hypothyroidism. The blood alkaline phosphatase (a bone enzyme) level is often raised in patients with Paget's disease of the bone. The CPK (a muscle enzyme) level is often elevated in patients with polymyositis, a disease with diffuse muscle inflammation. Therefore, obtaining alkaline phosphatase and CPK blood levels can help the doctor decide whether Paget's disease and polymyositis are the causes of bone and muscle pains. A complete blood count (CBC), and liver tests help in the diagnosis of hepatitis and other infections.

Fibromyalgia can occur alone, or in association with other systemic rheumatic conditions. Systemic rheumatic conditions refer to diseases that can cause inflammation and damage to numerous different tissues and organs in the body. Systemic rheumatic conditions associated with fibromyalgia include systemic lupus erythematosus, rheumatoid arthritis, polymyositis, and polymyalgia rheumatica. Blood tests which are helpful in evaluating these diseases include erythrocyte sedimentation rate (ESR), serum protein electrophoresis (SPEP), antinuclear antibody (ANA), and rheumatoid factor (RF). In patients with fibromyalgia without associated systemic illnesses, the ESR, SPEP, ANA, and RF blood tests are usually normal.

What is the treatment for fibromyalgia?

Since the symptoms of fibromyalgia are diverse and vary among patients, treatment programs must be individualized for each patient. Treatment programs are most effective when they combine patient education, stress reduction, regular exercise, and medications. Recent studies have verified that the best outcome for each patient results from a combination of approaches that involves the patient in customization of the treatment plan.

Patient Education

Patient education is an important first step in helping patients understand and cope with the diverse symptoms. Unfortunately, not all physicians are intimately acquainted with the vagaries of this illness. Therefore, community hospital support groups and the local chapters of the Arthritis Foundation have become important educational resources for patients and their doctors. Arthritis Foundation is a national voluntary health organization that provides community education through their many local chapters. Community hospital support groups also provide an arena for patients to share their experiences and treatment successes and failures.

Stress Reduction

It is extremely difficult to measure stress levels in different patients. For some people, spilling milk on the table can represent a significant tragedy. For others, a tank rolling into the living room might represent "just another day!" Therefore, stress reduction in the treatment of fibromyalgia must be individualized. Stress reduction might include simple stress modification at home or work, biofeedback, relaxation tapes, psychological counseling, and/or support among family members, friends, and doctors. Sometimes, changes in environmental factors (such as noise, temperature, and weather exposure) can exacerbate the symptoms of fibromyalgia, and these factors need to be modified.

Exercise

Low-impact aerobic exercises, such as swimming, cycling, walking and stationary cross-country ski machines can be effective treatments for fibromyalgia. Exercise regimens are most beneficial when performed on an every-other-day basis, in the morning. How exercise benefits fibromyalgia is unknown. Exercise may exert its beneficial effect by promoting a deep level of sleep (non-REM sleep). Similarly, avoiding alcohol and caffeine before bedtime can also help promote a more restful sleep.

Medications

Traditionally, the most effective medications in the treatment of fibromyalgia have been the tricyclic antidepressants, medications traditionally used in treating depression. In treating fibromyalgia, tricyclic antidepressants are taken at bedtime in doses that are a fraction of those used for treating depression. Tricyclic antidepressants appear to reduce fatigue, relieve muscle pain and spasm, and promote deep restorative sleep in patients with fibromyalgia. Scientists believe that tricyclics work by interfering with a nerve transmitter chemical in the brain called "serotonin." Examples of tricyclic antidepressants commonly used in treating fibromyalgia include amitriptyline (Elavil) and doxepin (Sinequan).

Studies have shown that adding fluoxetine (Prozac), or related medications, to low dose amitriptyline (Elavil) further reduces muscle pain, anxiety, and depression in patients with fibromyalgia. The combination is also more effective in promoting restful sleep, and improving an overall sense of well-being. These two medications also tend to cancel out certain side effects each can have. Tricyclic medications can cause tiredness and fatigue while fluoxetine can make patients more cheerful and awake. Even more recently, study of patients with resistant fibromyalgia found that lorazepam (Ativan) was helpful in relieving symptoms. Fluoxetine (Prozac) has also been shown to be effective when used alone for some patients with fibromyalgia.

In 2007, pregabalin (Lyrica) became the first medication approved specifically for treating fibromyalgia.

Other Treatments

Local injections of analgesics and/or cortisone medication into the trigger point areas can also be helpful in relieving painful soft tissues, while breaking cycles of pain and muscle spasm. Some studies indicate that the pain-reliever tramadol (Ultram) and tramadol/acetaminophen (Ultracet) may be helpful for the treatment of fibromyalgia pains. The muscle relaxant cyclobenzaprine (Flexeril) has been helpful for reducing pain symptoms and improving sleep.

The nonsteroidal antiinflammatory drugs (NSAIDs), while very helpful in treating other rheumatic conditions, have only a limited value in treating fibromyalgia pain. Narcotic pain relievers and cortisone medications have not been shown to be beneficial in this condition. Narcotics and cortisone medications are avoided because they have not been shown to be beneficial and they have potential adverse side effects, including dependency, when used long-term.

Both biofeedback and electroacupuncture have been used for relief of symptoms with some success. Standard acupuncture was recently reported to be effective in treating some patients with fibromyalgia.

What is in the future for fibromyalgia therapy?

The key to unlocking the mystery of fibromyalgia has yet to be found. Research scientists have been studying numerous viruses as potential causes for fibromyalgia. Identification of an infectious agent or toxin which causes the disease may one day lead to a laboratory test which can help doctors diagnose fibromyalgia. Until further research uncovers the exact cause of the disease, specific treatment aimed at a cure remains unattainable.

New drugs may be developed that block substance P or nerve growth factor to relieve pain of fibromyalgia. Many fibromyalgia patients can be helped by improved patient education, proper exercise, and medications. With ongoing research, the future will certainly improve for those affected by fibromyalgia.

Recent research has suggested that drugs that block more than one brain nerve transmitter, such as duloxetine (Cymbalta), can be effective in treating fibromyalgia. Duloxetine has been effective in treating depression and relieving pain in persons with depression. Additional research suggests that the drug pregabalin may be helpful by blocking nerve pain in patients with fibromyalgia. More research is underway to evaluate the potential of these new treatments.

Fibromyalgia At A Glance

Fibromyalgia causes pain, stiffness, and tenderness of muscles, tendons, and joints without detectable inflammation.
Fibromyalgia does not cause body damage or deformity.
Fatigue occurs in 90% of patients with fibromyalgia.
Irritable bowel syndrome can occur with fibromyalgia.
Sleep disorder is common in patients with fibromyalgia.
There is no test for the diagnosis of fibromyalgia.
Fibromyalgia can be associated with other rheumatic conditions.
Treatment of fibromyalgia is most effective with combinations of education, stress reduction, exercise, and medications.

Diabetes Mellitus

2008-01-14T18:13:00.000-08:00

What is diabetes?

Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels, which result from defects in insulin secretion, or action, or both. Diabetes mellitus, commonly referred to as diabetes (as it will be in this article) was first identified as a disease associated with “sweet urine," and excessive muscle loss in the ancient world. Elevated levels of blood glucose (hyperglycemia) lead to spillage of glucose into the urine, hence the term sweet urine. Normally, blood glucose levels are tightly controlled by insulin, a hormone produced by the pancreas. Insulin lowers the blood glucose level. When the blood glucose elevates (for example, after eating food), insulin is released from the pancreas to normalize the glucose level. In patients with diabetes, the absence or insufficient production of insulin causes hyperglycemia. Diabetes is a chronic medical condition, meaning that although it can be controlled, it lasts a lifetime.

What is the impact of diabetes?

Over time, diabetes can lead to blindness, kidney failure, and nerve damage. These types of damage are the result of damage to small vessels, referred to as microvascular disease. Diabetes is also an important factor in accelerating the hardening and narrowing of the arteries (atherosclerosis), leading to strokes, coronary heart disease, and other large blood vessel diseases. This is referred to as macrovascular disease. Diabetes affects approximately 17 million people (about 8% of the population) in the United States. In addition, an estimated additional 12 million people in the United States have diabetes and don't even know it. From an economic perspective, the total annual cost of diabetes in 1997 was estimated to be 98 billion dollars in the United States. The per capita cost resulting from diabetes in 1997 amounted to $10,071.00; while healthcare costs for people without diabetes incurred a per capita cost of $2,699.00. During this same year, 13.9 million days of hospital stay were attributed to diabetes, while 30.3 million physician office visits were diabetes related. Remember, these numbers reflect only the population in the United States. Globally, the statistics are staggering.

Diabetes is the third leading cause of death in the United States after heart disease and cancer.

What causes diabetes?

Insufficient production of insulin (either absolutely or relative to the body's needs), production of defective insulin (which is uncommon), or the inability of cells to use insulin properly and efficiently leads to hyperglycemia and diabetes. This latter condition affects mostly the cells of muscle and fat tissues, and results in a condition known as "insulin resistance." This is the primary problem in type 2 diabetes. The absolute lack of insulin, usually secondary to a destructive process affecting the insulin producing beta cells in the pancreas, is the main disorder in type 1 diabetes. In type 2 diabetes, there also is a steady decline of beta cells that adds to the process of elevated blood sugars. For more, please read the Insulin Resistance article. Essentially, if someone is resistant to insulin, the body can, to some degree, increase production of insulin and overcome the level of resistance. After time, if production decreases and insulin cannot be released as vigorously, hyperglycemia develops.

Glucose is a simple sugar found in food. Glucose is an essential nutrient that provides energy for the proper functioning of the body cells. Carbohydrates are broken down in the small intestine and the glucose in digested food is then absorbed by the intestinal cells into the bloodstream, and is carried by the bloodstream to all the cells in the body where it is utilized. However, glucose cannot enter the cells alone and needs insulin to aid in its transport into the cells. Without insulin, the cells become starved of glucose energy despite the presence of abundant glucose in the bloodstream. In certain types of diabetes, the cells' inability to utilize glucose gives rise to the ironic situation of "starvation in the midst of plenty". The abundant, unutilized glucose is wastefully excreted in the urine.

Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. (The pancreas is a deep-seated organ in the abdomen located behind the stomach.) In addition to helping glucose enter the cells, insulin is also important in tightly regulating the level of glucose in the blood. After a meal, the blood glucose level rises. In response to the increased glucose level, the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. When the blood glucose levels are lowered, the insulin release from the pancreas is turned down. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. In normal individuals, such a regulatory system helps to keep blood glucose levels in a tightly controlled range. As outlined above, in patients with diabetes, the insulin is either absent, relatively insufficient for the body's needs, or not used properly by the body. All of these factors cause elevated levels of blood glucose (hyperglycemia).

What are the different types of diabetes?

There are two major types of diabetes, called type 1 and type 2. Type 1 diabetes was also called insulin dependent diabetes mellitus (IDDM), or juvenile onset diabetes mellitus. In type 1 diabetes, the pancreas undergoes an autoimmune attack by the body itself, and is rendered incapable of making insulin. Abnormal antibodies have been found in the majority of patients with type 1 diabetes. Antibodies are proteins in the blood that are part of the body's immune system. The patient with type 1 diabetes must rely on insulin medication for survival.

In autoimmune diseases, such as type 1 diabetes, the immune system mistakenly manufactures antibodies and inflammatory cells that are directed against and cause damage to patients' own body tissues. In persons with type 1 diabetes, the beta cells of the pancreas, which are responsible for insulin production, are attacked by the misdirected immune system. It is believed that the tendency to develop abnormal antibodies in type 1 diabetes is, in part, genetically inherited, though the details are not fully understood. Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. These antibodies can be measured in the majority of patients, and may help determine which individuals are at risk for developing type 1 diabetes.

At present, the American Diabetes Association does not recommend general screening of the population for type 1 diabetes, though screening of high risk individuals, such as those with a first degree relative (sibling or parent) with type 1 diabetes should be encouraged. Type 1 diabetes tends to occur in young, lean individuals, usually before 30 years of age, however, older patients do present with this form of diabetes on occasion. This subgroup is referred to as latent autoimmune diabetes in adults (LADA). LADA is a slow, progressive form of type 1 diabetes. Of all the patients with diabetes, only approximately 10% of the patients have type 1 diabetes and the remaining 90% have type 2 diabetes.

Type 2 diabetes was also referred to as non-insulin dependent diabetes mellitus (NIDDM), or adult onset diabetes mellitus (AODM). In type 2 diabetes, patients can still produce insulin, but do so relatively inadequately for their body's needs, particularly in the face of insulin resistance as discussed above. In many cases this actually means the pancreas produces larger than normal quantities of insulin. A major feature of type 2 diabetes is a lack of sensitivity to insulin by the cells of the body (particularly fat and muscle cells). In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.

While it is said that type 2 diabetes occurs mostly in individuals over 30 years old and the incidence increases with age, we are seeing an alarming number patients with type 2 diabetes who are barely in their teen years. In fact, for the first time in the history of humans, type 2 diabetes is now more common than type 1 diabetes in childhood. Most of these cases are a direct result of poor eating habits, higher body weight, and lack of exercise.

While there is a strong genetic component to developing this form of diabetes, there are other risk factors - the most significant of which is obesity. There is a direct relationship between the degree of obesity and the risk of developing type 2 diabetes, and this holds true in children as well as adults. It is estimated that the chance to develop diabetes doubles for every 20% increase over desirable body weight.

Regarding age, data shows that for each decade after 40 years of age regardless of weight there is an increase in incidence of diabetes. The prevalence of diabetes in persons 65 to 74 years of age is nearly 20%. Type 2 diabetes is also more common in certain ethnic groups. Compared with a 6% prevalence in Caucasians, the prevalence in African Americans and Asian Americans is estimated to be 10%, in Hispanics 15%, and in certain Native American communities 20% to 50%. Finally, diabetes occurs much more frequently in women with a prior history of diabetes that develops during pregnancy (gestational diabetes - see below).

Diabetes can occur temporarily during pregnancy. Significant hormonal changes during pregnancy can lead to blood sugar elevation in genetically predisposed individuals. Blood sugar elevation during pregnancy is called gestational diabetes. Gestational diabetes usually resolves once the baby is born. However, 25-50% of women with gestational diabetes will eventually develop Type 2 diabetes later in life, especially in those who require insulin during pregnancy and those who remain overweight after their delivery. Patients with gestational diabetes are usually asked to undergo an oral glucose tolerance test about 6 weeks after giving birth to determine if their diabetes has persisted beyond the pregnancy, or if any evidence (such as impaired glucose tolerance) is present that may be a clue to the patient's future risk for developing diabetes.

"Secondary" diabetes refers to elevated blood sugar levels from another medical condition. Secondary diabetes may develop when the pancreatic tissue responsible for the production of insulin is destroyed by disease, such as chronic pancreatitis (inflammation of the pancreas by toxins like excessive alcohol), trauma, or surgical removal of the pancreas. Diabetes can also result from other hormonal disturbances, such as excessive growth hormone production (acromegaly) and Cushing's syndrome. In acromegaly, a pituitary gland tumor at the base of the brain causes excessive production of growth hormone, leading to hyperglycemia. In Cushing's syndrome, the adrenal glands produce an excess of cortisol, which promotes blood sugar elevation.

In addition, certain medications may worsen diabetes control, or "unmask" latent diabetes. This is seen most commonly when steroid medications (such as prednisone) are taken and also with medications used in the treatment of HIV infection (AIDS).

What are diabetes symptoms?

The early symptoms of untreated diabetes are related to elevated blood sugar levels, and loss of glucose in the urine. High amounts of glucose in the urine can cause increased urine output and lead to dehydration. Dehydration causes increased thirst and water consumption. The inability of insulin to perform normally has effects on protein, fat and carbohydrate metabolism. Insulin is an anabolic hormone, that is, one that encourages storage of fat and protein. A relative or absolute insulin deficiency eventually leads to weight loss despite an increase in appetite. Some untreated diabetes patients also complain of fatigue, nausea and vomiting. Patients with diabetes are prone to developing infections of the bladder, skin, and vaginal areas. Fluctuations in blood glucose levels can lead to blurred vision. Extremely elevated glucose levels can lead to lethargy and coma.

How is diabetes diagnosed?

The fasting blood glucose (sugar) test is the preferred way to diagnose diabetes. It is easy to perform and convenient. After the person has fasted overnight (at least 8 hours), a single sample of blood is drawn and sent to the laboratory for analysis. This can also be done accurately in a doctor's office using a glucose meter.

Normal fasting plasma glucose levels are less than 100 milligrams per deciliter (mg/dl). Fasting plasma glucose levels of more than 126 mg/dl on two or more tests on different days indicate diabetes. A random blood glucose test can also be used to diagnose diabetes A blood glucose level of 200 mg/dl or higher indicates diabetes.

When fasting blood glucose stays above 100mg/dl, but in the range of 100-126mg/dl, this is known as impaired fasting glucose (IFG). While patients with IFG do not have the diagnosis of diabetes, this condition carries with it its own risks and concerns, and is addressed elsewhere.

The oral glucose tolerance test

Though not routinely used anymore, the oral glucose tolerance test (OGTT) is a gold standard for making the diagnosis of type 2 diabetes. It is still commonly used for diagnosing gestational diabetes. With an oral glucose tolerance test, the person fasts overnight (at least eight but not more than 16 hours). Then first, the fasting plasma glucose is tested. After this test, the person receives 75 grams of glucose (100 grams for pregnant women). There are several methods employed by obstetricians to do this test, but the one described here is standard. Usually, the glucose is in a sweet-tasting liquid that the person drinks. Blood samples are taken at specific intervals to measure the blood glucose.

For the test to give reliable results, the person must be in good health (not have any other illnesses, not even a cold). Also, the person should be normally active (not lying down, for example, as an inpatient in a hospital) and should not be taking medicines that could affect the blood glucose. For three days before the test, the person should have eaten a diet high in carbohydrates (150- 200 grams per day). The morning of the test, the person should not smoke or drink coffee.

The classic oral glucose tolerance test measures blood glucose levels five times over a period of three hours. Some physicians simply get a baseline blood sample followed by a sample two hours after drinking the glucose solution. In a person without diabetes, the glucose levels rise and then fall quickly. In someone with diabetes, glucose levels rise higher than normal and fail to come back down as fast.

People with glucose levels between normal and diabetic have impaired glucose tolerance (IGT). People with impaired glucose tolerance do not have diabetes, but are at high risk for progressing to diabetes. Each year, 1-5% of people whose test results show impaired glucose tolerance actually eventually develop diabetes. Weight loss and exercise may help people with impaired glucose tolerance return their glucose levels to normal. In addition, some physicians advocate the use of medications, such as metformin (Glucophage), to help prevent/delay the onset of overt diabetes. Recent studies have shown that impaired glucose tolerance itself may be a risk factor for the development of heart disease. In the medical community, most physicians are now understanding that impaired glucose tolerance is nor simply a precursor of diabetes, but is its own clinical disease entity that requires treatment and monitoring.

Evaluating the results of the oral glucose tolerance test

Glucose tolerance tests may lead to one of the following diagnoses:

Normal response: A person is said to have a normal response when the 2-hour glucose level is less than 140 mg/dl, and all values between 0 and 2 hours are less than 200 mg/dl.
Impaired glucose tolerance: A person is said to have impaired glucose tolerance when the fasting plasma glucose is less than 126 mg/dl and the 2-hour glucose level is between 140 and 199 mg/dl.
Diabetes: A person has diabetes when two diagnostic tests done on different days show that the blood glucose level is high.
Gestational diabetes: A woman has gestational diabetes when she has any two of the following: a 100g OGTT, a fasting plasma glucose of more than 95 mg/dl, a 1-hour glucose level of more than 180 mg/dl, a 2-hour glucose level of more than 155 mg/dl, or a 3-hour glucose level of more than 140 mg/dl.

Why is blood sugar checked at home?

Home blood sugar (glucose) testing is an important part of controlling blood sugar. One important goal of diabetes treatment is to keep the blood glucose levels near the normal range of 70 to 120 mg/dl before meals and under 140 mg/dl at two hours after eating. Blood glucose levels are usually tested before and after meals, and at bedtime. The blood sugar level is typically determined by pricking a fingertip with a lancing device and applying the blood to a glucose meter, which reads the value. There are many meters on the market, for example, Accu-Check Advantage, One Touch Ultra, Sure Step and Freestyle. Each meter has its own advantages and disadvantages (some use less blood, some have a larger digital readout, some take a shorter time to give you results, etc). The test results are then used to help patients make adjustments in medications, diets, and physical activities.

There are some interesting developments in blood glucose monitoring. Currently, at least three continuous glucose sensors are being considered for approval in the United States (Dexcom, Medtronic and Navigator). The new continuous glucose sensor systems involve an implantable cannula placed just under the skin in the abdomen or in the arm. This cannula allows for frequent sampling of blood glucose levels. Attached to this is a transmitter that sends the data to a pager-like device. This device has a visual screen that allows the wearer to see, not only the current glucose reading, but also the graphic trends. In some devices, the rate of change of blood sugar is also shown. There are alarms for low and high sugar levels. Certain models will alarm if the rate of change indicates the wearer is at risk for dropping or rising blood glucose too rapidly. The Medtronic version is specifically designed to interface with their insulin pumps. However, at this time the patient still must manually approve any insulin dose (the pump cannot blindly respond to the glucose information it receives, it can only give a calculated suggestion as to whether the wearer should give insulin, and if so, how much). All of these devices need to be correlated to fingersticks for a few hours before they can function independently. The devices can then provide readings for 3-5 days.

Diabetes experts feel that these blood glucose monitoring devices give patients a significant amount of independence to manage their disease process; and they are a great tool for education as well. It is also important to remember that these devices can be used intermittently with fingersticks. For example, a well-controlled patient with diabetes can rely on fingerstick glucose checks a few times a day and do well. If they become ill, if they decide to embark on a new exercise regimen, if they change their diet and so on, they can use the sensor to supplement their fingerstick regimen, providing more information on how they are responding to new lifestyle changes or stressors. This kind of system takes us one step closer to closing the loop, and to the development of an artifical pancreas that senses insulin requirements based on glucose levels and the body's needs and releases insulin accordingly - the ultimate goal.

Hemoglobin A1c (A1c)

To explain what an A1c is, think in simple terms. Sugar sticks, and when it's around for a long time, it's harder to get it off. In the body, sugar sticks too, particularly to proteins. The red blood cells that circulate in the body live for about three months before they die off. When sugar sticks to these cells, it gives us an idea of how much sugar is around for the preceding three months. In most labs, the normal range is 4-5.9 %. In poorly controlled diabetes, its 8.0% or above, and in well controlled patients it's less than 7.0% (optimal is <6.5%).>

While there are no guidelines to use A1c as a screening tool, it gives a physician a good idea that someone is diabetic if the value is elevated. Right now, it is used as a standard tool to determine blood sugar control in patients known to have diabetes.

A1c(%)	Mean blood sugar (mg/dl)
6	135
7	170
8	205
9	240
10	275
11	310
12	345

The American Diabetes Association currently recommends an A1c goal of less than 7.0%. Other Groups such as the American Association of Clinical Endocrinologists feel that an A1c of <>

Of interest, studies have shown that there is about a 10% decrease in relative risk for microvascular disease for every 1 % reduction in A1c. So, if a patient starts off with an A1c of 10.7 and drops to 8.2, though there are not yet at goal, they have managed to decrease their risk of microvascular complications by about 20%. The closer to normal the A1c, the lower the absolute risk for microvascular complications. Data also suggests that the risk of macrovascular disease decreases by about 24% for every 1% reduction in A1c values.

It should be mentioned here that there are a number of conditions in which an A1c value may not be accurate. For example, with significant anemia, the red blood cell count is low, and thus the A1c is falsely low as is similarly in cases of sickle cell disease and other hemoglobinopathies. For more, please read the Hemoglobin A1c article.

What are the acute complications of diabetes?

Severely elevated blood sugar levels due to an actual lack of insulin or a relative deficiency of insulin.
Abnormally low blood sugar levels due to too much insulin or other glucose-lowering medications.

Insulin is vital to patients with type 1 diabetes - they cannot live with out a source of exogenous insulin. Without insulin, patients with type 1 diabetes develop severely elevated blood sugar levels. This leads to increased urine glucose, which in turn leads to excessive loss of fluid and electrolytes in the urine. Lack of insulin also causes the inability to store fat and protein along with breakdown of existing fat and protein stores. This dysregulation, results in the process of ketosis and the release of ketones into the blood. Ketones turn the blood acidic, a condition called diabetic ketoacidosis (DKA). Symptoms of diabetic ketoacidosis include nausea, vomiting, and abdominal pain. Without prompt medical treatment, patients with diabetic ketoacidosis can rapidly go into shock, coma, and even death.

Diabetic ketoacidosis can be caused by infections, stress, or trauma all which may increase insulin requirements. In addition, missing doses of insulin is also an obvious risk factor for developing diabetic ketoacidosis. Urgent treatment of diabetic ketoacidosis involves the intravenous administration of fluid, electrolytes, and insulin, usually in a hospital intensive care unit. Dehydration can be very severe, and it is not unusual to need to replace 6-7 liters of fluid when a person presents in diabetic ketoacidosis. Antibiotics are given for infections. With treatment, abnormal blood sugar levels, ketone production, acidosis, and dehydration can be reversed rapidly, and patients can recover remarkably well.

In patients with type 2 diabetes, stress, infection, and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Accompanied by dehydration, severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). This condition can lead to coma (hyperosmolar coma). A hyperosmolar coma usually occurs in elderly patients with type 2 diabetes. Like diabetic ketoacidosis, a hyperosmolar coma is a medical emergency. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. Unlike patients with type 1 diabetes, patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. Since in general, type 2 diabetes occurs in an older population, concomitant medical conditions are more likely to exist, and these patients may actually be sicker overall. The complication and death rates from hyperosmolar coma is thus higher than in DKA.

Hypoglycemia means abnormally low blood sugar (glucose). In patients with diabetes, the most common cause of low blood sugar is excessive use of insulin or other glucose-lowering medications, to lower the blood sugar level in diabetic patients in the presence of a delayed or absent meal. When low blood sugar levels occur because of too much insulin, it is called an insulin reaction. Sometimes, low blood sugar can be the result of an insufficient caloric intake or sudden excessive physical exertion.

Blood glucose is essential for the proper functioning of brain cells. Therefore, low blood sugar can lead to central nervous system symptoms such as dizziness, confusion, weakness, and tremors. The actual level of blood sugar at which these symptoms occur varies with each person, but usually it occurs when blood sugars are less than 65 mg/dl. Untreated, severely low blood sugar levels can lead to coma, seizures, and, in the worse case scenario, irreversible brain death. At this point, the brain is suffering from a lack of sugar, and this usually occurs somewhere around levels of <40>

The treatment of low blood sugar consists of administering a quickly absorbed glucose source. These include glucose containing drinks, such as orange juice, soft drinks (not sugar-free), or glucose tablets in doses of 15-20 grams at a time (for example, the equivalent of half a glass of juice). Even cake frosting applied inside the cheeks can work in a pinch if patient cooperation is difficult. If the individual becomes unconscious, glucagon can be given by intramuscular injection.

Glucagon causes the release of glucose from the liver (i.e., it promotes gluconeogenesis). Glucagon can be lifesaving and every patient with diabetes who has a history of hypoglycemia (particularly those on insulin) should have a glucagon kit. Families and friends of those with diabetes need to be taught how to administer glucagon, since obviously the patients will not be able to do it themselves in an emergency situation. Another lifesaving device that should be mentioned is very simple; a medic alert bracelet should be worn by all patients with diabetes.

For more, please read the Hypoglycemia article.

What are the chronic complications of diabetes?

These diabetes complications are related to blood vessel diseases and are generally classified into small vessel disease, such as those involving the eyes, kidneys and nerves (microvascular disease), and large vessel disease involving the heart and blood vessels (macrovascular disease). Diabetes accelerates hardening of the arteries (atherosclerosis) of the larger blood vessels, leading to coronary heart disease (angina or heart attack), strokes, and pain in the lower extremities because of lack of blood supply (claudication). For more information, please read the following articles: Stroke, Angina, and Heart Attack.

Eye Complications

The major eye complication of diabetes is called diabetic retinopathy. Diabetic retinopathy occurs in patients who have had diabetes for at least five years. Diseased small blood vessels in the back of the eye cause the leakage of protein and blood in the retina. Disease in these blood vessels also causes the formation of small aneurysms (microaneurysms), and new but brittle blood vessels (neovascularization). Spontaneous bleeding from the new and brittle blood vessels can lead to retinal scarring and retinal detachment, thus impairing vision.

To treat diabetic retinopathy a laser is used to destroy and prevent the recurrence of the development of these small aneurysms and brittle blood vessels. Approximately 50% of patients with diabetes will develop some degree of diabetic retinopathy after 10 years of diabetes, and 80% of diabetics have retinopathy after 15 years of the disease. Poor control of blood sugar and blood pressure further aggravates eye disease in diabetes. For more, please read the Diabetic Eye Disease article.

Cataracts and glaucoma are also more common among diabetics. It is also important to note that since the lens of the eye lets water through, if blood sugar concentrations vary a lot, the lens of the eye will shrink and swell with fluid accordingly. As a result, blurry vision is very common in poorly controlled diabetes. Patients are usually discouraged from getting a new eyeglass prescription until their blood sugar is controlled. This allows for a more accurate assessment of what kind of glasses prescription is required.

Kidney damage

Kidney damage from diabetes is called diabetic nephropathy. The onset of kidney disease and its progression is extremely variable. Initially, diseased small blood vessels in the kidneys cause the leakage of protein in the urine. Later on, the kidneys lose their ability to cleanse and filter blood. The accumulation of toxic waste products in the blood leads to the need for dialysis. Dialysis involves using a machine that serves the function of the kidney by filtering and cleaning the blood. In patients who do not want to undergo chronic dialysis, kidney transplantation can be considered. For more about dialysis, please read the Kidney Dialysis article.

The progression of nephropathy in patients can be significantly slowed by controlling high blood pressure, and by aggressively treating high blood sugar levels. Angiotensin converting enzyme inhibitors (ACE inhibitors) or angiotensin receptor blockers (ARBs) used in treating high blood pressure may also benefit kidney disease in diabetic patients.

Nerve damage

Nerve damage in diabetes is called diabetic neuropathy and is also caused by disease of small blood vessels. In essence, the blood flow to the nerves is limited, leaving the nerves without blood flow, and they get damaged or die as a result (a term known as ischemia). Symptoms of diabetic nerve damage include numbness, burning, and aching of the feet and lower extremities. When the nerve disease causes a complete loss of sensation in the feet, patients may not be aware of injuries to the feet, and fail to properly protect them. Shoes or other protection should be worn as much as possible. Seemingly minor skin injuries should be attended to promptly to avoid serious infections. Because of poor blood circulation, diabetic foot injuries may not heal. Sometimes, minor foot injuries can lead to serious infection, ulcers, and even gangrene, necessitating surgical amputation of toes, feet, and other infected parts.

Diabetic nerve damage can affect the nerves that are important for penile erection, causing erectile dysfunction (ED, impotence). Erectile dysfunction can also be caused by poor blood flow to the penis from diabetic blood vessel disease.

Diabetic neuropathy can also affect nerves to the stomach and intestines, causing nausea, weight loss, diarrhea, and other symptoms of gastroparesis (delayed emptying of food contents from the stomach into the intestines, due to ineffective contraction of the stomach muscles).

The pain of diabetic nerve damage may respond to traditional treatments with gabapentin (Neurontin), phenytoin (Dilantin), carbamazepine (Tegretol), desipramine (Norpraminine), amitriptyline (Elavil), or with topically-applied capsaicin (an extract of pepper). Neurontin, Dilantin and Tegretol are medications that are traditionally used in the treatment of seizure disorders. Elavil and Norpraminine are medications that are traditionally used for depression. While many of these medications are not FDA indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly. The pain of diabetic nerve damage may also improve with better blood sugar control, though unfortunately blood glucose control and the course of neuropathy do not always go hand in hand. Newer medications for nerve pain have recently come to market in the US. Pregabalin (Lyrica) which has an indication for diabetic neuropathic pain and duloxetine (Cymbalta) are newer agents used in the treatment of diabetic neuropathy. For more, please read the Diabetic Neuropathy article.

What can be done to slow diabetes complications?

Findings from the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS) have clearly shown that aggressive and intensive control of elevated levels of blood sugar in patients with type 1 and type 2 diabetes decreases the complications of nephropathy, neuropathy, retinopathy, and may reduce the occurrence and severity of large blood vessel diseases. Aggressive control with intensive therapy means achieving fasting glucose levels between 70-120 mg/dl; glucose levels of less than 160 mg/dl after meals; and a near normal hemoglobin A1C levels (see below).

Studies in type 1 patients have shown that in intensively treated patients, diabetic eye disease decreased by 76%, kidney disease decreased by 54%, and nerve disease decreased by 60%. More recently the EDIC trial has shown that type 1 diabetes is also associated with increased heart disease, similar to type 2 diabetes. However, the price for aggressive blood sugar control is a two to three fold increase in the incidence of abnormally low blood sugar levels (caused by the diabetes medications). For this reason, tight control of diabetes to achieve glucose levels between 70-120 mg/dl is not recommended for children under 13 years of age, patients with severe recurrent hypoglycemia, patients unaware of their hypoglycemia, and patients with far advanced diabetes complications. To achieve optimal glucose control without an undue risk of abnormally lowering blood sugar levels, patients with type 1 diabetes must monitor their blood glucose at least four times a day and administer insulin at least three times per day. In patients with type 2 diabetes, aggressive blood sugar control has similar beneficial effects on the eyes, kidneys, nerves and blood vessels.

How is diabetes treated?

Please see the Diabetes Treatment article.

Diabetes At A Glance

Diabetes is a chronic condition associated with abnormally high levels of sugar (glucose) in the blood.
Insulin produced by the pancreas lowers blood glucose.
Absence or insufficient production of insulin causes diabetes.
The two types of diabetes are referred to as type 1 (insulin dependent) and type 2 (non-insulin dependent).
Symptoms of diabetes include increased urine output, thirst and hunger as well as fatigue.
Diabetes is diagnosed by blood sugar (glucose) testing.
The major complications of diabetes are both acute and chronic.
- Acutely: dangerously elevated blood sugar, abnormally low blood sugar due to diabetes medications may occur.
- Chronically: disease of the blood vessels (both small and large) which can damage the eye, kidneys, nerves, and heart may occur
Diabetes treatment depends on the type and severity of the diabetes. Type 1 diabetes is treated with insulin, exercise, and a diabetic diet. Type 2 diabetes is first treated with weight reduction, a diabetic diet, and exercise. When these measures fail to control the elevated blood sugars, oral medications are used. If oral medications are still insufficient, insulin medications are considered.

Crohn's Disease

2008-01-14T18:09:00.000-08:00

What is Crohn's disease?

Crohn's disease is a chronic inflammatory disease of the intestines. It primarily causes ulcerations (breaks in the lining) of the small and large intestines, but can affect the digestive system anywhere from the mouth to the anus. It is named after the physician who described the disease in 1932. It also is called granulomatous enteritis or colitis, regional enteritis, ileitis, or terminal ileitis.

Crohn's disease is related closely to another chronic inflammatory condition that involves only the colon called ulcerative colitis. Together, Crohn's disease and ulcerative colitis are frequently referred to as inflammatory bowel disease (IBD). Ulcerative colitis and Crohn's disease have no medical cure. Once the diseases begin, they tend to fluctuate between periods of inactivity (remission) and activity (relapse). They affect approximately 500,000 to two million people in the United States. Men and women are equally affected. IBD most commonly begins during adolescence and early adulthood, but it also can begin during childhood and later in life.

Crohn's disease tends to be more common in relatives of patients with Crohn's disease. It also is more common among relatives of patients with ulcerative colitis.

What causes Crohn's disease?

The cause of Crohn's disease is unknown. Some scientists suspect that infection by certain bacteria, such as strains of mycobacterium, may be the cause of Crohn's disease. To date, however, there has been no convincing evidence that the disease is caused by infection. Crohn's disease is not contagious. Although diet may affect the symptoms in patients with Crohn's disease, it is unlikely that diet is responsible for the disease.

Activation of the immune system in the intestines appears to be important in IBD. The immune system is composed of immune cells and the proteins that these immune cells produce. Normally, these cells and proteins defend the body against harmful bacteria, viruses, fungi, and other foreign invaders. Activation of the immune system causes inflammation within the tissues where the activation occurs. (Inflammation is an important mechanism of defense used by the immune system.)

Normally, the immune system is activated only when the body is exposed to harmful invaders. In patients with IBD, however, the immune system is abnormally and chronically activated in the absence of any known invader. The continued abnormal activation of the immune system results in chronic inflammation and ulceration. The susceptibility to abnormal activation of the immune system is genetically inherited. Thus, first degree relatives (brothers, sisters, children, and parents) of patients with IBD are more likely to develop these diseases. Recently a gene called NOD2 has been identified as being associated with Crohn's disease. This gene is important in determining how the body responds to some bacterial products. Individuals with mutations in this gene are more susceptible to developing Crohn's disease.

How does Crohn's disease affect the intestines?

In the early stages, Crohn's disease causes small, scattered, shallow, crater–like areas (erosions) on the inner surface of the bowel. These erosions are called aphthous ulcers. With time, the erosions become deeper and larger, ultimately becoming true ulcers (which are deeper than erosions) and causing scarring and stiffness of the bowel. As the disease progresses, the bowel becomes increasingly narrowed, and ultimately can become obstructed. Deep ulcers can puncture holes in the wall of the bowel, and bacteria from within the bowel can spread to infect adjacent organs and the surrounding abdominal cavity.

When Crohn's disease narrows the small intestine to the point of obstruction, the flow of the contents through the intestine ceases. Sometimes, the obstruction can be caused suddenly by poorly–digestible fruit or vegetables that plug the already–narrowed segment of the intestine. When the intestine is obstructed, digesting food, fluid and gas from the stomach and the small intestine cannot pass into the colon. The symptoms of small intestinal obstruction then appear, including severe abdominal cramps, nausea, vomiting, and abdominal distention. Obstruction of the small intestine is much more likely since the small intestine is much narrower than the colon to begin with.

Deep ulcers can puncture holes in the walls of the small intestine and the colon, and create a tunnel between the intestine and adjacent organs. If the ulcer tunnel reaches an adjacent empty space inside the abdominal cavity, a collection of infected pus (an abdominal abscess) is formed. Patients with abdominal abscesses can develop tender abdominal masses, high fevers, and abdominal pain.

When the ulcer tunnels into an adjacent organ, a channel (fistula) is formed. The formation of a fistula between the intestine and the bladder (enteric–vesicular fistula) can cause frequent urinary tract infections and the passage of gas and feces during urination. When a fistula develops between the intestine and the skin (enteric–cutaneous fistula), pus and mucous emerge from a small painful opening on the skin of the abdomen. The development of a fistula between the colon and the vagina (colonic–vaginal fistula) causes gas and feces to emerge through the vagina. The presence of a fistula from the intestines to the anus (anal fistula) leads to a discharge of mucous and pus from the fistula's opening around the anus.

How is Crohn's disease different from ulcerative colitis?

While ulcerative colitis causes inflammation only in the colon (colitis) and/or the rectum (proctitis), Crohn's disease may cause inflammation in the colon, rectum, small intestine (jejunum and ileum), and, occasionally, even the stomach, mouth, and esophagus.

The patterns of inflammation in Crohn's disease are different from ulcerative colitis. Except in the most severe cases, the inflammation of ulcerative colitis tends to involve the superficial layers of the inner lining of the bowel. The inflammation also tends to be diffuse and uniform. (All of the lining in the affected segment of the intestine is inflamed.) Unlike ulcerative colitis, the inflammation of Crohn's disease is concentrated in some areas more than others and involves layers of the bowel that are deeper than the superficial inner layers. Therefore, the affected segment(s) of bowel in Crohn's disease often is studded with deeper ulcers with normal lining between these ulcers.

What are the symptoms of Crohn's disease?

Common symptoms of Crohn's disease include abdominal pain, diarrhea, and weight loss. Less common symptoms include poor appetite, fever, night sweats, rectal pain, and rectal bleeding. The symptoms of Crohn's disease are dependent on the location, the extent, and the severity of the inflammation. The different subtypes of Crohn's disease and their symptoms are:

Crohn's colitis is inflammation that is confined to the colon. Abdominal pain and bloody diarrhea are the common symptoms. Anal fistulae and peri–rectal abscesses also can occur.

Crohn's enteritis refers to inflammation confined to the small intestine (the first part, called the jejunum or the second part, called the ileum). Involvement of the ileum alone is referred to as Crohn's ileitis. Abdominal pain and diarrhea are the common symptoms. Obstruction of the small intestine also can occur.

Crohn's terminal ileitis is inflammation that affects only the very end of the small intestine (terminal ileum), the part of the small intestine closest to the colon. Abdominal pain and diarrhea are the common symptoms. Small intestinal obstruction also can occur.

Crohn's entero–colitis and ileo–colitis are terms to describe inflammation that involve both the small intestine and the colon. Bloody diarrhea and abdominal pain are the common symptoms. Small intestinal obstruction also can occur.

Crohn's terminal ileitis and ileo–colitis are the most common types of Crohn's disease. (Ulcerative colitis frequently involves only the rectum or rectum and sigmoid colon at the distal end of the colon. These are called ulcerative proctitis and procto–sigmoiditis, respectively.)

Up to one third of patients with Crohn's disease may have one or more of the following conditions involving the anal area:

Swelling of the tissue of the anal sphincter, the muscle at the end of the colon that controls defecation.

Development of ulcers and fissures (long ulcers) within the anal sphincter. These ulcers and fissures can cause bleeding and pain with defecation.

Development of anal fistulae (abnormal tunnels) between the anus or rectum and the skin surrounding the anus). Mucous and pus may drain from the openings of the fistulae on the skin.

Development of peri–rectal abscesses (collections of pus in the anal and rectal area). Peri–rectal abscesses can cause fever, pain and tenderness around the anus.

What are the complications of Crohn's disease?

Complications of Crohn's disease may be related or unrelated to the inflammation within the intestine (such as intestinal or extra–intestinal). Intestinal complications of Crohn's disease include obstruction and perforation of the small intestine, abscesses (collections of pus), fistulae, and intestinal bleeding. Massive distention or dilatation of the colon (megacolon), and rupture (perforation) of the intestine are potentially life–threatening complications. Both generally require surgery, but, fortunately, these two complications are rare. Recent data suggest that there is an increased risk of cancer of the small intestine and colon in patients with long–standing Crohn's disease.

Extra–intestinal complications involve the skin, joints, spine, eyes, liver, and bile ducts. Skin involvement includes painful red raised spots on the legs (erythema nodosum) and an ulcerating skin condition generally found around the ankles called pyoderma gangrenosum. Painful eye conditions (uveitis, episcleritis) can cause visual difficulties. Arthritis can cause pain, swelling, and stiffness of the joints of the extremities. Inflammation of the low back (sacroiliac joint arthritis) and of the spine (ankylosing spondylitis) can cause pain and stiffness of the spine. Inflammation of the liver (hepatitis) or bile ducts (primary sclerosing cholangitis) also can occur. Sclerosing cholangitis causes narrowing and obstruction of the ducts draining the liver and can lead to yellow skin (jaundice), recurrent bacterial infections, and liver cirrhosis with liver failure. Sclerosing cholangitis with liver failure is one of the reasons for performing liver transplantation. Sclerosing cholangitis frequently is complicated by the development of cancer of the bile ducts.

How is Crohn's disease diagnosed?

The diagnosis of Crohn's disease is suspected in patients with fever, abdominal pain and tenderness, diarrhea with or without bleeding, and anal diseases. Laboratory blood tests may show elevated white cell counts and sedimentation rates, both of which suggest infection or inflammation. Other blood tests may show low red blood cell counts (anemia), low blood proteins, and low body minerals, reflecting loss of these elements due to chronic diarrhea.

Barium x–ray studies can be used to define the distribution, nature, and severity of the disease. Barium is a chalky material that is visible by x–ray and appears white on x–ray films. When barium is ingested orally (upper GI series) it fills the intestine and pictures (x–rays) can be taken of the stomach and the small intestines. When barium is administered through the rectum (barium enema), pictures of the colon and the terminal ileum can be obtained. Barium x–rays can show ulcerations, narrowing, and, sometimes, fistulae of the bowel.

Direct visualization of the rectum and the large intestine can be accomplished with flexible viewing tubes (colonoscopes). Colonoscopy is more accurate than barium x–rays in detecting small ulcers or small areas of inflammation of the colon and terminal ileum. Colonoscopy also allows for small tissue samples (biopsies) to be taken and sent for examination under the microscope to confirm the diagnosis of Crohn's disease. Colonoscopy also is more accurate than barium x–rays in assessing the degree (activity) of inflammation.

Computerized axial tomography (CAT or CT) scanning is a computerized x–ray technique that allows imaging of the entire abdomen and pelvis. It can be especially helpful in detecting abscesses.

Most recently, video capsule endoscopy has been added to the list of diagnostic tests for diagnosing Crohn's disease. For video capsule endoscopy, a capsule containing a miniature video camera is swallowed. As the capsule travels through the small intestine, it sends video images of the lining of the small intestine to a receiver carried on a belt at the waist. The images are downloaded and then reviewed on a computer. The value of video capsule endoscopy is that it can identify the early, mild abnormalities of Crohn's disease. Video capsule endoscopy may be particularly useful when there is a strong suspicion of Crohn's disease but the barium x–rays are normal. (Barium x–rays are not as good at identifying early, mild Crohn's disease.)

Video capsule endoscopy should not be performed in patients who have obstruction of the small intestine. The capsule may get stuck behind the obstruction and make the obstruction worse. Doctors usually also are reluctant to perform video–capsule endoscopy for the same reason in patients who they suspect of having small intestinal strictures (narrowed segments of small intestine that can result from prior surgery, prior radiation, or chronic ulceration, for example, from Crohn's disease). There is also a theoretical concern for electrical interference between the capsule and implanted cardiac pacemakers and defibrillators; however, so far in a small number of patients with pacemakers or defibrillators who have undergone video capsule endoscopy there have been no problems.

How is Crohn's disease treated?

The symptoms and severity of Crohn's disease vary among patients. Patients with mild or no symptoms may not need treatment. Patients whose disease is in remission (where symptoms are absent) also may not need treatment.

There is no medication that can cure Crohn's disease. Patients with Crohn's disease typically will experience periods of relapse (worsening of inflammation) followed by periods of remission (reduced inflammation) lasting months to years. During relapses, symptoms of abdominal pain, diarrhea, and rectal bleeding worsen. During remissions, these symptoms improve. Remissions usually occur because of treatment with medications or surgery, but occasionally they occur spontaneously without any treatment.

Since there is no cure for Crohn's disease, the goals of treatment are to 1) induce remissions, 2) maintain remissions, 3) minimize side effects of treatment, and 4) improve the quality of life. Treatment of Crohn's disease and ulcerative colitis with medications is similar though not always identical.

Medications for treating Crohn's disease include 1) antiinflammatory agents such as 5–ASA compounds, corticosteroids, topical antibiotics, 2) immuno–modulators, 3) other medications.

Antiinflammatory medications

Antiinflammatory medications that decrease intestinal inflammation are analogous to arthritis medications that decrease joint inflammation. Different types of antiinflammatory medications used in the treatment of Crohn's disease are:

5–ASA compounds such as sulfasalazine (Azulfidine) and mesalamine (Pentasa, Asacol, Dipentum, Colazal, Rowasa enema, Canasa suppository) that act via direct contact (topically) with the inflamed tissue in order to be effective.
Corticosteroids that act systemically (without the need for direct contact with the inflamed tissue) to decrease inflammation throughout the body. Systemic corticosteroids have important and predictable side effects if used long–term.
A new class of topical corticosteroid (for example, budesonide) that acts via direct contact (topically) with the inflamed tissue. This class of corticosteroids has fewer side effects than systemic corticosteroids which are absorbed into the body.
Antibiotics such as metronidazole (Flagyl) and ciprofloxacin (Cipro) that decrease inflammation by an unknown mechanism

5–ASA (mesalamine) oral medications

5–aminosalicylic acid (5–ASA), also called mesalamine, is similar chemically to aspirin. Aspirin has been used for many years for treating arthritis, bursitis, and tendonitis (conditions of tissue inflammation). Aspirin, however, is not effective in treating Crohn's disease and ulcerative colitis, and even may worsen the inflammation. On the other hand, 5–ASA can be effective in treating Crohn's disease and ulcerative colitis if the drug can be delivered topically onto the inflamed intestinal lining. For example, mesalamine (Rowasa) is an enema containing 5–ASA that is effective in treating inflammation in the rectum. However, the enema solution cannot reach high enough to treat inflammation in the upper colon and the small intestine. Therefore, for most patients with Crohn's disease involving both the ileum (distal small intestine) and colon, 5–ASA must be taken orally.

If pure 5–ASA is taken orally, however, most of the 5–ASA would be absorbed in the stomach and the upper small intestine, and very little 5–ASA would reach the ileum and colon. To be effective as an oral agent in treating Crohn's disease, 5–ASA has to be modified chemically to escape absorption by the stomach and the upper intestines.

Sulfasalazine (Azulfidine)

Sulfasalazine (Azulfidine) was the first modified 5–ASA compound used in the treatment of Crohn's colitis and ulcerative colitis. It has been used successfully for many years to induce remissions among patients with mild to moderate ulcerative colitis. Sulfasalazine also has been used for prolonged periods for maintaining remissions.

Sulfasalazine consists of a 5–ASA molecule linked chemically to a sulfapyridine molecule. (Sulfapyridine is a sulfa antibiotic.) Connecting the two molecules together prevents absorption by the stomach and the upper intestines. When sulfasalazine reaches the ileum and the colon, the bacteria that normally are present break the link between the two molecules. After breaking away from 5–ASA, sulfapyridine is absorbed into the body and later eliminated in the urine. Most of the active 5–ASA, however, is available within the terminal ileum and colon to treat the colitis.

Most of the side effects of sulfasalazine are due to the sulfapyridine molecule. These side effects include nausea, heartburn, headache, anemia, skin rashes, and, in rare instances, hepatitis and kidney inflammation. In men, sulfasalazine can reduce the sperm count. The reduction in sperm count is reversible, and the count usually becomes normal after the sulfasalazine is discontinued or changed to a different 5– ASA compound.

Because the newer 5–ASA compounds [for example, mesalamine (Asacol and Pentasa)] do not have the sulfapyridine component and have fewer side effects than sulfasalazine, they are being used more frequently in treating Crohn's disease and ulcerative colitis.

Asacol

Asacol is a tablet consisting of the 5–ASA compound surrounded by an acrylic resin coating. Asacol is sulfa–free. The resin coating prevents the 5–ASA from being absorbed as it passes through the stomach and the small intestine. When the tablet reaches the terminal ileum and the colon, the resin coating dissolves, and the active 5–ASA drug is released.

Asacol is effective in inducing remissions in patients with mild to moderate ulcerative colitis. It also is effective when used in the longer term to maintain remissions. Some studies have shown that Asacol also is effective in treating Crohn's ileitis and ileo–colitis, as well as in maintaining remission in patients with Crohn's disease.

The recommended dose of Asacol for inducing remissions is two 400 mg tablets three times daily (a total of 2.4 grams a day). At least two tablets of Asacol twice daily (1.6 grams a day) is recommended for maintaining remission. Occasionally, the maintenance dose is higher.

As with Azulfidine, the benefits of Asacol are dose–related. If patients do not respond to 2.4 grams a day of Asacol, the dose frequently is increased to 3.6 – 4.8 grams a day to induce remission. If patients fail to respond to the higher doses of Asacol, then other alternatives such as corticosteroids are considered.

Pentasa

Pentasa is a capsule consisting of small spheres containing 5–ASA. Pentasa is sulfa–free. As the capsule travels down the intestines, the 5–ASA inside the spheres is released slowly into the intestine. Unlike Asacol, the active drug 5–ASA in Pentasa is released into the small intestine as well as the colon. Therefore, Pentasa can be effective in treating inflammation in the small intestine and is currently the most commonly used 5–ASA compound for treating mild to moderate Crohn's disease in the small intestine.

Patients with Crohn's disease occasionally undergo surgery to relieve small intestinal obstruction, drain abscesses, or remove fistulae. Usually, the diseased portions of the intestines are removed during surgery. After successful surgery, patients can be free of disease and symptoms (in remission) for a while. In many patients, however, Crohn's disease eventually returns. Pentasa helps maintain remissions and reduces the chances of the recurrence of Crohn's disease after surgery.

In the treatment of Crohn's ileitis or ileocolitis, the dose of Pentasa usually is four 250 mg capsules four times daily (a total of 4 grams a day). For maintenance of remission in patients after surgery, the dose of Pentasa is between 3–4 grams daily.

Olsalazine (Dipentum)

Olsalazine (Dipentum) is a capsule in which two molecules of 5–ASA are joined together by a chemical bond. In this form, the 5–ASA cannot be absorbed from the stomach and intestine. Intestinal bacteria are able to break apart the two molecules releasing the active individual 5–ASA molecules into the intestine. Since intestinal bacteria are more abundant in the ileum and colon, most of the active 5–ASA is released in these areas. Therefore, olsalazine is most effective for disease that is limited to the ileum or colon. Although clinical studies have shown that olsalazine is effective for maintenance of remission in ulcerative colitis, up to 11% of patients experience diarrhea when taking olsalazine. Because of this, olsalazine is not often used. The recommended dose of olsalazine is 500 mg twice a day.

Balsalazide (Colazal)

Balsalazide (Colazal) is a capsule in which the 5–ASA is linked by a chemical bond to another molecule that is inert (without effect on the intestine) and prevents the 5–ASA from being absorbed. This drug is able to travel through the intestine unchanged until it reaches the end of the small bowel (terminal ileum) and colon. There, intestinal bacteria break apart the 5–ASA and the inert molecule releasing the 5–ASA. Because intestinal bacteria are most abundant in the terminal ileum and colon, balsalazide is used to treat inflammatory bowel disease predominantly localized to the colon.

Side effects of oral 5–ASA compounds

The 5–ASA compounds have fewer side effects than Azulfidine and also do not reduce sperm counts. They are safe medications for long–term use and are well–tolerated.

Patients allergic to aspirin should avoid 5–ASA compounds because they are similar chemically to aspirin.

Rare kidney and lung inflammation has been reported with the use of 5–ASA compounds. Therefore, 5–ASA should be used with caution in patients with kidney disease. It also is recommended that blood tests of kidney function be done before starting and periodically during treatment.

Rare instances of worsening of diarrhea, cramps, and abdominal pain, at times accompanied by fever, rash, and malaise, may occur. This reaction is believed to represent an allergy to the 5–ASA compound.

5–ASA rectal medications (Rowasa Canasa)

Rowasa is 5–ASA in enema form. 5–ASA by enema is most useful for treating ulcerative colitis involving only the distal colon since the enema easily can reach the inflamed tissues of the distal colon. Rowasa also is used in treating Crohn's disease in which there is inflammation in and near the rectum. Each Rowasa enema contains 4 grams of 5–ASA. The enema usually is administered at bedtime, and patients are encouraged to retain the enema through the night. The enema contains sulfite and should not be used by patients with sulfite allergy. Otherwise, Rowasa enemas are safe and well–tolerated.

Canasa is 5–ASA in suppository form. It is used for treating ulcerative proctitis. Each suppository contains 500 mg of 5–ASA and usually is administered twice daily.

Both enemas and suppositories have been shown to be effective in maintaining remission in patients with ulcerative colitis limited to the distal colon and rectum.

Corticosteroids

Corticosteroids (for example, prednisone, prednisolone, hydrocortisone, etc.) have been used for many years to treat patients with moderate to severe Crohn's disease and ulcerative colitis and to treat patients who fail to respond to 5–ASA. Unlike 5–ASA, corticosteroids do not require direct contact with the inflamed intestinal tissues to be effective.

Oral corticosteroids are potent antiinflammatory medications. After absorption, corticosteroids exert prompt antiinflammatory actions throughout the body, including the intestines. Consequently, they are used in treating Crohn's disease anywhere in the small intestine, as well as ulcerative and Crohn's colitis. In critically ill patients, intravenous corticosteroids (such as hydrocortisone) can be given in the hospital. For patients with proctitis, hydrocortisone enemas (Cortenema) can be used to deliver the corticosteroid directly to the inflamed tissue. By using the corticosteroid topically, less of it is absorbed into the body and the frequency and severity of side effects are lessened (but not eliminated) as compared with systemic corticosteroids.

Corticosteroids are faster–acting than 5–ASA, and patients frequently experience improvement in their symptoms within days of beginning them. Corticosteroids, however, do not appear to be useful in maintaining remission in Crohn's disease and ulcerative colitis or in preventing the return of Crohn's disease after surgery.

Side effects of corticosteroids

The frequency and severity of side effects of corticosteroids depend on the dose and duration of their use. Short courses of corticosteroids, for example, usually are well–tolerated with few and mild side effects. Long–term use of high doses of corticosteroids usually produces predictable and potentially serious side effects. Common side effects include:

rounding of the face (moon face),
acne,
increased body hair,
diabetes,
weight gain,
high blood pressure,
cataracts,
glaucoma,
increased susceptibility to infections,
muscle weakness,
depression,
insomnia,
mood swings,
personality changes,
irritability, and
thinning of the bones (osteoporosis) with fractures of the spine.

Children receiving corticosteroids experience stunted growth.

The most serious complication from long term corticosteroid use is aseptic necrosis of the hip joints. Aseptic necrosis is a condition in which there is death and degeneration of the hip bone. It is a painful condition that can ultimately lead to the need for surgical replacement of the hip. Aseptic necrosis also has been reported in the knee joints. It is not known how corticosteroids cause aseptic necrosis. The estimated incidence of aseptic necrosis among corticosteroid users is 3%–4%. Patients on corticosteroids who develop pain in the hips or knees should report the pain to their doctors promptly. Early diagnosis of aseptic necrosis with cessation of corticosteroids might decrease the severity of the aseptic necrosis and the need for hip replacement surgery.

Prolonged use of corticosteroids can depress the ability of the body's adrenal glands to produce cortisol (a natural corticosteroid necessary for proper functioning of the body). Therefore, abruptly discontinuing corticosteroids can cause symptoms due to a lack of natural cortisol (a condition called adrenal insufficiency). Symptoms of adrenal insufficiency include nausea, vomiting, and even shock. Withdrawing corticosteroids too quickly also can produce symptoms of joint pain, fever, and malaise. Therefore, when corticosteroids are discontinued, the dose usually is tapered gradually rather than stopped abruptly.

Even after corticosteroids are discontinued, the adrenal glands' ability to produce cortisol can remain depressed from months up to two years. The depressed adrenal glands may not be able to produce increased amounts of cortisol to help the body handle the stress of accidents, surgery, and infections. Therefore, patients need additional corticosteroids during stressful situations to avoid developing adrenal insufficiency. Because corticosteroids are not useful in maintaining remission in ulcerative colitis and Crohn's disease, and because they have predictable and potentially serious side effects, they should be used for the shortest possible length of time.

Proper use of corticosteroids

Once the decision is made to use systemic corticosteroids, treatment usually is initiated with prednisone, 40–60 mg daily. The majority of patients with Crohn's disease respond with an improvement in symptoms within a few weeks. Once symptoms have improved, prednisone is reduced by 5–10 mg per week until a dose of 20 mg per day is reached. The dose then is reduced at a slower rate until the corticosteroid is discontinued. Gradually reducing corticosteroids not only minimizes the symptoms of adrenal insufficiency, it also reduces the chances of an abrupt recurrence of inflammation.

Many doctors use 5–ASA compounds and corticosteroids together. In patients who achieve remission with corticosteroids, 5–ASA compounds often are continued alone to maintain remission.

In patients whose symptoms return corticosteroids are slowly being reduced, the dose of corticosteroids is increased slightly to control the symptoms. Once the symptoms are under control, the reduction of corticosteroids can resume at a slower pace. Unfortunately, many patients who require corticosteroids to induce remissions become corticosteroid dependent. These patients consistently develop symptoms whenever the corticosteroid dose falls below a certain level. In such patients who are corticosteroid dependent as well as in patients who are unresponsive to corticosteroids and other antiinflammatory medications, immuno–modulator medications or surgery must be considered. The management of patients who are corticosteroid dependent or patients with severe disease that responds poorly to medications is complex. Doctors who are experienced in treating ulcerative colitis and Crohn's disease and in using immuno–modulators should evaluate these patients.

Prevention of osteoporosis

Long–term use of corticosteroids can cause osteoporosis. Calcium is very important in the formation and maintenance of healthy bones. Corticosteroids decrease the absorption of calcium from the intestine and increase the loss of calcium from the kidneys. Increasing dietary calcium intake is important but alone cannot halt corticosteroid–induced osteoporosis. To prevent or minimize osteoporosis, management of patients on long–term corticosteroids should include:

Adequate intake of calcium (1000 mg daily in premenopausal women, 1,500 mg daily in postmenopausal women) and vitamin D (800 units daily).
Periodic review with the doctor of the need for continued corticosteroid treatment and use of the lowest effective dose if continued treatment is necessary.
For patients taking corticosteroids for more than three months, a bone density study may be helpful in determining the extent of bone loss and the need for more aggressive treatment.
Regular weight–bearing exercise and stopping smoking (cigarettes).
Discussion with the doctor regarding the use of alendronate (Fosamax), risedronate (Actonel), or etidronate (Didronel) to prevent or treat corticosteroid–induced osteoporosis.

Budesonide (Entocort EC)

Budesonide (Entocort EC) is a new type of corticosteroid for treating Crohn's disease. Like other corticosteroids, budesonide is a potent antiinflammatory medication. Unlike other corticosteroids, however, budesonide acts only via direct contact with the inflamed tissues (topically) and not systemically. As soon as budesonide is absorbed into the body, the liver converts it into inactive chemicals. Therefore, for effective treatment of Crohn's disease, budesonide, like topical 5–ASA, must be brought into direct contact with the inflamed intestinal tissue.

Budesonide capsules contain granules that allow a slow release of the drug into the ileum and the colon. In a double–blind multicenter study (published in 1998), 182 patients with Crohn's ileitis and/or Crohn's disease of the right colon were treated with either budesonide (9 mg daily) or Pentasa (2 grams twice daily). Budesonide was more effective than Pentasa in inducing remissions while the side effects were similar to Pentasa. In another study comparing the effectiveness of budesonide with corticosteroids, budesonide was not better than corticosteroids in treating Crohn's disease but had fewer side effects.

Because budesonide is broken down by the liver into inactive chemicals, it has fewer side effects than systemic corticosteroids. It also suppresses the adrenal glands less than systemic corticosteroids. Budesonide will be available as an enema for the treatment of proctitis.

Budesonide has not been shown to be effective in maintaining remission in patients with Crohn's disease. If used long–term, budesonide also may cause some of the same side effects as corticosteroids. Because of this, the use of budesonide should be limited to short–term treatment for inducing remission. Most budesonide is released in the terminal ileum, it will have its best results in Crohn's disease limited to the terminal ileum.

It is not known whether budesonide is effective in treating patients with ulcerative colitis, and it is currently not recommended for the treatment of ulcerative colitis.

Antibiotics for Crohn's disease

Antibiotics such as metronidazole (Flagyl) and ciprofloxacin (Cipro) have been used for treating Crohn's colitis. Flagyl also has been useful in treating anal fistulae in patients with Crohn's disease. The mechanism of action of these antibiotics in Crohn's disease is not well understood.

Metronidazole (Flagyl)

Metronidazole (Flagyl) is an antibiotic that is used for treating several infections caused by parasites (for example, giardia) and bacteria (for example, infections caused by anaerobic bacteria, and vaginal infections). It is effective in treating Crohn's colitis and is particularly useful in treating patients with anal fistulae. Chronic use of metronidazole in doses higher than 1 gram daily can be associated with permanent nerve damage (peripheral neuropathy). The early symptoms of peripheral neuropathy are numbness and tingling in the fingertips, toes, and other parts of the extremities. Metronidazole should be stopped promptly if these symptoms appear. Metronidazole and alcohol together can cause severe nausea, vomiting, cramps, flushing, and headache. Patients taking metronidazole should avoid alcohol. Other side effects of metronidazole include nausea, headaches, loss of appetite, a metallic taste, and, rarely, a rash.

Ciprofloxacin (Cipro)

Ciprofloxacin (Cipro) is another antibiotic used in the treatment of Crohn's disease. It can be used in combination with metronidazole.

Summary of antiinflammatory medications

Azulfidine, Asacol, Pentasa, Dipentum, Colazal and Rowasa all contain 5–ASA which is the active topical antiinflammatory ingredient. Azulfidine was the first 5–ASA medication used in treating ulcerative colitis and Crohn's disease, but the newer 5–ASA medications have fewer side effects.
Pentasa and Asacol have been found to be effective in treating patients with Crohn's ileitis and ileo–colitis. Rowasa enemas and Canasa suppositories are safe and effective for treating patients with proctitis. For mild to moderate Crohn's ileitis or ileo–colitis, doctors usually start with Pentasa or Asacol. If Pentasa or Asacol is ineffective, doctors may try antibiotics such as Cipro or Flagyl for prolonged periods (often months).
In patients with moderate to severe disease and in patients who fail to respond to 5–ASA compounds and/or antibiotics, systemic corticosteroids can be used. Systemic corticosteroids are potent and fast–acting antiinflammatory agents for treating Crohn's enteritis and colitis as well as ulcerative colitis.
Systemic corticosteroids are not effective in maintaining remission in patients with Crohn's disease. Serious side effects can result from prolonged corticosteroid treatment.
To minimize side effects, corticosteroids should be gradually tapered as soon as a remission is achieved. In patients who become corticosteroid dependent or are unresponsive to corticosteroid treatment, surgery or immuno–modulator treatment are considered.
A new class of topical corticosteroids (budesonide) may have fewer side effects than systemic corticosteroids.

Immuno–modulator medications

Immuno–modulators are medications that affect the body's immune system. The immune system is composed of immune cells and the proteins that they produce. These cells and proteins serve to protect the body against harmful bacteria, viruses, fungi, and other foreign invaders. Activation of the immune system causes inflammation within the tissues where the activation occurs. (Inflammation is, in fact, an important mechanism used by the immune system to defend the body.) Normally, the immune system is activated only when the body is exposed to foreign invaders. In patients with Crohn's disease and ulcerative colitis, however, the immune system is abnormally and chronically activated in the absence of any known invader.

Immuno–modulators decrease tissue inflammation by reducing the population of immune cells and/or by interfering with their production of proteins. Decreasing the activity of the immune system with immuno–modulators increases the risk of infections; however, the benefits of controlling moderate to severe Crohn's disease usually outweigh the risks of infection due to weakened immunity. Examples of immuno–modulators are 6–mercaptopurine (6–MP), azathioprine (Imuran), methotrexate (Rheumatrex, Trexall), infliximab (Remicade), adalimumab (Humira).

Azathioprine (Imuran) and 6–mercaptopurine (6–MP, Purinethol)

Azathioprine (Imuran) and 6–mercaptopurine (6–MP, Purinethol) are medications that weaken the body's immune system by reducing the population of a class of immune cells called lymphocytes. Azathioprine and 6–MP are related chemically. (Actually, azathioprine is converted into 6–MP within the body.) In high doses, these two drugs have been useful in preventing rejection of transplanted organs and in treating leukemia. In low doses, they have been used for many years to treat patients with moderate to severe Crohn's disease and ulcerative colitis.

Azathioprine and 6–MP are increasingly recognized by doctors as valuable drugs in treating Crohn's disease and ulcerative colitis. Some 70% of patients with moderate to severe disease will benefit from these drugs. Azathioprine and 6–MP are used primarily in the following situations:

Severe Crohn's disease and ulcerative colitis not responding to corticosteroids.

The presence of undesirable corticosteroid–related side effects.

Corticosteroid dependency, a condition in which patients are unable to discontinue corticosteroids without developing relapses of their disease.

Maintenance of remission.

When azathioprine and 6–MP are added to corticosteroids in the treatment of Crohn's disease not responding to corticosteroids alone, there may be an improved response. Also, smaller doses and shorter courses of corticosteroids may be able to be used. Some patients can discontinue corticosteroids altogether without experiencing relapses of their disease. This corticosteroid–lowering effect has earned azathioprine and 6–MP their reputation as "steroid–sparing" medications.

In Crohn's disease patients with severe disease who suffer frequent relapses, 5–ASA may not be sufficient, and the more potent azathioprine and 6–MP will be necessary to maintain remissions. In the lower doses used to treat Crohn's disease, the long–term side effects of azathioprine or 6– MP are less serious than those of long–term corticosteroids or repeated courses of corticosteroids.

Patients with Crohn's disease may undergo surgery to remove a segment of the intestine that is obstructed or contains a fistula. After surgical removal of the diseased segments, the patients often will be free of disease and symptoms for a while, but many eventually will have their disease recur. During these recurrences, previously healthy intestine can become inflamed. Long–term 5–ASA (such as Pentasa) and 6–MP both are effective in reducing the chances of recurrence after surgery.

Anal fistulae can develop in some patients with Crohn's disease. Anal fistulae are abnormal tracts (tunnels) that form between the small intestine or colon and the skin around the anus. Drainage of fluid and mucous from the opening of the fistula is a troublesome problem. These fistulae are difficult to treat and do not heal readily. Metronidazole (Flagyl) has been used with some success in promoting healing of these fistulae. In difficult cases, azathioprine and 6–MP may be successful in promoting healing.

Side effects of azathioprine and 6–MP

Side effects of azathioprine and 6–MP include increased vulnerability to infections, inflammation of the liver (hepatitis) and the pancreas (pancreatitis), and bone marrow toxicity (interference with the formation of cells that circulate in the blood).

The goal of treatment with azathioprine and 6–MP is to lower the body's production of certain types of white blood cells (lymphocytes) in order to decrease the inflammation in the intestines; however, lowering the number of lymphocytes may increase vulnerability to infections. For example, in a group of patients with severe Crohn's disease unresponsive to standard doses of azathioprine, raising the dose of azathioprine helped to control the disease, but two patients developed cytomegalovirus (CMV) infection. (CMV typically infects individuals with weakened immune systems such as patients with AIDS and cancer patients receiving chemotherapy).

Azathioprine and 6–MP can induce inflammation of the liver (hepatitis) and pancreas (pancreatitis). Pancreatitis typically causes severe abdominal pain and sometimes vomiting. Pancreatitis due to azathioprine or 6–MP occurs in 3%–5% of patients, usually during the first several weeks of treatment. Patients who develop pancreatitis should not receive either of these two medications again.

Azathioprine and 6–MP also suppress the bone marrow. The bone marrow is where the red blood cells, white blood cells, and platelets are made. Actually, a slight reduction in the white cell count during treatment is desirable since it suggests that the dose of azathioprine or 6–MP is high enough to have an effect; however, excessively low red or white blood cell counts indicates bone marrow toxicity. Therefore, patients on azathioprine or 6–MP should have periodic blood counts (usually every two weeks initially and then every three months during maintenance) to monitor the effect of the drugs on the bone marrow.

Patients on long–term, high dose azathioprine to prevent rejection of the kidney after kidney transplantation have an increased risk of developing lymphoma, a malignant disease of lymph cells. There is no evidence at present that long term use of azathioprine or 6–MP, in the lower doses used in Crohn's disease, increases the risk of lymphoma, leukemia or other malignancies.

The use of azathioprine and 6–MP in pregnant women must be carefully considered. There are reports suggesting that the use of azathioprine or 6–MP in pregnancy is safer than once thought. The risk of continuing azathioprine or 6–MP during conception and pregnancy must be weighed against the risk of worsening disease if they are stopped. On the other hand, worsening disease has been shown clearly to be a significant risk to the fetus.

Other issues with azathioprine and 6–MP

One problem with 6–MP and azathioprine is their slow onset of action. Typically, full benefit of these drugs is not realized for three months or longer. During this time, corticosteroids frequently have to be maintained at high levels to control inflammation.

The reason for this slow onset of action is partly due to the way doctors prescribe these drugs. For example, 6–MP is typically started at a dose of 50 mg daily. The blood count is then checked two weeks later. If the lymphocytes are not reduced, the dose of 6–MP is increased. This cautious, stepwise approach helps reduce bone marrow and liver toxicity but also delays benefit from the drug.

Studies have shown that giving higher doses of 6–MP early can hasten the benefit of 6–MP without increasing the toxicity in most patients, but some patients do develop severe bone marrow toxicity. Scientists now believe that an individual's vulnerability to 6–MP toxicity is genetically inherited. Blood tests can be performed to identify those individuals with increased vulnerability to 6–MP toxicity. Blood tests also can be performed to measure the levels of certain by–products of 6–MP. The levels of these by–products in the blood help doctors more quickly determine whether the dose of 6–MP is right for the patient.

TPMT genetics and safety of azathioprine and 6–MP

Azathioprine is converted into 6–MP in the body and 6–MP then is partially converted in the body into inactive and non–toxic chemicals by an enzyme called thiopurine methyltransferase (TPMT). These chemicals then are eliminated from the body. The activity of TPMT enzyme (the ability of the enzyme to convert 6–MP into inactive and non–toxic chemicals) is genetically determined, and approximately 10% of the population in the Untied States has a reduced or absent TPMT activity. In this 10% of patients, 6–MP accumulates and is converted into chemicals that are toxic to the bone marrow where blood cells are produced. Thus, when given normal doses of azathioprine or 6–MP, these patients with reduced or absent TPMT activities can develop seriously low white blood cell counts for prolonged periods of time, exposing them to serious life–threatening infections.

Doctors now can perform genetic testing for TPMT before starting azathioprine or 6–MP. Patients found to have genes associated with reduced or absent TPMT activity are treated with alternative medications or are prescribed substantially lower than normal doses of 6–MP or Azathioprine.

A word of caution is in order, however. Having normal TPMT genes is no guarantee against azathioprine or 6–MP toxicity. Rarely, a patient with normal TPMT genes can develop severe toxicity in the bone marrow and a low white blood cell count even with normal doses of 6–MP or azathioprine. Therefore, all patients taking 6–MP or azathioprine (regardless of TPMT genetics) have to be closely monitored by a doctor who will order periodic blood counts for as long as the medication is taken.

Another cautionary note; allopurinol (Zyloprim), used in treating high blood uric acids levels, can induce bone marrow toxicity when used together with azathioprine or 6–MP. Zyloprim used together with azathioprine or 6–MP has similar effect as having reduced TPMT activity, causing increased accumulation of the 6–MP metabolite that is toxic to the bone marrow.

6–MP metabolite levels

In addition to monitoring blood cell counts and liver tests, doctors also may measure blood levels of the chemicals that are formed from 6–MP (6–MP metabolites), which can be helpful in several situations such as:

If a patient's disease is not responding to standard doses of 6–MP or azathioprine and his/her 6–MP blood metabolite levels are low, doctors may increase the 6–MP or azathioprine dose.

If a patient's disease is not responding to treatment and his/her 6–MP blood metabolite levels are zero, he/she is not taking his/her medication. The lack of response in this case is due to patient non–compliance.

Duration of treatment with azathioprine and 6–MP

Patients have been maintained on 6–MP or azathioprine for years without important long–term side effects. Patients on long–term azathioprine or 6–MP, however, should be closely monitored by their doctors. There are data suggesting that patients on long–term maintenance fare better than those who stop these medications. Thus, those who stop azathioprine or 6–MP are more likely to experience recurrence of their disease and are more likely to need corticosteroids or undergo surgery.

Infliximab (Remicade)

Infliximab (Remicade) is an antibody that attaches to a protein called tumor necrosis factor–alpha (TNF–alpha). TNF–alpha is one of the proteins produced by immune cells during activation of the immune system. TNF–alpha, in turn, stimulates other cells of the immune system to produce and release other proteins that promote inflammation. In Crohn's disease, there is continued production of TNF–alpha as part of the immune activation. Infliximab, by attaching to TNF–alpha, blocks its activity and in so doing decreases the inflammation.

Infliximab, an antibody to TNF–alpha, is produced by the immune system of mice after the mice are injected with human TNF–alpha. The mouse antibody then is modified to make it look more like a human antibody, and this modified antibody is infliximab. Such modifications are necessary to decrease the likelihood of allergic reactions when the antibody is administered to humans. Infliximab is given by intravenous infusion over two hours. Patients are monitored throughout the infusion for adverse reactions.

In August 1998 the United States Food and Drug Administration approved the use of infliximab for the short–term treatment of moderate to severe Crohn's disease patients who respond inadequately to corticosteroids, azathioprine, or 6–MP.

Effectiveness of infliximab

Infliximab is an effective and fast–acting drug for the treatment of active Crohn's disease. In a study involving patients with moderate to severe Crohn's disease who were not responding to corticosteroids or immuno–modulators, 65% experienced improvement in their disease after one infusion of infliximab. Some patients noticed improvement in symptoms within days of the infusion. Most patients experienced improvement within two weeks.

In patients who respond to infliximab, the improvements in symptoms can be dramatic. Moreover, there can be impressively rapid healing of the ulcers and the inflammation in the intestines after just one infusion.

The anal fistulae of Crohn's disease are troublesome and often difficult to treat. Infliximab has been found to be effective for treating fistulae.

Duration of benefits with infliximab

The majority of the patients who responded to a first infusion of infliximab developed recurrence of their disease within three months. However, studies have shown that repeated infusions of infliximab every eight weeks are safe and effective in maintaining remission in many patients over a one to two year period. Response to infliximab after repeated infusions sometimes is lost if the patient starts to develop antibodies to the infliximab (which attach to the infliximab and prevent it from working). Studies are now being done to determine the long–term safety and effectiveness of repeated infusions of infliximab.

One potential use of infliximab is to quickly control active and severe disease. The use of infliximab then may be followed by maintenance treatment with azathioprine, 6–MP or 5–ASA compounds. Azathioprine or 6–MP also may be helpful in preventing the development of antibodies against infliximab.

Side effects of infliximab

Infliximab generally is well–tolerated. There have been rare reports of side effects during infusions, including chest pain, shortness of breath, and nausea. These effects usually resolve spontaneously within minutes if the infusion is stopped. Other commonly–reported side effects include headache and upper respiratory tract infection.

TNF–alpha is an important protein for defending the body against infections. Infliximab, like immuno–modulators, increases the risk for infection. One case of salmonella colitis and several cases of pneumonia have been reported with the use of infliximab. There also have been cases of tuberculosis (TB) reported after the use of infliximab.

Because infliximab is partly a mouse protein, it may induce an immune reaction when given to humans, especially with repeated infusions. In addition to the side effects that occur while the infusion is being given, patients also may develop a "delayed allergic reaction" that occurs 7–10 days after receiving the infliximab. This type of reaction may cause flu–like symptoms with fever, joint pain and swelling, and a worsening of Crohn's disease symptoms. It can be serious, and if it occurs, a physician should be contacted. Paradoxically, those patients who have more frequent infusions of infliximab are less likely to develop this type of delayed reaction compared to those patients who receive infusions separated by long intervals (6–12 months). Although infliximab is only FDA approved for a single infusion at this time, patients should be aware that they are likely to require repeated infusions once Remicade therapy has been initiated.

Rare cases of nerve inflammation such as optic neuritis (inflammation of the nerve of the eye) and mother neuropathy has been reported with the use of infliximab.

Precautions with infliximab

Infliximab can aggravate and cause the spread of an existing infection. Therefore, it should not be given to patients with pneumonia, urinary tract infection or abscess (localized collection of pus). It now is recommended that patients be tested for TB prior to receiving infliximab. Patients who previously had TB should inform their physician of this before they receive infliximab infliximab can cause the spread of cancer cells; therefore, it should not be given to patients with cancer.

Infliximab can promote intestinal scarring (part of the process of healing) and, therefore, can worsen strictures (narrowed areas of the intestine caused by inflammation and subsequent scaring) and lead to intestinal obstruction. It also can cause partial healing (partial closure) of anal fistulae. Partial closure of fistulae impedes drainage of fluid through the fistulae, and may result in collections of fluid in which bacteria multiply, which can result in abscesses.

The effects infliximab on the fetus are not known.

Because infliximab is partly a mouse protein, some patients can develop antibodies against infliximab with repeated infusions. Such antibodies can decrease the effectiveness of the drug. The chance of developing such antibodies can be decreased by the concomitant use of 6–MP and corticosteroids. There are some reports of worsening heart disease in patients who have received Remicade. The precise mechanism and role of infliximab in the development of this side effect is unclear. As a precaution, individuals with heart disease should inform their physician of this condition before receiving infliximab.

While infliximab represents an exciting new class of medications in the fight against Crohn's disease, caution is warranted in its use. The long–term safety and effectiveness is not yet known.

Adalimumab (Humira)

Adalimumab is an anti–TNF agent similar to infliximab and decreases inflammation by blocking tumor necrosis factor (TNF–alpha). In contrast to infliximab, adalimumab is a fully humanized anti–TNF antibody (no mouse protein). Adalimumab is administered subcutaneously (under the skin) instead of intravenously as in the case of infliximab.

Rheumatologists have been using adalimumab for treating inflammation of the joints in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Four recent clinical trials (involving almost 1,500 patients) comparing adalimumab to placebo, have demonstrated that adalimumab is also effective in treating inflammation in the intestines of patients with Crohn's disease and in reducing signs and symptoms of Crohn's disease.

Adalimumab is comparable to infliximab in effectiveness and safety for inducing and maintaining remission in patients suffering from Crohn's disease. Adalimumab is also effective in healing Crohn's anal fistulas. Adalimumab has been shown to be effective for patients who either failed or cannot tolerate infliximab.

The Food and Drug Administration in February 2007, approved Humira (adalimumab) to treat adult patients with moderately to severely active Crohn's disease. Adalimumab (Humira) is administered subcutaneously every two weeks.

The side effects of Adalimumab

Adalimumab generally is well–tolerated. The most common side effect is skin reactions at the site of injection with swelling, itching, or redness. Other common side effects include upper respiratory infections, sinusitis, and nausea.

TNF–alpha is an important protein for defending the body against infections. Adalimumab, like infliximab, increases the risk of infection. There have been cases of tuberculosis (TB) reported after the use of infliximab and adalimumab. It now is recommended that patients be tested for TB prior to receiving these agents. Patients who previously had TB should inform their physician of this before they receive these agents. Adalimumab, like infliximab, can aggravate and cause the spread of an existing infection. Therefore, it should not be given to patients with pneumonia, urinary tract infection or abscess (localized collection of pus).

Rare cases of lymphoma (cancer of the lymphatic system) have been reported with the use of adalimumab. Rare cases of nervous system inflammation have been reported with the use of adalimumab. The symptoms may include numbness and tingling, vision disturbances, weakness in legs. Some patients receiving adalimumab may rarely develop symptoms that mimic systemic lupus; these symptoms include skin rash, arthritis, chest pain, or shortness of breath. These lupus–like symptoms resolve after stopping the drug.

There are some reports of worsening heart disease such as heart failure in patients who have received infliximab or adalimumab. The precise mechanism and role of these agents in the development of this side effect is unclear. As a precaution, individuals with heart disease should inform their physician of this condition before receiving infliximab or adalimumab.

Severe allergic reactions with rash, difficulty breathing, and severe low blood pressure or shock are rare, but serious allergic reactions can occur either after the fist injection or after many injections. Patients experiencing symptoms of serious allergic reactions should seek emergency care are immediately.

Methotrexate (Rheumatrex, Trexall)

Methotrexate (Rheumatrex, Trexall) is both an immuno–modulator and antiinflammatory medication. Methotrexate has been used for many years in the treatment of severe rheumatoid arthritis and psoriasis. It has been helpful in treating patients with moderate to severe Crohn's disease who are either not responding to azathioprine and 6– MP or are intolerant of them. Methotrexate also may be effective in patients with moderate to severe ulcerative colitis who are not responding to corticosteroids, azathioprine, or 6–MP. It can be given orally or by weekly injections under the skin or into the muscles, but it is more reliably absorbed with the injections.

One major complication of methotrexate is the development of liver cirrhosis when the medication is given over a prolonged period of time (years). The risk of liver damage is higher in patients who also abuse alcohol or are severely obese. Although it has been recommended that a liver biopsy should be obtained in patients who have received a cumulative (total) methotrexate dose of 1.5 grams or higher, the need for such biopsies is controversial.

Other side effects of methotrexate include low white blood cell counts and inflammation of the lungs.

Methotrexate should not be used in pregnant women because of toxic effects on the fetus.

Surgery in Crohn's disease

There is no surgical cure for Crohn's disease. Even when all of the diseased parts of the intestines are removed, inflammation frequently recurs in previously healthy intestines months to years after the surgery. Therefore, surgery in Crohn's disease is used primarily for:

Removal of a diseased segment of the small intestine that is causing obstruction.

Drainage of pus from abdominal and peri–rectal abscesses.

Treatment of severe anal fistulae that do not respond to drugs.

Resection of internal fistulae (such as a fistula between the colon and bladder) that are causing infections.

Usually, after the diseased portions of the intestines are removed surgically, patients can be free of disease and symptoms for some time, often years. Surgery, when successfully performed, can lead to a marked improvement in a patient's quality of life. In many patients, however, Crohn's disease eventually returns, affecting previously healthy intestines. The recurrent disease usually is located at or near the previous site of surgery. In fact, 50% of patients can expect to have a recurrence of symptoms within four years of surgery. Drugs such as Pentasa or 6–MP have been useful in some patients to reduce the chances of relapse of Crohn's disease after surgery.

General measures

General measures which may help control Crohn's disease include dietary changes and supplementation. Since fiber is poorly digestible, it can worsen the symptoms of intestinal obstruction. Hence, a low fiber diet may be recommended, especially in those patients with small intestinal disease. A liquid diet may be of benefit when symptoms are more severe. Intravenous nutrition or TPN (total peripheral nutrition) may be utilized when it is felt that the intestine needs to "rest." Supplementation of calcium, folate and vitamin B12 is helpful when malabsorption of these nutrients is apparent. The use of anti–diarrheal agents [diphenoxylate and atropine (Lomotil), loperamide (Imodium)] and anti–spasmotics also can help relieve symptoms of cramps and diarrhea.

Conclusions

Crohn's disease is a chronic inflammatory disease involving predominantly the small intestine and colon. The symptoms and the activity of the disease can come and go. Even though many effective medications are available to control the activity of the disease, there is as yet no cure for Crohn's disease. Surgery can significantly improve the quality of life in selected individuals, but recurrence of the disease after surgery is common. The disease can have complications, both within and outside of the intestine. Newer treatments are actively being evaluated. A better understanding of the role of genetics and environmental factors in the cause of Crohn's disease may lead to improved treatments and prevention of the disease.

Crohn's Disease At A Glance

Crohn's disease is a chronic inflammatory disease of the intestines.
The cause of Crohn's disease is unknown.
Crohn's disease can cause ulcers in the small intestine, colon, or both.
Abdominal pain, diarrhea, vomiting, fever, and weight loss are symptoms of Crohn's disease.
Crohn's disease of the small intestine may cause obstruction of the intestine.
Crohn's disease can be associated with reddish, tender skin nodules, and inflammation of the joints, spine, eyes, and liver.
The diagnosis of Crohn's disease is made by barium enema, barium x–ray of the small bowel, and colonoscopy.
The choice of treatment for Crohn's disease depends on the location and severity of the disease.
Treatment of Crohn's disease includes drugs for suppressing inflammation or the immune system, antibiotics, and surgery.

Asthma

2008-01-14T18:03:00.000-08:00

What do each of these individuals have in common: First, an 18-year-old suddenly develops wheezing and shortness of breath when visiting his grandmother who happens to have a cat. Second, a 30-year-old woman has colds that "always go into her chest," causing coughing and difficulty breathing. Lastly, a 60-year-old man develops shortness of breath with only slight exertion even though he has never smoked. The answer is that they all have asthma. These are some of the many faces of asthma.

Most researchers believe that the different patterns of asthma are all related to one condition. But some researchers feel that separate forms of lung conditions exist. There is currently no cure for asthma and no single exact cause has been identified. Therefore, understanding the changes that occur in asthma, how it makes you feel, and how it can behave over time is vital. This knowledge can empower persons with asthma to take an active role in your own health.

Myths, facts, and statistics about asthma

Before we present the typical symptoms of asthma, we should dispel some common myths about this condition. This is best achieved by conducting a short true or false quiz.

T or F Asthma is "all in the mind."
T or F You will "grow out of it."
T or F Asthma can be cured, so it is not serious and nobody dies from it.
T or F You are likely to develop asthma if someone in your family has it.
T or F You can "catch" asthma from someone else who has it.
T or F Moving to a different location, such as the desert, can cure asthma.
T or F People with asthma should not exercise.
T or F Asthma does not require medical treatment.
T or F Medications used to treat asthma are habit-forming.
T or F Someone with asthma can provoke episodes anytime they want in order to get attention.

Here are the answers:

F - Asthma is not a psychological condition. However, emotional triggers can cause flare-ups.
F - You cannot outgrow asthma. In about 50% of children with asthma, the condition may become inactive in the teenage years. The symptoms, however, may reoccur at any time in adulthood.
F - There is no cure for asthma, but the disease can be controlled in most patients with good medical care. The condition should be taken seriously, since uncontrolled asthma may result in emergency hospitalization and possible death.
T - You have a 6% chance of having asthma if neither parent has the condition; a 30% chance if one parent has it; and a 70% chance if both parents have it.
F - Asthma is not contagious.
F - A new environment may temporarily improve asthma symptoms, but it will not cure asthma. After a few years in the new location, many people become sensitized to the new environment and the asthma symptoms return with the same or even greater intensity than before.
F - Swimming is an optimal exercise for those with asthma. On the other hand, exercising in dry, cold air may be a trigger for asthma in some people.
F - Asthma is best controlled by having an asthma management plan designed by your doctor that includes the medications used for quick relief and those used as controllers.
F - Asthma medications are not addictive.
F - Asthma attacks cannot be faked.

What is asthma?

Asthma is a chronic inflammation of the bronchial tubes (airways) that causes swelling and narrowing (constriction) of the airways. The result is difficulty breathing. The bronchial narrowing is usually either totally or at least partially reversible with treatments.

Bronchial tubes that are chronically inflamed may become overly sensitive to allergens (specific triggers) or irritants (nonspecific triggers). The airways may become "twitchy" and remain in a state of heightened sensitivity. This is called "Bronchial Hyperreactivity" (BHR). It is likely that there is a spectrum of bronchial hyperreactivity in all individuals. However, it is clear that asthmatics and allergic individuals (without apparent asthma) have a greater degree of bronchial hyperreactivity than non-asthmatic and nonallergic people. In sensitive individuals, the bronchial tubes are more likely to swell and constrict when exposed to triggers such as allergens, tobacco smoke, or exercise. Amongst asthmatics, some may have mild BHR and no symptoms while others may have severe BHR and chronic symptoms.

Allergy Assist

Asthma affects people differently. Each individual is unique in their degree of reactivity to environmental triggers. This naturally influences the type and dose of medication prescribed, which may vary from one individual to another.

From the past to the present

Physicians in ancient Greece used the word "asthma" to describe breathlessness or gasping. They believed that asthma was derived from internal imbalances, which could be restored by healthy diet, plant and animal remedies, or lifestyle changes.

Allergy Jargon

Asthma is derived from the Greek word "Panos," meaning panting.

Chinese healers understood that "xiao-chiran," or "wheezy breathing," was a sign of imbalance in the life force they called "Qi." They restored "Qi" by means of herbs, acupuncture, massage, diet, and exercise.

The Hindu philosophers connected the soul and breath as part of the mind, body, and spirit connection. Yoga uses control of breathing to enhance meditation. Indian physicians taught these breathing techniques to help manage asthma.

Allergy Fact

Maimonides was a renowned 12th-century rabbi and physician who practiced in the court of the sultan of Egypt. He recommended to one of the Royal Princes with asthma that he eat, drink, and sleep less. He also advised that he engage in less sexual activity, avoid the polluted city environment, and eat a specific remedy–chicken soup.

The balance of the "four humors," which was derived from the Greco-Roman times, influenced European medicine until the middle of the 18th century. In a healthy person, the four humors, or bodily fluids–blood, black bile, yellow bile, and phlegm–were in balance. An excess of one of these humors determined what kinds of disorders were present. Asthmatics who were noted for their coughing, congestion, and excess mucus (phlegm) production were therefore regarded as "phlegmatic."

By the 1800s, aided by the invention of the stethoscope, physicians began to recognize asthma as a specific disease. However, patients still requested the traditional treatments of the day, such as bloodletting, herbs, and smoking tobacco. These methods were used for a variety of conditions, including asthma. Of the many remedies that were advertised for asthma throughout the 19th century, none were particularly helpful.

Allergy Fact

As early as 1892, the famous Canadian-American physician Sir William Osler suggested that inflammation played an important role in asthma.

Bronchial dilators first appeared in the 1930s and were improved in the 1950s. Shortly thereafter, corticosteroid drugs that treated inflammation appeared and have become the mainstay of therapy used today.

The scope of the problem

Asthma is now the most common chronic illness in children, affecting one in every 15. In North America, 5% of adults are also afflicted. In all, there are about 1 million Canadians and 15 million Americans who suffer from this disease.

The number of new cases and the yearly rate of hospitalization for asthma have increased about 30% over the past 20 years. Even with advances in treatment, asthma deaths among young people have more that doubled.

Allergy Fact

There are about 5,000 deaths annually from asthma in the U.S. and about 500 deaths per year in Canada.

Normal bronchial tubes

Before we can appreciate how asthma affects the bronchial airways, we should first take a quick look at the structure and function of normal bronchial tubes.

The air we breathe in through our nose and mouth passes through the vocal cords (larynx) and into the windpipe (trachea). The air then enters the lungs by way of two large air passages (bronchi), one for each lung. The bronchi divide within each lung into smaller and smaller air tubes (bronchioles), just like branches of an inverted tree. Inhaled air is brought through these airways to the millions of tiny air sacs (alveoli) that are contained in the lungs. Oxygen (O2) passes from the air sacs into the bloodstream through numerous tiny blood vessels called capillaries. Similarly, the body's waste product, carbon dioxide (CO2), is returned to the air sacs and then eliminated upon each exhalation.

Normal bronchial tubes allow rapid passage of air in and out of the lungs to ensure that the levels of O2 and CO2 remain constant in the blood stream. The outer walls of the bronchial tubes are surrounded by smooth muscles that contract and relax automatically with each breath. This allows the required amount of air to enter and exit the lungs to achieve this normal exchange of O2 and CO2. The contraction and relaxation of the bronchial smooth muscles are controlled by two different nervous systems that work in harmony to keep the airways open.

The inner lining of the bronchial tubes, called the bronchial mucosa, contains: (1) mucus glands that produce just enough mucus to properly lubricate the airways; and (2) a variety of so-called inflammatory cells, such as eosinophils, lymphocytes, and mast cells. These cells are designed to protect the bronchial mucosa from the microorganisms, allergens, and irritants we inhale, and which can cause the bronchial tissue to swell. Remember, however, that these inflammatory cells are also important players in the allergic reaction. Therefore, the presence of these cells in the bronchial tubes causes them to be a prime target for allergic inflammation.

How does asthma affect breathing?

Asthma causes a narrowing of the breathing airways, which interferes with the normal movement of air in and out of the lungs. Asthma involves only the bronchial tubes and does not affect the air sacs or the lung tissue. The narrowing that occurs in asthma is caused by three major factors: inflammation, bronchospasm, and hyperreactivity.

Inflammation

The first and most important factor causing narrowing of the bronchial tubes is inflammation. The bronchial tubes become red, irritated, and swollen. The inflammation occurs in response to an allergen or irritant and results from the action of chemical mediators (histamine, leukotrienes, and others). The inflamed tissues produce an excess amount of "sticky" mucus into the tubes. The mucus can clump together and form "plugs" that can clog the smaller airways. Specialized allergy and inflammation cells (eosinophils and white blood cells), which accumulate at the site, cause tissue damage. These damaged cells are shed into the airways, thereby contributing to the narrowing.

Bronchospasm

The muscles around the bronchial tubes tighten during an attack of asthma. This muscle constriction of the airways is called bronchospasm. Bronchospasm causes the airway to narrow further. Chemical mediators and nerves in the bronchial tubes cause the muscles to constrict.

Hyperreactivity (Hypersensitivity)

In patients with asthma, the chronically inflamed and constricted airways become highly sensitive, or reactive, to triggers such as allergens, irritants, and infections. Exposure to these triggers may result in progressively more inflammation and narrowing.

The combination of these three factors results in difficulty with breathing out, or exhaling. As a result, the air needs to be forcefully exhaled to overcome the narrowing, thereby causing the typical "wheezing" sound. People with asthma also frequently "cough" in an attempt to expel the thick mucus plugs. Reducing the flow of air may result in less oxygen passing into the bloodstream and if very severe, carbon dioxide may dangerously accumulate in the blood.

The importance of inflammation

Inflammation, or swelling, is a normal response of the body to injury or infection. The blood flow increases to the affected site and cells rush in and ward off the offending problem. The healing process has begun. Usually, when the healing is complete, the inflammation subsides. Sometimes, the healing process causes scarring. The central issue in asthma, however, is that the inflammation does not resolve completely on its own. In the short term, this results in recurrent "attacks" of asthma. In the long term, it may lead to permanent thickening of the bronchial walls, called airway "remodeling." If this occurs, the narrowing of the bronchial tubes may become irreversible and poorly responsive to medications. Therefore, the goals of asthma treatment are: (1) in the short term, to control airway inflammation in order to reduce the reactivity of the airways; and (2) in the long term, to prevent airway remodeling.

Allergy Assist

The hallmark of managing asthma is the prevention and treatment of airway inflammation. It is also likely that control of the inflammation will prevent airway remodeling and thereby prevent permanent loss of lung function.

Various triggers in susceptible individuals result in airway inflammation. Prolonged inflammation induces a state of airway hyperreactivity, which might progress to airway remodeling unless treated effectively.

Which triggers cause an asthma attack?

Asthma symptoms may be activated or aggravated by many agents. Not all asthmatics react to the same triggers. Additionally, the effect that each trigger has on the lungs varies from one individual to another. In general, the severity of your asthma depends on how many agents activate your symptoms and how sensitive your lungs are to them. Most of these triggers can also worsen nasal or eye symptoms.

Triggers fall into two categories:

Allergens ("specific")
Nonallergens - mostly irritants (nonspecific)

Once your bronchial tubes (nose and eyes) become inflamed from an allergic exposure, a re-exposure to the offending allergens will often activate symptoms. These "reactive" bronchial tubes might also respond to other triggers, such as exercise, infections, and other irritants. The following is a simple checklist.

Common Asthma Triggers:

Allergens

"Seasonal" pollens
Year-round dust mites, molds, pets, and insect parts
Foods, such as fish, egg, peanuts, nuts, cow's milk, and soy
Additives, such as sulfites
Work-related agents, such as latex

Allergy Fact

About 80% of children and 50% of adults with asthma also have allergies.

Irritants

Respiratory infections, such as those caused by viral "colds," bronchitis, and sinusitis
Drugs, such as aspirin, other NSAIDs (nonsteroidal antiinflammatory drugs), and beta blockers (used to treat blood pressure and other heart conditions)
Tobacco smoke
Outdoor factors, such as smog, weather changes, and diesel fumes
Indoor factors, such as paint, detergents, deodorants, chemicals, and perfumes
Nighttime
GERD (gastroesophageal reflux disorder)
Exercise, especially under cold dry conditions
Work-related factors, such as chemicals, dusts, gases, and metals
Emotional factors, such as laughing, crying, yelling, and distress
Hormonal factors, such as in premenstrual syndrome

The many faces of asthma - "Expected"

The many potential triggers of asthma largely explain the different ways in which asthma can present. In most cases, the disease starts in early childhood–age 2 to 6 years. In this age group, the cause of asthma is often linked to exposure to allergens, such as dust mites, tobacco smoke, and viral respiratory infections. In very young children, less than 2 years of age, asthma can be difficult to diagnose with certainty. Wheezing at this age often follows a viral infection and might disappear later, without ever leading to asthma. Asthma, however, can develop again in adulthood. Adult-onset asthma occurs more often in women, mostly middle-aged, and frequently follows a respiratory tract infection. The triggers in this group are usually nonallergic in nature.

Types: allergic (extrinsic) and nonallergic (intrinsic) asthma

Your doctor may refer to asthma as being "extrinsic" or "intrinsic." A better understanding of the nature of asthma can help explain the differences between them. Extrinsic, or allergic asthma, is more common (90% of all cases) and typically develops in childhood. Approximately 80% of children with asthma also have documented allergies. Typically, there is a family history of allergies. Additionally, other allergic conditions, such as nasal allergies or eczema, are often also present. Allergic asthma often goes into remission in early adulthood. However, in 75% of cases, the asthma reappears later.

Intrinsic asthma represents about 10% of all cases. It usually develops after the age of 30 and is not typically associated with allergies. Women are more frequently involved and many cases seem to follow a respiratory tract infection. The condition can be difficult to treat and symptoms are often chronic and year-round.

Typical symptoms and signs of asthma

The symptoms of asthma vary from person to person and in any individual from time to time. It is important to remember that many of these symptoms can be subtle and similar to those seen in other conditions. All of the symptoms mentioned below can be present in other respiratory, and sometimes, in heart conditions. This potential confusion makes identifying the settings in which the symptoms occur and diagnostic testing very important in recognizing this disorder.

The Four Major Recognized Symptoms:

Shortness of breath - especially with exertion or at night
Wheezing - a whistling or hissing sound when breathing out
Coughing - may be chronic; usually worse at night and early morning; and may occur after exercise or when exposed to cold, dry air
Chest tightness - may occur with or without the above symptoms

Asthma Fact

Asthma is classified according to the frequency and severity of symptoms, or "attacks," and the results of pulmonary (lung) function tests.
30% of affected patients have mild, intermittent (less than two episodes a week) symptoms of asthma with normal breathing tests
30% have mild, persistent (two or mores episodes a week) symptoms of asthma with normal or abnormal breathing tests
40% have moderate or severe, persistent (daily or continuous) symptoms of asthma with abnormal breathing tests

Acute asthma attack

An acute, or sudden, asthma attack is usually caused by an exposure to allergens or an upper respiratory tract infection. The severity of the attack depends on how well your underlying asthma is being controlled (reflecting how well the airway inflammation is being controlled). An acute attack is potentially life-threatening because it may continue despite the use of your usual quick-relief medications (inhaled bronchodilators). Asthma that is unresponsive to treatment with an inhaler should prompt you to seek medical attention at the closest hospital emergency room or your asthma specialist office, depending on the circumstances and time of day. Asthma attacks do not stop on their own without treatment. If you ignore the early warning signs, you put yourself at risk of developing "status asthmaticus."

Allergy Fact

Prolonged attacks of asthma that do not respond to treatment with bronchodilators are a medical emergency. Physicians call these severe attacks "status asthmaticus," and they require immediate emergency care.

The symptoms of severe asthma are persistent coughing and the inability to speak full sentences or walk without shortness of breath. Your chest may feel closed and your lips may have a bluish tint. In addition, you may feel agitation, confusion, or an inability to concentrate. You may hunch your shoulders, sit or stand up to breathe more easily, and strain your abdominal and neck muscles. These are signs of an impending respiratory system failure. At this point, it is unlikely that inhaled medications will reverse this process. A mechanical ventilator may be needed to assist the lungs and respiratory muscles. A face mask or a breathing tube is inserted in the nose or mouth for this treatment. These breathing aids are temporary and are removed once the attack has subsided and the lungs have recovered sufficiently to resume the work of breathing on their own. A short hospital stay in an intensive care unit may be a result of a severe attack that has not been promptly treated. To avoid such hospitalization, it is best, at the onset of symptoms, to begin immediate early treatment at home or in your doctor's office.

What medications are used in the treatment of asthma?

Most asthma medications work by relaxing bronchospasm (bronchodilators) or reducing inflammation (corticosteroids). In the treatment of asthma, inhaled medications are generally preferred over tablet or liquid medicines which are swallowed (oral medications). Inhaled medications act directly on the airway surface and airway muscles where the asthma problems initiate. Absorption of inhaled medications into the rest of the body is minimal. Therefore, adverse side effects are fewer as compared to oral medications. Inhaled medications include beta-2 agonists, anticholinergics, corticosteroids, and cromolyn sodium. Oral medications include aminophylline, leukotriene antagonists, and corticosteroid tablets.

Historically, one of the first medications used for asthma was adrenaline (epinephrine). Adrenaline has a rapid onset of action in opening the airways (bronchodilation). It is still often used in emergency situations for asthma. Unfortunately, adrenaline has many side effects, including rapid heart rate, headache, nausea, vomiting, restlessness, and a sense of panic.

Medications chemically similar to adrenaline have been developed. These medications, called beta-2 agonists, have the bronchodilating benefits of adrenaline without many of its unwanted side-effects. Beta-2 agonists are inhaled bronchodilators which are called "agonists" because they promote the action of the beta-2 receptor of bronchial wall muscle. This receptor acts to relax the muscular wall of the airways (bronchi), resulting in bronchodilation. The bronchodilator action of beta- 2 agonists starts within minutes after inhalation and lasts for about four hours. Examples of these medications include albuterol (Ventolin, Proventil), metaproterenol (Alupent), pirbuterol acetate (Maxair), and terbutaline sulfate (Brethaire).

A new group of long-acting beta-2 agonists has been developed with a sustained duration of effect of 12 hours. These inhalers can be taken twice a day. Salmeterol xinafoate (Serevent) is an example of this group of medications. The long-acting beta-2 agonists are generally not used for acute attacks. Beta-2 agonists can have side effects, such as anxiety, tremor, palpitations or fast heart rate, and lowering of blood potassium.

Just as beta-2 agonists can dilate the airways, beta blocker medications impair the relaxation of bronchial muscle by beta-2 receptors and can cause constriction of airways, aggravating asthma. Therefore, beta blockers, such as the blood pressure medications propanolol (Inderal), and atenolol (Tenormin), should be avoided by asthma patients if possible.

The anticholinergic agents act on a different type of nerves than the beta-2 agonists to achieve a similar relaxation and opening of the airway passages. These two groups of bronchodilator inhalers when used together can produce an enhanced bronchodilation effect. An example of a commonly used anticholinergic agent is ipratropium bromide (Atrovent). Ipratropium takes longer to work as compared with the beta-2 agonists, with peak effectiveness occurring two hours after intake and lasting six hours. Anticholinergic agents can also be very helpful medications for patients with emphysema.

When symptoms of asthma are difficult to control with beta-2 agonists, inhaled corticosteroids (cortisone) are often added. Corticosteroids can improve lung function and reduce airway obstruction over time. Examples of inhaled corticosteroids include beclomethasone dipropionate (Beclovent, Beconase, Vancenase, and Vanceril), triamcinolone acetonide (Azmacort), and flunisolide (Aerobid). The ideal dose of corticosteroids is still unknown. The side effects of inhaled corticosteroids include hoarseness, loss of voice, and oral yeast infections. Early use of inhaled corticosteroids may prevent irreversible damage to the airways.

Cromolyn sodium (Intal) prevents the release of certain chemicals in the lungs, such as histamine, which can cause asthma. Exactly how cromolyn works to prevent asthma needs further research. Cromolyn is not a corticosteroid and is usually not associated with significant side effects. Cromolyn is useful in preventing asthma but has limited effectiveness once acute asthma starts. Cromolyn can help prevent asthma triggered by exercise, cold air, and allergic substances, such as cat dander. Cromolyn may be used in children as well as adults.

Theophylline (Theodur, Theoair, Slo-bid, Uniphyl, Theo-24) and aminophylline are examples of methylxanthines. Methylxanthines are administered orally or intravenously. Before the inhalers became popular, methylxanthines were the mainstay of treatment of asthma. Caffeine that is in common coffee and soft drinks is also a methylxanthine drug! Theophylline relaxes the muscles surrounding the air passages and prevents certain cells lining the bronchi (mast cells) from releasing chemicals, such as histamine, which can cause asthma. Theophylline can also act as a mild diuretic, causing an increase in urination. For asthma that is difficult to control, methylxanthines can still play an important role. Dosage levels of theophylline or aminophylline are closely monitored. Excessive levels can lead to nausea, vomiting, heart rhythm problems, and even seizures. In certain medical conditions, such as heart failure or cirrhosis, dosages of methylxanthines are lowered to avoid excessive blood levels. Drug interactions with other medications, such as cimetidine (Tagamet), calcium channel blockers (Procardia), quinolones (Cipro), and allopurinol (Xyloprim) can further affect drug blood levels.

Corticosteroids are given orally for severe asthma unresponsive to other medications. Unfortunately, high doses of corticosteroids over long periods can have serious side effects, including osteoporosis, bone fractures, diabetes mellitus, high blood pressure, thinning of the skin and easy bruising, insomnia, emotional changes, and weight gain.

Expectorants help thin airway mucus, making it easier to clear the mucus by coughing. Potassium iodide is not commonly used and has the potential side-effects of acne, increased salivation, hives, and thyroid problems. Guaifenesin (Entex, Humibid) can increase the production of fluid in the lungs and help thin the mucus, but can also be an airway irritant for some people.

In addition to bronchodilator medications for those patients with atopic asthma, avoiding allergens or other irritants can be very important. In patients who cannot avoid the allergens, or in those whose symptoms cannot be controlled by medications, allergy shots are considered. The benefits of allergy shots (desensitization) in the prevention of asthma has not been firmly established. Some doctors are still concerned about the risk of anaphylaxis, which occurs in one in 2 million doses given. Allergy shots most commonly benefit children allergic to house dust mites. Other benefits can be seen with pollens and animal dander.

In some asthma patients, avoidance of aspirin, or other NSAIDs (commonly used in treating arthritis inflammation) is important. In other patients, adequate treatment of backflow of stomach acid (esophageal reflux) prevents irritation of the airways. Measures to prevent esophageal reflux include medications, weight loss, dietary changes, and stopping cigarettes, coffee, and alcohol. Examples of medications used to reduce reflux include omeprazole (Prilosec) and ranitidine (Zantac). Patients with severe reflux problems causing lung problems may need surgery to strengthen the esophageal sphincter in order to prevent acid reflux (fundoplication surgery). For further information, please read the Gastroesophageal Reflux Disease article.

Asthma At A Glance

Asthma is a chronic inflammation of the bronchial tubes (airways) that causes swelling and narrowing (constriction) of the airways. The bronchial narrowing is usually either totally or at least partially reversible with treatments.

Asthma is now the most common chronic illness in children, affecting one in every 15.

Asthma involves only the bronchial tubes and usually does not affect the air sacs or the lung tissue. The narrowing that occurs in asthma is caused by three major factors; inflammation, bronchospasm, and hyperreactivity.

Allergy can play a role in some, but not all, asthma patients.

Many factors can precipitate asthma attacks and are they are classified as either allergens or irritants.

Symptoms of asthma include shortness of breath, wheezing, cough, and chest tightness.

Asthma is usually diagnosed based on the presence of wheezing and confirmed with breathing tests.

Chest x-rays are usually normal in asthma patients.

Avoiding precipitating factors is important in the management of asthma.

Medications can be used to reverse or prevent bronchospasm in patients with asthma.

REFERENCES: Murray, J., Nadel, J. (2000). Textbook of Respiratory Medicine. Third edition. Philadelphia: W.B Saunders Company.

Davies, S. Peak expiratory flow rate monitoring in asthma. In: UpToDate, Rose, BD (Ed), UpToDate, Wellesley, MA, 2005.

Kohler, C. Metered dose inhaler techniques in adults. In: UpToDate, Rose, BD (Ed), UpToDate, Wellesley, MA, 2005.

Medically Reviewed By: Ellen Reich, MD, Board Certified in Allergy and Immunology, Board Certified in Pediatrics

Arthritis

2008-01-14T18:01:00.000-08:00

What is arthritis?

Arthritis is a joint disorder featuring inflammation. A joint is an area of the body where two different bones meet. A joint functions to move the body parts connected by its bones. Arthritis literally means inflammation of one or more joints.

Arthritis is frequently accompanied by joint pain. Joint pain is referred to as arthralgia.

There are many forms of arthritis (over 100 and growing). The forms range from those related to wear and tear of cartilage (such as osteoarthritis) to those associated with inflammation resulting from an overactive immune system (such as rheumatoid arthritis). Together, the many forms of arthritis make up the most common chronic illness in the United States.

The causes of arthritis depend on the form of arthritis. Causes include injury (leading to osteoarthritis), abnormal metabolism (such as gout and pseudogout), inheritance, infections, and unclear reasons (such as rheumatoid arthritis and systemic lupus erythematosus).

Arthritis is classified as one of the rheumatic diseases. These are conditions that are different individual illnesses, with differing features, treatments, complications, and prognosis. They are similar in that they have a tendency to affect the joints, muscles, ligaments, cartilage, tendons, and many have the potential to affect internal body areas.

What are symptoms of arthritis?

Symptoms of arthritis include pain and limited function of joints. Inflammation of the joints from arthritis is characterized by joint stiffness, swelling, redness, and warmth. Tenderness of the inflamed joint can be present.

Many of the forms of arthritis, because they are rheumatic diseases, can cause symptoms affecting various organs of the body that do not directly involve the joints. Therefore, symptoms in some patients with certain forms of arthritis can also include fever, gland swelling, weight loss, fatigue, feeling unwell, and even symptoms from abnormalities of organs such as the lungs, heart, or kidneys.

Who is affected by arthritis?

Arthritis sufferers include men and women, children and adults. Approximately 350 million people worldwide have arthritis. Nearly 40 million persons in the United States are affected by arthritis, including over a quarter million children!

More than 21 million Americans have osteoarthritis. Approximately 2.1 million Americans suffer from rheumatoid arthritis.

More than half of those with arthritis are under 65 years of age. Nearly 60% of Americans with arthritis are women.

How is arthritis diagnosed and why is a diagnosis important?

The first step in the diagnosis of arthritis is a meeting between the doctor and the patient. The doctor will review the history of symptoms, examine the joints for inflammation and deformity, as well as ask questions about or examine other parts of the body for inflammation or signs of diseases that can affect other body areas. Furthermore, certain blood, urine, joint fluid, and/or x-ray tests might be ordered. The diagnosis will be based on the pattern of symptoms, the distribution of the inflamed joints, and any blood and x-ray findings. Several visits may be necessary before the doctor can be certain of the diagnosis. A doctor with special training in arthritis and related diseases is called a rheumatologist (see below).

Many forms of arthritis are more of an annoyance than serious. However, millions of patients suffer daily with pain and disability from arthritis or its complications.

Earlier and accurate diagnosis can help to prevent irreversible damage and disability. Properly guided programs of exercise and rest, medications, physical therapy, and surgery options can idealize long-term outcomes for arthritis patients.

It should be noted that both before and especially after the diagnosis of arthritis, communication with the treating doctor is essential for optimal health. This is important from the standpoint of the doctor, so that he/she can be aware of the vagaries of the patient's symptoms as well as their tolerance to and acceptance of treatments. It is important from the standpoint of patients, so that they can be assured that they have an understanding of the diagnosis and how the condition does and might affect them. It is also crucial for the safe use of medications.

What is the national financial impact of arthritis?

It has been estimated that the total cost of the arthritis bill for the United States, in terms of hospitalization, doctor visits, medications, physical therapies, nursing home care, lost wages, early death, and family discord is over $50 billion dollars annually.

This does not include the nearly $2 billion spent each year in the United States on unproven remedies by patients addressing their symptoms on their own.

What is a rheumatologist?

A rheumatologist is a medical doctor who specializes in the nonsurgical treatment of rheumatic illnesses, especially arthritis.

Rheumatologists have special interests in unexplained rash, fever, arthritis, anemia, weakness, weight loss, fatigue, joint or muscle pain, autoimmune disease, and anorexia. They often serve as consultants, acting like medical detectives at the request of other doctors.

Rheumatologists have particular skills in the evaluation of the over 100 forms of arthritis and have special interest in rheumatoid arthritis, spondylitis, psoriatic arthritis, systemic lupus erythematosus, antiphospholipid syndrome, Still's disease, dermatomyositis, Sjogren's syndrome, vasculitis, scleroderma, mixed connective tissue disease, sarcoidosis, Lyme disease, osteomyelitis, osteoarthritis, back pain, gout, pseudogout, relapsing polychondritis, Henoch-Schonlein purpura, serum sickness, reactive arthritis, Kawasaki disease, fibromyalgia, erythromelalgia, Raynaud's disease, growing pains, iritis, osteoporosis, reflex sympathetic dystrophy, and others.

Classical adult rheumatology training includes four years of medical school, one year of internship in internal medicine, two years of internal medicine residency, and two years of rheumatology fellowship. There is a subspecialty board for rheumatology certification, offered by the American Board of Internal Medicine, which can provide board certification to approved rheumatologists.

Pediatric rheumatologists are physicians who specialize in providing comprehensive care to children (as well as their families) with rheumatic diseases, especially arthritis.

Pediatric rheumatologists are pediatricians who have completed an additional two to three years of specialized training in pediatric rheumatology and are usually board-certified in pediatric rheumatology.

What is the Arthritis Foundation?

The Arthritis Foundation is the only national voluntary health organization whose purpose is directed solely to all forms of arthritis. The Arthritis Foundation has national and international programs involving support for scientific research, public information and education for affected patients and their families, training of specialists, public awareness, and local community assistance.

Local branch chapters of the Arthritis Foundation serve to disseminate information about arthritis and rheumatic diseases as well as functioning as referral centers. Moreover, many of the various forms of arthritis have their own foundations that serve as information and referral resources for local communities.

Summary

It is the ultimate goal of scientific arthritis research that optimal treatment programs are designed for each of the many form of arthritis. This field will continue to evolve as improvements develop in the diagnosis and treatment of arthritis and related conditions.

Arthritis At A Glance

Arthritis is inflammation of one or more joints.
Symptoms of arthritis include pain and limited function of joints.
Arthritis sufferers include men and women, children and adults.
A rheumatologist is a medical arthritis expert.
Earlier and accurate diagnosis can help to prevent irreversible damage and disability.

REFERENCES: The Arthritis Foundation (http://www.arthritis.org), "Arthritis Prevalence: A Nation in Pain," "The Facts About Arthritis."

Allergy/Allergies

2008-01-14T17:51:00.000-08:00

Introduction

In this review you will learn how allergy relates to the immune system. You will begin understanding how and why certain people become allergic. The most common allergic diseases are discussed briefly in this article.

What does an allergy mean?

An allergy refers to an exaggerated reaction by our immune system in response to bodily contact with certain foreign substances. It is exaggerated because these foreign substances are usually seen by the body as harmless and no response occurs in non- allergic people. Allergic people's bodies recognize the foreign substance and one part of the immune system is turned on. Allergy-producing substances are called "allergens." Examples of allergens include pollens, dust mite, molds, danders, and foods. To understand the language of allergy it is important to remember that allergens are substances that are foreign to the body and can cause an allergic reaction in certain people.

When an allergen comes in contact with the body, it causes the immune system to develop an allergic reaction in persons who are allergic to it. When you inappropriately react to allergens that are normally harmless to other people, you are having an allergic reaction and can be referred to as allergic or atopic. Therefore, people who are prone to allergies are said to be allergic or "atopic."

Austrian pediatrician Clemens Pirquet (1874-1929) first used the term allergy. He referred to both immunity that was beneficial and to the harmful hypersensitivity as "allergy." The word allergy is derived from the Greek words "allos," meaning different or changed and "ergos," meaning work or action. Allergy roughly refers to an "altered reaction." The word allergy was first used in 1905 to describe the adverse reactions of children who were given repeated shots of horse serum to fight infection. The following year, the term allergy was proposed to explain this unexpected "changed reactivity."

What causes allergies?

To help answer this question, let's look at a common household example. A few months after the new cat arrives in the house, dad begins to have itchy eyes and episodes of sneezing. One of the three children develops coughing and wheezing, especially when the cat comes into her bedroom. The mom and the other two children experience no reaction whatsoever to the presence of the cat. How can we explain this?

The immune system is the body's organized defense mechanism against foreign invaders, particularly infections. Its job is to recognize and react to these foreign substances, which are called antigens. Antigens are substances that are capable of causing the production of antibodies. Antigens may or may not lead to an allergic reaction. Allergens are certain antigens that cause an allergic reaction and the production of IgE.

The aim of the immune system is to mobilize its forces at the site of invasion and destroy the enemy. One of the ways it does this is to create protective proteins called antibodies that are specifically targeted against particular foreign substances. These antibodies, or immunoglobulins (IgG, IgM, IgA, IgD), are protective and help destroy a foreign particle by attaching to its surface, thereby making it easier for other immune cells to destroy it. The allergic person however, develops a specific type of antibody called immunoglobulin E, or IgE, in response to certain normally harmless foreign substances, such as cat dander. To summarize, immunoglobulins are a group of protein molecules that act as antibodies. There are five different types; IgA, IgM, IgG, IgD, and IgE. IgE is the allergy antibody.

(In 1967, the husband and wife team of Kimishige and Teriko Ishizaka detected a previously unrecognized type of immunoglobulin in allergic people. They called it gamma E globulin or IgE.)

In the pet cat example, the dad and the youngest daughter developed IgE antibodies in large amounts that were targeted against the cat allergen, the cat dander. The dad and daughter are now sensitized or prone to develop allergic reactions on subsequent and repeated exposures to cat allergen. Typically, there is a period of "sensitization" ranging from months to years prior to an allergic reaction. Although it might occasionally appear that an allergic reaction has occurred on the first exposure to the allergen, there must have been a prior contact in order for the immune system to be poised to react in this way.

IgE is an antibody that all of us have in small amounts. Allergic persons, however, produce IgE in large quantities. Normally, this antibody is important in protecting us from parasites, but not from cat dander or other allergens. During the sensitization period, cat dander IgE is being overproduced and coats certain potentially explosive cells that contain chemicals. These cells are capable of causing an allergic reaction on subsequent exposures to the dander. This is because the reaction of the cat dander with the dander IgE irritates the cells and leads to the release of various chemicals, including histamine. These chemicals, in turn, cause inflammation and the typical allergic symptoms. This is how the immune system becomes exaggerated and primed to cause an allergic reaction when stimulated by an allergen.

On exposure to cat dander, the mom and the other two children produce other classes of antibodies, none of which cause allergic reactions. In these non-allergic members of the family, the dander particles are eliminated uneventfully by the immune system and the cat has no effect on them.

Figure 1

The Immune System Foreign Substance alt="-" (cat dander, pollen, virus, bacteria)

Normal Immune Response IgM, IgG, IgA, IgD and various immune cells respond to attack.		Exaggerated Immune Response IgE is overproduced in response to cat dander, pollens, and other harmless allergens.

Foreign substance is eliminated.		Subsequent exposure results in an allergic reaction.

Non-Allergic Individual		Allergic Individual

Who is at risk and why?

Allergies can develop at any age, possibly even in the womb. They commonly occur in children but may give rise to symptoms for the first time in adulthood. Asthma may persist in adults while nasal allergies tend to decline in old age.

Why, you may ask, are some people "sensitive" to certain allergens while most are not? Why do allergic persons produce more IgE than those who are non-allergic? The major distinguishing factor appears to be heredity. For some time, it has been known that allergic conditions tend to cluster in families. Your own risk of developing allergies is related to your parents' allergy history. If neither parent is allergic, the chance that you will have allergies is about 15%. If one parent is allergic, your risk increases to 30% and if both are allergic, your risk is greater than 60%.

Although you may inherit the tendency to develop allergies, you may never actually have symptoms. You also do not necessarily inherit the same allergies or the same diseases as your parents. It is unclear what determines which substances will trigger a reaction in an allergic person. Additionally, which diseases might develop or how severe the symptoms might be is unknown.

Another major piece of the allergy puzzle is the environment. It is clear that you must have a genetic tendency and be exposed to an allergen in order to develop an allergy. Additionally, the more intense and repetitive the exposure to an allergen and the earlier in life it occurs, the more likely it is that an allergy will develop.

There are other important influences that may conspire to cause allergic conditions. Some of these include smoking, pollution, infection, and hormones.

What are common allergic conditions and their symptoms and signs?

The parts of the body that are prone to react to allergies include the eyes, nose, lungs, skin, and stomach. Although the various allergic diseases may appear different, they all result from an exaggerated immune response to foreign substances in sensitive people. The following brief descriptions will serve as an overview of common allergic disorders.

Allergic Rhinitis

Allergic rhinitis ("hay fever") is the most common of the allergic diseases and refers to seasonal nasal symptoms that are due to pollens. Year round or perennial allergic rhinitis is usually due to indoor allergens, such as dust mites, animal dander, or molds. It can also be caused by pollens. Symptoms result from the inflammation of the tissues that line the inside of the nose (mucus lining or membranes) after allergens are inhaled. Adjacent areas, such as the ears, sinuses, and throat can also be involved. The most common symptoms include:

Runny nose
Stuffy nose
Sneezing
Nasal itching (rubbing)
Itchy ears and throat
Post nasal drip (throat clearing)

In 1819, an English physician, John Bostock, first described hay fever by detailing his own seasonal nasal symptoms, which he called "summer catarrh." The condition was called hay fever because it was thought to be caused by "new hay."

Asthma

Asthma is a breathing problem that results from the inflammation and spasm of the lung's air passages (bronchial tubes). The inflammation causes a narrowing of the air passages, which limits the flow of air into and out of the lungs. Asthma is most often, but not always, related to allergies. Common symptoms include:

Shortness of breath
Wheezing
Coughing
Chest tightness

Allergic Eyes

Allergic eyes (allergic conjunctivitis) is inflammation of the tissue layers (membranes) that cover the surface of the eyeball and the undersurface of the eyelid. The inflammation occurs as a result of an allergic reaction and may produce the following symptoms:

Redness under the lids and of the eye overall
Watery, itchy eyes
Swelling of the membranes

Allergic Eczema

Allergic eczema (atopic dermatitis) is an allergic rash that is usually not caused by skin contact with an allergen. This condition is commonly associated with allergic rhinitis or asthma and features the following symptoms:

Itching, redness, and or dryness of the skin
Rash on the face, especially children
Rash around the eyes, in the elbow creases, and behind the knees, especially in older children and adults (rash can be on the trunk of the body)

Hives

Hives (urticaria) are skin reactions that appear as itchy swellings and can occur on any part of the body. Hives can be caused by an allergic reaction, such as to a food or medication, but they also may occur in non-allergic people. Typical hive symptoms are:

Raised red welts
Intense itching

Allergic Shock

Allergic shock (anaphylaxis or anaphylactic shock) is a life-threatening allergic reaction that can affect a number of organs at the same time. This response typically occurs when the allergen is eaten (for example, foods) or injected (for example, a bee sting). Some or all of the following symptoms may occur:

Hives or reddish discoloration of the skin
Nasal congestion
Swelling of the throat
Stomach pain, nausea, vomiting
Shortness of breath, wheezing
Low blood pressure or shock

Shock refers to the insufficient circulation of blood to the body's tissues. Shock is most commonly caused by blood loss or an infection. Allergic shock is caused by dilated and "leaky" blood vessels, which result in a drop in blood pressure.

Where are allergens?

Everywhere...

We have seen that allergens are special types of antigens that cause allergic reactions. The symptoms and diseases that result depend largely on the route of entry and level of exposure to the allergens. The chemical structure of allergens affects the route of exposure. Airborne pollens, for example, will have little effect on the skin. They are easily inhaled and will thus cause more nasal and lung symptoms and limited skin symptoms. When allergens are swallowed or injected they may travel to other parts of the body and provoke symptoms that are remote from their point of entry. For example, allergens in foods may prompt the release of mediators in the skin and cause hives.

We will assume that allergens are defined as: the source of the allergy producing substance (for example, cat), the substance itself (cat dander), or the specific proteins that provoke the immune response (for example, Feld1). Feld1, from the Felis domesticus (the domesticated cat), is the most important chemical allergen in cat dander.

Allergens may be inhaled, ingested (eaten or swallowed), applied to the skin, or injected into the body either as a medication or inadvertently by an insect sting.

In the Air We Breathe

Breathing can be hazardous if you are allergic. Aside from oxygen, the air contains a wide variety of particles; some toxic, some infectious, and some "innocuous," including allergens. The usual diseases that result from airborne allergens are hay fever, asthma, and conjunctivitis. The following allergens are usually harmless, but can trigger allergic reactions when inhaled by sensitized individuals.

Pollens: trees, grasses, and/or weeds
Dust mites
Animal proteins: dander, skin, and/or urine
Mold spores
Insect parts: cockroaches

In What We Ingest

When foods or medications are ingested, allergens may gain access to the blood stream and become attached to specific IgE on cells in remote sites such as the skin or nasal membranes. The ability of allergens to travel explains how symptoms can occur in areas other than the gastrointestinal tract. Food allergy reactions may begin with tongue or throat swelling and may be followed by tingling, nausea, diarrhea, or stomach cramps. Nasal breathing difficulties or skin reactions may also be seen. The two main allergen groups that are ingested are:

Foods
Drugs (when taken by mouth): for example, antibiotics and aspirin

Allergy Assist The most common foods that cause allergic reactions are cow's milk, fish, shellfish, eggs, peanuts, tree nuts, soy, and wheat.

Touching Our Skin

Allergic contact dermatitis is an inflammation of the skin that is caused by a local allergic reaction. The majority of these localized skin reactions do not involve IgE, but are caused by cells of inflammation. The rash produced is similar to that of a poison ivy rash. It should be noted that when some allergens (for example, latex) come into contact with the skin, they are absorbed by the skin and can also potentially cause reactions throughout the body, not just the skin. For most people, however, the skin is a formidable barrier that can be only locally affected. Examples of allergic contact dermatitis include:

Latex (causes IgE and non-IgE reactions)
Plants (poison ivy and oak)
Dyes
Chemicals
Metals (nickel)
Cosmetics

Allergic contact dermatitis does not involve IgE antibody, but involves cells of the immune system which are programmed to react when triggered by a sensitizing allergen. Touching or rubbing a substance to which you were previously sensitized can trigger a skin rash.

Injected into Our Body

The most severe reactions can occur when allergens are injected into the body and gain direct access to the blood stream. This access carries the risk of a generalized reaction, such as anaphylaxis, which can be life-threatening. The following are commonly injected allergens that can cause severe allergic reactions:

Insect venom
Medications
Vaccines (including allergy shots)
Hormones (for example, insulin)

Allergy At A Glance

Allergy involves an exaggerated response of the immune system.
The immune system is the body's organized defense mechanism against foreign invaders, particularly infections.
Allergens are substances that are foreign to the body and can cause an allergic reaction.
IgE is the allergy antibody.
Allergies can develop at any age.
Your risk of developing allergies is related to your parents' allergy history.

REFERENCES: Fiocchi A, Assa'ad A, Bahna S; Adverse Reactions to Foods Committee; American College of Allergy, Asthma and Immunology. Food allergy and the introduction of solid foods to infants: a consensus document. Adverse Reactions to Foods Committee, American College of Allergy, Asthma and Immunology. Ann Allergy Asthma Immunol. 2006 Jul;97(1):10-20; quiz 21, 77.

Price D, Bond C, Bouchard J, Costa R, Keenan J, Levy ML, Orru M, Ryan D, Walker S, Watson M. International Primary Care Respiratory Group (IPCRG) Guidelines: management of allergic rhinitis. Prim Care Respir J. 2006 Feb;15(1):58-70. Epub 2005 Dec 27.

American College of Allergy, Asthma, & Immunology. Food allergy: a practice parameter. Ann Allergy Asthma Immunol. 2006 Mar;96(3 Suppl 2):S1-68. No abstract available.

Flinterman AE, Pasmans SG, Hoekstra MO, Meijer Y, van Hoffen E, Knol EF, Hefle SL, Bruijnzeel-Koomen CA, Knulst AC. Determination of no-observed-adverse-effect levels and eliciting doses in a representative group of peanut-sensitized children. J Allergy Clin Immunol. 2006 Feb;117(2):448-54.

Scibilia J, Pastorello EA, Zisa G, Ottolenghi A, Bindslev-Jensen C, Pravettoni V, Scovena E, Robino A, Ortolani C. Wheat allergy: a double-blind, placebo-controlled study in adults. J Allergy Clin Immunol. 2006 Feb;117(2):433-9.

Medically Reviewed By: Ellen Reich, MD, Board Certified in Allergy and Immunology, Board Certified in Pediatrics

Diseases & Conditions

Child Abuse

Boils(Skin Abscesses)

Abscessed Tooth

Cuts, Scrapes and Puncture Wounds

Miscarriage(Spontaneous Abortion)

Vaginal Bleeding(Menstruation)

Liver Blood Tests

Ablation Therapy for Arrhythmias

Tummy Tuck ( Abdominoplasty)

Abdominal Pain

Abdominal Aortic Aneurysm

Rheumatoid Arthritis

What is rheumatoid arthritis?

What causes rheumatoid arthritis?

What are the symptoms of rheumatoid arthritis?

How is rheumatoid arthritis diagnosed?

How is rheumatoid arthritis treated?

"First-line" drugs

"Second-line" or "slow-acting" drugs(Disease-modifying anti-rheumatic drugs or DMARDs)

Newer treatments

Other treatments

Future treatments

Rheumatoid Arthritis At A Glance

Osteoporosis

What is osteoporosis?

What are the symptoms of osteoporosis?

What are the consequences of osteoporosis?

Why is osteoporosis an important public health issue?

What factors determine bone strength?

What are the risk factors for developing osteoporosis?

How is osteoporosis diagnosed?

Who should have bone density testing?

How is osteoporosis treated and prevented?

Lifestyle changes

Calcium Supplements

Vitamin D

Hormone therapy (menopausal hormone therapy)

Medications that prevent bone loss and breakdown

Choosing an osteoporosis medication

Prevention of osteoporosis due to long term corticosteroids

Monitoring osteoporosis therapy

Prevention of hip fractures in elderly persons with osteoporosis

Osteoporosis At A Glance

Multiple Sclerosis

What is multiple sclerosis?

What causes multiple sclerosis?

Is multiple sclerosis inherited?

What are the types of multiple sclerosis?

What are the symptoms of multiple sclerosis?

How is multiple sclerosis diagnosed?

How is multiple sclerosis treated?

Interferon

Other medications

How are the manifestations of multiple sclerosis treated?

What are the future directions for managing multiple sclerosis?

Multiple Sclerosis At A Glance

Fibromyalgia

What is fibromyalgia?

What causes fibromyalgia?

Who does fibromyalgia affect?

What are symptoms of fibromyalgia?

How is fibromyalgia diagnosed?

What is the treatment for fibromyalgia?

What is in the future for fibromyalgia therapy?

Fibromyalgia At A Glance

Diabetes Mellitus

What is diabetes?

What is the impact of diabetes?

What causes diabetes?

What are diabetes symptoms?

How is diabetes diagnosed?

Why is blood sugar checked at home?

What are the acute complications of diabetes?

What are the chronic complications of diabetes?

What can be done to slow diabetes complications?

How is diabetes treated?

Diabetes At A Glance

Crohn's Disease

What is Crohn's disease?

"Second-line" or "slow-acting" drugs
(Disease-modifying anti-rheumatic drugs or DMARDs)