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« on: December 24, 2005, 10:40:51 am »

Autoimmune Disease

The term "autoimmune disease" refers to a varied group of more than 80 serious, chronic illnesses that involve almost every human organ system. It includes diseases of the nervous, gastrointestinal, and endocrine systems as well as skin and other connective tissues, eyes blood, and blood vessel. In all of these diseases, the underlying problem is similar--the body's immune system becomes misdirected, attacking the very organs it was designed to protect.

Table I
Female:Male Ratios
in Autoimmune Diseases
Hashimoto's disease/hypothyroiditis  50:1
Systemic lupus erythematosus  9:1 
Sjogren's syndrome  9:1 
Antiphospholipid syndrome  9:1 
Primary biliary cirrhosis  9:1 
Mixed connective tissue disease  8:1
Chronic active hepatitis  8:1
Graves' disease/hyperthyroiditis  7:1
Rheumatoid arthritis  4:1
Scleroderma  3:1
Myasthenia gravis  2:1
Multiple sclerosis  2:1
Chronic idiopathic thrombo-
cytopenic purpura 2:1

A WOMEN'S ISSUE

For reasons we do not understand, about 75 percent of autoimmune diseases occur in women, most frequently during the childbearing years. Table I(list above) lists the female-to-male ratios in autoimmune diseases. Hormones are thought to play a role, because some autoimmune illnesses occur more frequently after menopause, others suddenly improve during pregnancy, with flare-ups occurring after delivery, while still others will get worse during pregnancy.

Autoimmune diseases also seem to have a genetic component, but, mysteriously, they can cluster in families as different illnesses. For example, a mother may have lupus erythematosus; her daughter, diabetes; her grandmother, rheumatoid arthritis. Research is shedding light on genetic as well as hormonal and environmental risk factors that contribute to the causes of these diseases.

Individually, autoimmune diseases are not very common, with the exception of thyroid disease, diabetes, and systemic lupus erythematosus (SLE). However, taken as a whole, they represent the fourth-largest cause of disability among women in the United States.

A NEED FOR KNOWLEDGE

Autoimmune diseases remain among the most poorly understood and poorly recognized of any category of illnesses. Individual diseases range from the benign to the severe. Symptoms vary widely, notably from one illness to another, but even within the same disease. And because the diseases affect multiple body systems, their symptoms are often misleading, which hinders accurate diagnosis. To help women live longer, healthier lives, a better understanding of these diseases is needed, as well as providing early diagnosis and treatment.


MAJOR AUTOIMMUNE DISEASES
CONNECTIVE TISSUE DISEASES
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SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
An inflammation of the connective tissues, SLE can afflict every organ system. It is up to nine times more common in women than men and strikes black women three times as often as white women. The condition is aggravated by sunlight.

Symptoms: Fever, weight loss, hair loss, moth and nose sores, malaise, fatigue, seizures and symptoms of mental illness. Ninety percent of patients experience joint inflammation similar to rheumatoid arthritis. Fifty percent develop a classic "butterfly" rash on the nose and cheeks. Raynaud's phenomenon (extreme sensitivity to cold in the hands and feet) appears in about 20 percent of people with SLE.

Treatment: Anti-inflammatory drugs can help control arthritis symptoms; skin lesions may respond to topical treatment such as corticosteroid creams. Oral steroids, such as prednisone, are used for the systemic symptoms. Wearing protective clothing and sunscreen when outdoors is recommended.


--------------------------------------------------------------------------------
RHEUMATOID ARTHRITIS
Rheumatoid arthritis is a systemic disorder in which immune cells attack and inflame the membrane around joints. It also can affect the heart, lungs, and eyes. Of the estimated 2.1 million Americans with rheumatoid arthritis, approximately 1.5 million (71 percent) are women.

Symptoms: Inflamed and/or deformed joints, loss of strength, swelling, pain.

Treatment: Rest and exercise; anti-inflammatory drugs when necessary.


--------------------------------------------------------------------------------
SYSTEMIC SCLEROSIS (SCLERODERMA)
Scleroderma is an activations of immune cells which produces scar tissue in the skin, internal organs, and small blood vessels. It affects women three times more often than men overall, but increases to a rate 15 times greater for women during childbearing years, and appears to be more common among black women.

Symptoms: In most patients, the first symptoms are Raynaud's phenomenon and swelling and puffiness of the fingers or hands. Skin thickening follows a few months later. Other symptoms include skin ulcers on the fingers, joint stiffness in the hands, pain , sore throat, and diarrhea.

Treatment: The drug D-penicillamine has been shown to decrease skin thickening. Symptoms involving other organs such as the kidneys, esophagus, intestines, and blood vessels are treated individually.


--------------------------------------------------------------------------------
SJÖGREN'S SYNDROME
Sjögren's syndrome (also called Sjögren's disease) is a chronic, slowly progressing inability to secrete saliva and tears. It can occur alone or with rheumatoid arthritis, scleroderma, or systemic lupus erythematosus. Nine out of 10 cases occur in women, most often at or around mid-life.

Symptoms: Dryness of the eyes and mouth, swollen neck glands, difficulty swallowing or talking, unusual tastes or smells, thirst, tongue ulcers, and severe dental caries.

Treatment: Interventions to keep the mouth and eyes moist include drinking a lot of fluids and using eye drops, as well as good oral hygiene and eye care.


--------------------------------------------------------------------------------

NEUROMUSCULAR DISEASES


--------------------------------------------------------------------------------
MULTIPLE SCLEROSIS (MS)
A disease of the central nervous system that usually first appears between the ages of 20 and 40, and affects women twice as often as men. MS is the leading cause of disability among young adults.

Symptoms: Numbness, weakness, tingling or paralysis in one or more limbs, impaired vision and eye pain, tremor, lack of coordination or unsteady gait and rapid involuntary eye movement. A history of at least two episodes of a cluster of symptoms is necessary for a diagnosis of MS. Because MS affects the central nervous system, symptoms may be misdiagnosed as mental illness.

Treatment: The drug baclofen is used to suppress muscle spasticity, and corticosteroids help reduce inflammation. Interferons also are being used to treat this disease.


--------------------------------------------------------------------------------
MYASTHENIA GRAVIS
This is a chronic autoimmune disorder characterized by gradual muscle weakness, often appearing first in the face.

Symptoms: Drooping eyelids, double vision, and difficulty breathing, talking, chewing, and swallowing.

Treatment: The drug edrophonium along with daily rest periods can improve muscle strength.


--------------------------------------------------------------------------------
GUILLAIN-BARRÉ SYNDROME
Guillain-Barré syndrome is an acute illness that causes severe nerve damage. Two-thirds of all cases occur after a viral infection.

Symptoms: Tingling in the fingers and toes, general muscle weakness, difficulty breathing, and, in severe cases, paralysis.

Treatment: Supportive care until the condition is stabilized, then rehabilitation therapy combined with whirlpool baths to relieve pain and facilitate retraining of movements. A process called plasmapheresis, which removes plasma and nerve-damaging antibodies from the blood, is used during the first few weeks after a severe attack and may improve the chance of a full recovery.


--------------------------------------------------------------------------------

ENDOCRINE DISEASES


--------------------------------------------------------------------------------
HASHIMOTO'S THYROIDITIS
Hashimoto's Thyroiditis is a type of autoimmune disease in which the immune system destroys the thyroid, the gland that helps set the rate of metabolism. It attacks women 50 times more often than men.

Symptoms: Low levels of thyroid hormone cause mental and physical slowing, greater sensitivity to cold, weight gain, coarsening of the skin, and goiter (a swelling of the neck due to an enlarged thyroid gland).

Treatment: Thyroid hormone replacement therapy.


--------------------------------------------------------------------------------
GRAVES' DISEASE
Graves' disease is one of the most common autoimmune diseases, affecting 13 million people and targeting women seven times as often as men.. Patients with Graves' disease produce an excessive amount of thyroid hormone.

Symptoms: Weight loss due to increased energy expenditure; increased appetite, heart rate, and blood pressure; tremors, nervousness and sweating; frequent bowel movements.

Treatment: Antithyroid drug therapy or removal of the thyroid gland surgically or by radioiodine.


--------------------------------------------------------------------------------
INSULIN-DEPENDENT (TYPE 1) DIABETES
Type 1 diabetes is caused by too little insulin production in the pancreas, and usually occurs in children and young adults, but it can occur at any age.

Symptoms: Increased thirst, increased urination, weight loss, fatigue, nausea, vomiting, frequent infections.

Treatment: Monitoring of diet and insulin.


--------------------------------------------------------------------------------

GASTROINTESTINAL DISEASES


--------------------------------------------------------------------------------
INFLAMMATORY BOWEL DISEASE
Inflammatory bowel disease describes two autoimmune disorder of the small intestine--Crohn's disease and ulcerative colitis.

Symptoms of Crohn's disease: Persistent diarrhea, abdominal pain, fever, and general fatigue.

Symptoms of ulcerative colitis: Bloody diarrhea, pain, urgent bowel movements, joint pains, and skin lesions.

In both diseases, there is a risk of significant weight loss and malnutrition.

Treatment: Antidiarrheal pills or bulk formers for mild cases. For more serious cases, anti-inflammatory drugs are effective. Corticosteroids are reserved for acute flare-ups of these diseases. In some cases, surgery may be required to remove obstructions or repair perforation of the colon.



--------------------------------------------------------------------------------
OTHER AUTOIMMUNE DISEASES VASCULITIS SYNDROMES
This is a broad and heterogeneous group of diseases characterized by inflammation and damage to the blood vessels, thought to be brought on by an autoimmune response. Any type, size, and location of blood vessel may be involved. Vasculitis may occur alone or in combination with other diseases, and may be confined to one organ or involve several organ systems.


--------------------------------------------------------------------------------
HEMATOLOGIC AUTOIMMUNE DISEASES
Blood also can be affected by autoimmune disorder. In autoimmune hemolytic anemia, red blood cells are prematurely destroyed by antibodies. Other autoimmune diseases of the blood include autoimmune thrombocytopenic purpura and autoimmune neutropenia.


--------------------------------------------------------------------------------
AUTOIMMUNE SKIN DISEASES
The skin frequently gives the first sign that an autoimmune diseases is present. In many of the diseases mentioned, the skin is only peripherally involved, but in others, the skin is the primary site of the disease. One of the foremost is psoriasis, a common skin disease that results from a malfunction in the life cycle of skin cells. The process of skin cell production that normally takes about a month is speeded up to several days, resulting in a build-up of thick scales.


SUMMARY

Autoimmune diseases run the gamut from mild to disabling and potentially life threatening. Nearly all affect women at far greater rates than men. The question before the scientific community is "why?" We have come a long way in the diagnosis and treatment of autoimmune disease. But more work is needed, especially in the areas of discovering the causes and developing more effective treatments and prevention strategies.

The U.S. Public Health Service's (PHS) Office on Women's Health in the Department of Health and Human Services, was established to redress the inequities in research, health services, and education that have placed the health of American women at risk. Its mission is to direct, stimulate, and coordinate women's health research, health care services, and public and health care professional education and training across the Public Health Service agencies and to collaborate with other government organizations, foundations, private industry, consumer and health care professional groups to advance women's health. The focal point for women's health activities in the Department of Health and Human Services, the PHS Office on Women's Health is working to improve the health of American women in this decade and beyond into the 21st century.

The programs and activities in autoimmune diseases of the PHS Office on Women's Health, joined with initiatives and programs across the agencies and office of the Department of Health and Human Services, are providing a solid foundation from which to increase knowledge about autoimmune disorders in women.

For more information on autoimmune diseases, contact:
American Autoimmune Related Diseases Association
15475 Gratiot Avenue
Detroit, MI 48205
Phone: (313) 371-8600

Definitions of Autoimmune disorders on the Web:

Autoimmune disorders are conditions in which the body’s immune system attacks its own cells, causing tissue destruction.


Autoimmunity is a result of a misdirected immune system that causes one’s own immune system to attack itself. Rheumatic heart disease, multiple sclerosis, Graves disease, Sjogren syndrome, autoimmune thyroiditis, psoriasis, Kawasaki disease and insulin-dependent diabetes mellitus are all autoimmune disorders that have been linked to several foodborne bacteria including, Staphylococcus, Streptococcus, Yersinia and Clostridium.


A disease whereby an individual's immune system mounts an attack on a portion of its own tissues. Tissues undergoing such an attack can be destroyed in the process. Rheumatoid arthritis is an example of an autoimmune disease.


Autoimmune diseases arise from an overactive immune response of the body against substances and tissues normally present in the body. Today there are more than 40 human diseases classified as either definite or probable autoimmune diseases and they affect 5-7% of the population. Almost all autoimmune diseases appear without warning or apparent cause and most patients suffer from fatigue.
« Last Edit: May 17, 2006, 06:33:57 pm by Kathy » Logged


I look normal, as I have an "Invisible Illness". You can not catch it, you can not see it. It's called Lupus.My body is attacking itself on the inside.
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« Reply #1 on: December 24, 2005, 12:32:11 pm »

Drug-induced lupus erythematosus

Definition: 
Drug-induced lupus erythematosus is an inflammatory autoimmune disorder that may affect many organ systems. It is caused from an adverse reaction to a medication. 
Causes, incidence, and risk factors: 
Several medications are known to cause a syndrome that resembles systemic lupus erythematosus (SLE) -- a chronic inflammatory autoimmune disorder that may affect many organ systems.

Drug-induced lupus erythematosus occurs as a result of a hypersensitivity reaction to a medication. The drug may react with cell materials, causing the body to react to itself and form antinuclear antibodies.

Drugs that are known to cause this type of reaction in some people include: procainamide, isoniazid, chlorpromazine, penicillamine, sulfasalazine, hydralazine, methyldopa, and quinidine. Symptoms tend to occur after taking the drug for a reasonable period of time, usually at least 3 to 6 months.

In drug-induced lupus erythematosus, the features of arthritis, systemic symptoms, and cardiac and pulmonary (lung) symptoms may be present. Other symptoms associated with SLE, such as lupus nephritis and neurological disease, are rare.

Drug-induced lupus erythematosus also differs from SLE in that the course of the disease is usually not as severe as SLE. Usually, the symptoms resolve within a few days to weeks after stopping the medication. The sex distribution of drug-induced lupus erythematosus is equal, whereas in SLE, women are affected more often than men
 
« Last Edit: May 17, 2006, 06:32:06 pm by Kathy » Logged


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« Reply #2 on: January 14, 2006, 07:03:21 pm »

What is mixed connective tissue disease (MCTD)? 

An autoimmune disease first described in 1972
Combines symptoms of lupus, scleroderma and polymyositis


Mixed connective tissue disease (MCTD) is an autoimmune disease first described in 1972 and is considered an "overlap" of three diseases, systemic lupus erythematosus (lupus), scleroderma and polymyositis. People with MCTD experience symptoms of each of these three diseases.  In many cases, this mixed set of symptoms is eventually dominated by symptoms characteristic of one of the three illnesses, especially scleroderma or lupus.


How common is MCTD? 

MCTD is rare.
It mostly affects women.


Mixed connective tissue disease is relatively rare, and the vast majority of people with the disease (80 percent) are women. MCTD occurs among people of all ages.


What are the warning signs of MCTD? 

Can start with subtle symptoms and is often misdiagnosed
Initial symptoms can include swollen fingers, joint pain, Raynaud’s phenomenon, a purplish rash on the face, fatigue and more
Blood tests can help to confirm a diagnosis of MCTD


Most people with MCTD experience subtle signs of the disease many years before having it diagnosed.  These symptoms can include swollen fingers, joint or muscule pain, acid reflux or difficulty swallowing, Raynaud's phenomenon (fingers become pale and numb in response to cold or emotional stress), muscle weakness, shortness of breath on activity, dry cough, a general malaise and fatigue. .
 Symptoms of MCTD vary widely and each person's illness can be quite different.
 
Often a person with MCTD will visit many doctors before they receive a confirmed diagnosis. Although the diagnosis is often made based on the overlapping symptoms of lupus, scleroderma and polymyositis, a blood test for the ANA (anti-nuclear antibodies) – a general test of autoimmune disease – is taken.

 Abnormally high test results for ANA are an indicator for MCTD. Further testing of the blood will detect a more specific antibody, anti-ribonucleoprotein (RNP), which is present in almost all people who have MCTD.
 
Almost everyone with MCTD will have aching joints. The disease also damages the muscle fibres causing weakness and soreness, especially in the muscles around the shoulders and hips.
 
Frequently, MCTD causes swollen hands and fingers. A purplish butterfly-shaped rash on the cheeks and the bridge of the nose, red patches on the knuckles, a violet discolouration of the eyelids and spidery veins on the face and hands may also occur.



What causes MCTD? 

The cause of MCTD is not known.

The cause of MCTD is not known. There may be a genetic predisposition and it is known that autoimmune diseases like MCTD run in families. It also appears that hormones may play a role in increasing susceptibility to developing the disease.


What can you do about MCTD? 

Treatment is similar to treatment for lupus and other autoimmune diseases
Mild cases can be treated with NSAIDs
Severe cases may require immunosuppressive drugs
As the disease progresses it can become less responsive to treatment



Medicine
Treatment of MCTD is directed at suppressing immune-related inflammation of tissues and is similar to treatment for lupus. Corticosteroids (for example, prednisone) are usually effective, especially when the disease is diagnosed early. Mild cases can be treated with nonsteroidal anti-inflammatory drugs (NSAIDs), hydroxychloroquine or similar drugs, and low doses of corticosteroids.
 
The more severe the disease, the higher the dose of corticosteroid needed. Prednisone is the most common corticosteroid used and is taken in pill form. Prednisone is usually considered when the symptoms of MCTD are not being controlled by other treatments.
 
Prednisone use needs to be carefully monitored because of its many side effects, and the drug must never be stopped abruptly. Some of the side effects from long-term use include cataracts, high blood pressure, sleep problems, muscle loss, bruising, thinning of the bones (osteoporosis), weight gain and increased risk of infections.  The goal with this and most drugs is to find the lowest effective dose to avoid as many of the side effects as possible.

In severe cases of MCTD, immunosuppressive drugs (e.g. cytotoxic drugs) may also be needed. These drugs are powerful medications that suppress inflammation and the immune system. You may be prescribed these if your MCTD symptoms are difficult to control with prednisone alone or if you are experiencing side effects from prednisone.
 
Cyclophosphamide (Procytox) and Imuran (azathioprine) are commonly prescribed immunosuppressant drugs. Serious side effects from these drugs include decreased blood cell counts, increased risk of infection, and a risk of developing certain types of cancer. People taking these medications must have regular blood tests and be monitored very closely by their doctor.
 
In general, the more advanced the disease and the greater the organ damage, the less effective the treatment will be. Scleroderma-like damage to the skin and esophagus (pronounced e-sof-a-gus) is least likely to respond to treatment. Symptom-free periods can sometimes last for many years through minimal or no ongoing treatment.
However, MCTD will progress in spite of treatment in about 13 percent of cases.

A Word about Medication Safety
The need to effectively monitor new drugs once they have been approved and introduced into the market has been a key advocacy issue for The Arthritis Society for several years. This advocacy helps to ensure that unfavorable side effects are reported, documented, and addressed.

All medications have potential side effects whether they are taken by themselves or in combination with other herbal, over-the-counter and prescription medications. It is therefore important for patients to discuss the benefits and potential side effects of all their medications with their doctor.


Additional tips for living well with MCTD 

The Arthritis Society offers a variety of programs and services that can be helpful
You can also reach them throughr their website at www.arthritis.ca
 

Along with the physical symptoms of MCTD, many people experience feelings of helplessness and depression. Learning daily living strategies to manage your arthritis gives you a greater feeling of control and a more positive outlook.

From another website:


Mixed connective tissue disease (MCTD) is a rare autoimmune disorder. People with this disorder have signs and symptoms of three diseases — lupus, scleroderma and polymyositis. They also have antibodies to U1-RNP protein in their blood. This disorder occurs most often in females between the ages of 15 and 25. Signs and symptoms may include:

Raynaud's phenomenon — blood vessel spasms that interrupt blood flow to the finger, toes, ears and nose
Arthritis with painful, swollen joints
Swelling in the hands (edema)
Muscle weakness (myositis)
Shortness of breath
Skin changes, such as thickening or rash, typically on the face or hands
A doctor may make a diagnosis of MCTD based on:

Physical examination
Signs and symptoms
Blood tests that detect the presence of antibodies to U1-RNP protein
Your doctor may recommend further testing to help determine the severity of the disease and the appropriate treatment. There's no cure for MCTD. Treatment is usually directed at managing the signs and symptoms and may include:

Nonsteroidal anti-inflammatory drugs
Corticosteroids
Vasodilators, which improve blood flow
Immunosuppressant medications
 

Lupus & Connective Tissue Disorder Website Information
www.LupusMCTD.com


This website is provided for educational and informational purposes only. Lupus and Mixed Connective Tissue Disorder is not engaged in rendering medical advice or professional services and this information should not be used for diagnosing or treating a health problem. The site author and the content providers make no representation or warranties, expressed or implied. Providing links to other websites does not imply that Lupus and Connective Tissue Disorder endorses the information or services provided on those websites. The organizations operating those websites are solely responsible for the content found on their websites. All material on this web site is copyright © 2005 by Lupus and Mixed Connective Tissue Disorder.
« Last Edit: May 17, 2006, 06:19:44 pm by Kathy » Logged


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« Reply #3 on: April 03, 2006, 11:16:03 am »

MEDICAL GENOMICS GROUP
COMPARATIVE GENOMICS CENTRE
Mail Address: Comparative Genomics Centre,
Molecular Sciences Bldg 21, James Cook University,
Townsville, 4811, Queensland, Australia
Telephone: 61-7-4781 6265 Fax:  61-7-4781 6078


RESEARCH OVERVIEW:
    The Medical Genomics Group is working to determine the causes of autoimmune diseases using both cellular and genetic techniques. Current projects study: the genetics of autoimmune diabetes, gastritis and lupus in mice; the effects of mycobacteria on autoimmune diseases; and the role of immunoregulatory NKT cells in childhood diabetes.

     A major focus for the group is the study of interactions between genetic and environmental factors in causing autoimmune disease. Our understanding of these genetic and environmental factors has been greatly aided by the inbred NOD mouse model (pictured) which spontaneously develops autoimmune diabetes, but is protected by treatment with Mycobacterium bovis, the BCG vaccine.

   NOD mice are a well established model of both type 1 diabetes and systemic lupus erythematosus. They spontaneously develop lymphocytic infiltrates of their islets of Langerhans in the pancreas, and in the majority of females, this pathology progresses to complete destruction of the insulin-producing beta cells, resulting in diabetes. Many genes encoding susceptibility to diabetes in this model have been mapped by us and other groups.
 
    If NOD mice are exposed to mycobacteria between three and ten weeks of age, they are protected from the onset of diabetes, but tend to develop another autoimmune disease, systemic lupus erythematosus. Our group was responsible for all of the original characterisation of this model. Lupus in both patients and NOD mice is characterised by the production of antibodies specific for multiple cellular constituents. This results in antibody clumping and deposition in fine vascular beds (such as those in the kidneys and skin) resulting in the activation of inflammatory processes and tissue damage. About 50% of women with lupus develop kidney failure.

    We postulated that the autoimmune diseases diabetes and lupus represented two different expressions of the same basic tendency to autoimmune disease in these mice, and that exposure to the environmental factor mycobacteria was responsible for switching between the two expressions (phenotypes) of this underlying susceptibility.

    This hypothesis was disproved in two ways. Firstly, mycobacteria were sonnicated and then subfractionated, and the individual subfractions tested for their abilities to prevent diabetes and precipitate lupus. We have identified a single subcomponent, MAPG, which can prevent diabetes without inducing lupus. This product is in the final stages of preparation for clinical trials in children who are known to be at a high risk of developing type 1 diabetes.

    The second way in which we were able to demonstrate that diabetes and lupus were independent in the NOD mouse model, was by performing a whole genome screen of loci encoding susceptibility to lupus induced by mycobacteria. We then compared the genetic locations of the lupus genes with those of the diabetes genes. With the exception of the MHC region on chromosome 17, which is involved in almost all autoimmune diseases, the genes did not co-localise.

    NKT cells are a small population of white blood cells that play a critical role in controlling the size and character of immune responses against bacteria, viruses, parasites, tumours and the body's own tissues. Indeed, both diabetes and lupus are associated with numerical deficiencies in these cells; we were responsible for demonstrating this deficiency in NOD mice. When we mapped the genes controlling numbers of NKT cells in mice, only two genetic regions were identified: one was on distal chromosome 1 and mapped to the same location as our previously mapped major lupus gene, and the other was on chromosome 2, and mapped to the same region as an important diabetes susceptibility gene. It seems likely that these two regions play important roles in both autoimmune disease susceptibility and control of NKT cells, and it is possible that disease susceptibility is a consequence of these genes' effects on NKT cell numbers.

    Our current work is focussed on identifying the coding sequences responsible for these phenotypes. We have produced congenic mice for each segment in order to narrow down the region under consideration, and are now applying the candidate approach to positional cloning by examining the protein coding regions within these areas that could conceivably play a role in controlling NKT cell numbers. These protein coding regions are being characterised by sequencing the cDNA from both parental strains and characterising the levels of expression of the gene in each strain and the congenic lines by reverse transcriptase PCR.

    The Medical Genomics Research Group is very grateful for the generous support of Diabetes Australia and the National Health and Medical Research Council of Australia.


Autoimmune Diseases

    Autoimmune diseases are conditions in which the body's defence (immune) system attacks part of the body itself. The targeting of this attack is directed either by specialised proteins called antibodies, or else by a subset of white blood cells called T cells. It is not known why some individuals develop these diseases while most do not, but they are relatively common and can cause serious health problems and even death. The most common autoimmune diseases are:
  DISEASE FREQUENCY (%)
Autoimmune thyroid disease (Hashimoto's Disease, Graves Disease) 2
Rheumatoid arthritis 1
Vitiligo 0.5
Childhood Diabetes 0.25


One way of discovering the cause of these diseases is to examine the genes associated with them.



Childhood Diabetes

    Childhood diabetes (type 1, or Insulin dependent diabetes mellitus) is known to be caused by autoimmune mediated destruction of the insulin producing cells in the pancreas. The NOD mouse is a type of mouse which develops a disease equivalent to human type 1 diabetes and has been used as a model for testing new therapies for prevention and treatment of potential value in the human disease.  The genes responsible for diabetes in these mice have been well studied, but one hurdle facing future work is our ignorance of the mechanisms whereby they actually affect the immune system.

     In many immune responses, one or other pattern of reactivity dominates. In some reactions, a predominantly cellular response occurs and white blood cells (especially T lymphocytes) mediate tissue destruction. This is a common response to viral infections. In other reactions, antibody production predominates, often in response to bacterial infection. These two types of response are counter-regulated so that the cell hormones (lymphokines) which mediate cellular responses tend to ameliorate antibody responses. There are many lines of evidence to suggest that type 1 diabetes is mediated by an inappropriate cellular response to the insulin-producing beta cells (pictured) and may be  prevented by an ongoing antibody response.

Although NKT cells make up only a tiny proportion of the lymphocytes in the immune system, they have a powerful action and produce large amounts of the lymphokine (IL4) which enhances antibody responses and inhibits cellular responses. Two recent experiments suggest that they are responsible for determining whether a cellular or antibody response is made. NOD mice spontaneously develop type 1 diabetes and we have shown that they have very few NKT cells.

Other workers have shown that NOD mice make less IL4 than other strains, which is consistent with their relative lack of NKT cells. We think this defect may result in these mice being more likely to make cellular responses and may partly explain the nature of the autoimmune response to the islets in diabetes. In support of this hypothesis, we have shown that we can prevent diabetes in NOD mice by injecting them with extra NKT cells.

    We are currently trying to find out how these cells prevent diabetes, identify the genes which control them and examine their role in human diabetes.



Lupus

    Systemic lupus erythematosus (lupus) is an autoimmune disease in which the production of antibodies against many normal cell components results in the deposition of proteins in the small blood vessels, inflammation, and subsequent damage to many parts of the body, including the skin, joints, kidneys and brain.  About half of lupus patients develop significant kidney disease (termed lupus nephritis) and this is a strong predictor of a poor outcome. In lupus nephritis, immune complexes, consisting of antibody and cell components, are deposited in the filtering units of the kidney. This gives a characteristic "lumpy bumpy" pattern when stained with fluorescent reagents that bind either antibody or the inflammatory mediator complement.

   We have found that injecting BCG (the anti-tuberculosis vaccine, M.bovis) into NOD mice prevents diabetes, but causes the onset of lupus. We have been studying what genes are responsible for causing lupus in NOD mice, and comparing them to the genes already known to cause diabetes. We examined the idea that some genes cause both lupus and diabetes because they control how likely the immune system is to attack the body's own tissues. This project was a major undertaking for the group and has taken five years to complete.

Approximately 900 female mice were clinically monitored for almost a year after vaccination with BCG. Mice which developed haemolytic anaemia, antinuclear antibodies and  lupus nephritis (pictured), as well as a group of unaffected mice were then gene typed at over 150 genetic locations. This linkage analysis localised both genes which are shared with diabetes as well as other genes which are shared with other mouse models of lupus. The identification of these genes will be of great help in understanding what causes lupus and in developing safer ways of treating or preventing diabetes.
    We are now using the genetic information obtained in the gene mapping study to produce mice carrying only one or two disease susceptibility genes on a normal genetic background, in order to study the interactions between them and the environmental disease trigger, BCG.
 


Gastritis

    Gastritis is a disease in humans which destroys the acid-producing cells in the stomach and is associated with the development of pernicious anaemia (vitamin B12 deficiency) and cancer of the stomach. The thymus is the organ that produces T cells, which are the white blood cells that provide the cellular defence from infections and cancer. If the thymus is removed from some kinds of mice while they are still very young, the few T cells that have left the thymus start to damage the host's own tissues.

 Together with collaborators in Dr Ian van Driel's laboratory at the University of Melbourne, we are using this experimental approach to study the BALB/c inbred strain of mice. These mice, after removal of the thymus, develop T cell-mediated damage of the acid-producing cells of the stomach, resulting in a disease that closely resembles autoimmune gastritis in humans. We have identified the locations of four genes which are responsible for causing gastritis amd one of them appears to be especially important, because it has the strongest effect and may also be involved in diabetes and lupus. We currently characterizing this gene in more detail by locating it more exactly and by examining its effect on mice not normally prone to gastritis.
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« Reply #4 on: April 22, 2006, 10:47:18 am »

Faulty Cells Thought to Start Autoimmune Process
February 2006 Vol. 311. no. 5764, pp. 1160-1164 - Science 
 
Autoimmune diseases such as lupus have been linked to the body’s failure to clean up after an immune response, since there is a need to eliminate inflammatory cells once a virus or bacteria has been fought off.  In order to ensure the clean-up process is efficient, these inflammatory cells normally undergo a process known as apoptosis – or programmed cell death. When this occurs, the cells bring proteins up to their surface that attract the “clean-up” cells which come in and dispose of them.

 

When apoptosis is inefficient, the persistence of the used-up inflammatory cells in the blood stream will lead to more inflammation, and could be one of the key triggers of autoimmune diseases such as lupus.  However, research has found that inhibiting apoptosis in immune cells is not enough, in and of itself, to cause autoimmunity, suggesting the additional involvement of other cell types in causing autoimmune diseases.  The researchers of this study are working to fill in the gaps between what happens when apoptosis is prevented and the start of autoimmune disease.

 
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« Reply #5 on: May 28, 2006, 01:31:32 pm »

Lupus Fueled by Untimely Death of Body's Waste Disposal Cells

LRI-Funded Scientist Shows That Resulting Debris Exacerbates Disease

With the help of Lupus Research Institute (LRI) funds, Mariana J. Kaplan, M.D. and colleagues at the University of Michigan in Ann Arbor have found an invaluable clue as to what causes and promotes the autoimmune reaction in lupus, a chronic and often devastating multi-system disease that affects more than 1.5 million Americans.

The research, published in the February 15th issue of the Journal of Immunology, indicates that lupus worsens when the very agents designed to mop up dying cells in the body—specialized scavenger cells called macrophages—fail to get disposed of properly.

"Dr. Kaplan has elegantly shown that lupus autoimmunity occurs by chemically impairing the clearance of apoptotic [dead cell] material,” explains Roberto Caricchio, M.D. at the University of Pennsylvania. “This finding is highly interesting because it leads to possible new therapeutic venues."

The LRI is the nation's leading sponsor of new science to prevent, treat and cure lupus. It awarded Dr. Kaplan a Novel Research Grant in 2002 to examine, among other factors, the role of auto-reactive T cells in lupus and the molecular pathway by which they trigger the death of the endothelial cells that line blood vessels.

Problem Identified, Solution Proposed

The body’s waste disposal experts (macrophages) are designed to engulf and destroy dying cells—part of a complex and delicate balancing act designed to keep blood healthy. In people with lupus, macrophages and their precursors (monocytes) appear to be particularly susceptible to untimely death. Without the normal garbage disposal experts in attendance, the build-up of debris in the blood—dead cell material such as DNA and DNA-binding proteins—may eventually prompt the immune system to turn on itself.

To test whether this phenomenon actually explains why lupus develops and flares, Dr. Kaplan treated mice genetically prone to the disease with a chemical that destroys the scavenger macrophages. As expected, these mice developed lupus symptoms faster, and suffered more severe disease, than the lupus-prone mice spared administration of the macrophage-killing chemical. (Interestingly, mice that were not prone to lupus but that received the chemical that destroys macrophages developed autoantibodies, albeit not at the high levels seen in lupus. Nor did they develop kidney disease.)

"Based on the results from this study," explains Dr. Kaplan, "we propose that increased macrophage apoptosis [death] contributes to the pathogenesis [cause and development] of autoantibody formation and organ damage in lupus." The chemically treated mice not only had increased and sustained elevations of key antibodies (anti-nucleosome and anti-dsDNA Abs), but they also developed signs of kidney problems (indicated by increased protein in the urine) and got more severe lupus nephritis (kidney inflammation).

The authors point to T cells, which are designed to eliminate cells infected with viruses among other important functions, as the likely culprits in the early death of macrophages. Saving the macrophages from this untimely end, possibly by using agents that block the killer molecules on T cells, is now of interest as a way of slowing or stopping the autoimmune reaction.

Dr. Caricchio sees the possibility, "for example, of a system which would allow faster clearance of apoptotic material so that the lupus-prone immune system would be always scarce of “fuel” to sustain itself. In this scenario lupus disease would be milder and perhaps long-term inactive."

Multiple Institute-Funded Projects Explore Mishandling of Dead and Dying Cells in Lupus

Dr. Kaplan is one of several researchers funded by the LRI who is exploring the idea that lupus develops when leftover cell parts prompt the body to produce self-directed antibodies. Currently six LRI-funded projects tackle this particular hypothesis in novel ways.

As the nation’s leading sponsor of innovative and cutting-edge research in lupus, the LRI funds numerous other approaches to better understanding, preventing, and treating a disease that has baffled scientists for more than 40 years. Lupus can attack and damage vital organs and tissues such as the skin, brain, heart, lungs, blood, and kidneys. More than 90 percent of people with lupus are female, and it is a leading cause of kidney disease, stroke, and premature cardiovascular disease in women of childbearing age.

Since its founding in 2000, the LRI has awarded more than $14.5 million in grants to nearly 60 scientists at leading institutions nationwide. It has cast a broad net across the nation to identify, and then support and champion, the brightest novel ideas such as Dr. Kaplan's—the as-yet unasked questions—that have the potential to crack open the autoimmunity mystery.

For more on the LRI, visit www.LupusResearchInstitute.org
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« Reply #6 on: June 15, 2006, 10:23:47 pm »

What is CREST?
 
CREST is a form of Systemic Sclerosis (scleroderma) which is characterized by Calcinosis (calcium deposits), usually in the fingers; Raynaud's;loss of muscle control of the Esophagus, which can cause difficulty swallowing; Sclerodactyly, a tapering deformity of the bones of the fingers; and Telangiectasia, small red spots on the skin of the fingers, face, or inside of the mouth.
 
Calcinosis
 Raynaud's
 Esophagus
 Sclerodactyly
 Telangiectasia
 
 
It takes only two of the five CREST symptoms for a diagnosis of  CREST (either "pure" or "plus") to be made.  For example, a patient with Calcinosis and Raynaud's would have CREST (which for precision may also be written as CRest, but it is CREST nonetheless.)
 
CREST Syndrome "Patients with CREST syndrome are a subset of patients with scleroderma..."


"Pure" CREST
 
"Pure"CREST — by itself:  "Pure" CREST is diagnosed when patients have two or more symptoms of CREST but they do not meet the criteria for either Limited or Diffuse Scleroderma.  That is, they must not have tight skin above their wrists, and if there is tight skin on their fingers, they must not have either pitting digital ulcers or lung fibrosis.

  "Plus" CREST
 
"Plus" CREST — along with:   When CREST symptoms appear along with another form of Scleroderma, it is referred to as, for example, "Limited Scleroderma plus CREST" or "Diffuse Scleroderma plus CREST." A person may also have any other autoimmune disease " plus CREST."
 
Progression
 
Although some doctors still believe CREST is a useful subcategory, the existing research studies have been unable to predict consistently how (or whether) the disease will progress to Diffuse Systemic Scleroderma in any specific individual.
 
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« Reply #7 on: June 21, 2006, 07:33:39 pm »

General Description

Scleroderma (means "hard skin") is a rare connective tissue disorder characterized by abnormal thickening of the skin. It is generally considered to be an autoimmune disorder.

There are two major variants of the disease, as well as other less common forms. The more serious form is usually called "diffuse Scleroderma" and is characterized by rapid development of skin thickening beginning with the hands, and face and extending to the arms and trunk. People with diffuse Scleroderma are at greater risk for developing internal organ involvement early in the course of the disease.

The other major form is often called limited Scleroderma or CREST Syndrome. The name CREST is an acronym for its characteristic symptoms: calcinosis, Raynaud's phenomenon, esophageal involvement, sclerodactyly, and telangiectasia (these terms are discussed below). This form progresses more slowly and has a better prognosis.

Scleroderma can also occur in more localized forms without internal organ involvement. These variants are called Morphea and Linear Scleroderma. Scleroderma like symptoms can also appear in conjunction with other disorders such as Mixed Connective Tissue Disorder. These scleroderma-like conditions are discussed in more detail below.

Differential Diagnosis

In most cases, diagnosis can be made based on presenting symptoms in combination with a positive anti-nuclear antibody (ANA) test. Specific antibody tests can often be used to confirm or differentiate specific subsets of the disease.

The presence of anti-centromere (ACA) antibodies is very highly correlated with a diagnosis of CREST (limited Scleroderma). However, only about 57% of patients who are diagnosed with CREST by symptoms alone have detectable ACA antibodies. Similarly, the presence of anti-topoisomerase I (anti-SCL-70) antibodies is highly correlated with diffuse Scleroderma, while only about 40% of patients diagnosed with diffuse Scleroderma by symptoms alone have detectable anti-SCL-70 antibodies. It is very rare for an individual to have both antibodies.

Overall, only about 60% of patients diagnosed with Scleroderma have positive specific antibody tests. This means that the lack of specific antibodies does not rule out the diagnosis of Scleroderma. Measurement of these antibodies should be considered secondary to the clinical features when making a diagnosis of Scleroderma.

These findings also suggest that there are at least four different subsets of Scleroderma and possibly more: ACA positive CREST, ACA negative CREST, anti-SCL-70 positive diffuse Scleroderma, and anti-SCL-70 negative diffuse Scleroderma. This has significant implications when interpreting the results of research studies that do not distinguish between the specific subsets of the disease.

Scleroderma-Like Disorders

Morphea, or localized Scleroderma, usually begins between the ages of 20 to 50 years as patches of yellowish or ivory-colored rigid, dry skin. These are followed by the appearance of firm, hard, oval-shaped plaques with ivory centers that are encircled by a violet ring. These spots generally appear on the trunk, face, and/or extremities. Many patients with localized Morphea improve without treatment. Generalized Morphea is more rare and serious, and involves the skin but not the internal organs.

Linear Scleroderma appears as a band-like thickening of skin on the arms or legs. This type of Scleroderma is most likely to be on one side of the body but may be on both sides. Linear Scleroderma generally appears in young children and is characterized by the failure of one limb (i.e., arm or leg) to grow as rapidly as its counterpart.

Diffuse fasciitis with eosinophilia (DFE; also called eosinophilic fasciitis or Shulman’s syndrome) is a rare condition that mimics Scleroderma with swelling, stiffness, and decreased flexibility of the limbs associated with skin thickening. Although the symptoms can be widespread and involve the trunk and limbs, in contrast to Scleroderma, the fingers, hands, and face are usually not affected. In addition, there is no occurrence of Raynaud’s or GI involvement.

Eosinophilia-myalgia syndrome (EMS) and toxic oil syndrome (TOS) are toxin-induced disorders that mimic Scleroderma. Both conditions result in skin fibrosis and can become chronic.

Scleroderma-like skin changes have also been associated with insulin-dependent diabetes, carcinoid syndrome, myeloma, scleromyxedema, chronic graft-versus-host disease, porphyria cutanea tarda, Werner’s syndrome, progeria, phenylketonuria, bleomycin exposure, local lipodystrophies, and POEMS syndrome.

Affected Population

Scleroderma is a rare disorder that affects an estimated 40,000 to 165,000 people in the United States. The incidence rate of Scleroderma appears to be relatively stable at about 19 new cases per million per year in the US. A number of international studies suggest that Scleroderma occurs much more frequently in the United States than elsewhere. These regional differences may be a consequence of differential genetic susceptibility to Scleroderma, different exposure to possible environmental triggers, or a combination of both.

Scleroderma may occur at any age, but the symptoms most frequently begin in mid-life. The diffuse and limited forms of Scleroderma are very rare in children. The disease is 3 to 4 times more common in women than men. There is some evidence that black women have a significantly greater risk than white women. In addition, diffuse Scleroderma appears to occur more frequently among black women and starts at an earlier age.

There seems to be a relatively weak genetic link with Scleroderma. Close order relatives of an affected individual are much more likely to have elevated ANA levels, but without any Scleroderma symptoms, than the normal population.

Causes

The exact cause of Scleroderma is unknown. There are a number of environmental factors that appear to be related to Scleroderma or Scleroderma-like illnesses, including exposure to silica dust, vinyl chloride, epoxy resins, and other organic solvents. Several studies have shown some evidence of geographic clustering, which is also consistent with possible environmental risk factors

A number of researchers have investigated the possible link between Scleroderma and silicone breast implants. To date, all of these studies have shown no causal link. While there are certainly many reported cases of Scleroderma and other auto-immune disorders among women who have had breast implants, this is the same population which is most likely to develop auto-immune disorders such as Scleroderma in any case, and the incidence of auto-immune disorders among these women is consistent with the expected incidence in this population.

A few studies have suggested that certain viruses may have a causal role in some cases of Scleroderma, but the data is limited.

Symptoms

Clinical Features - General

Scleroderma normally begins with Raynaud's phenomenon - the fingers and toes lose circulation and turn white upon exposure to cold. Raynaud's phenomenon usually (but not always) precedes skin changes by several months with diffuse Scleroderma and often precedes skin changes by several years with limited Scleroderma. Other early symptoms may be painful joints, morning stiffness, red swollen hands, fatigue, and/or weight loss. It is important to note, however, that Raynaud’s phenomenon without any underlying disease is quite common in the general population, especially among women. This form of Raynaud’s is called "primary Raynaud’s". A key distinguishing characteristic is that with primary Raynaud’s, the anti-nuclear antibody (ANA) level will normally be negative, while with Raynaud’s which accompanies Scleroderma or other auto-immune disorders (secondary Raynaud’s), ANA levels are normally positive.

The first specific clinical symptom to suggest a diagnosis of Scleroderma is skin thickening that begins as swelling or "puffiness" of the fingers and hands. Later the skin becomes hard, shiny, and leathery. With diffuse Scleroderma, these areas of hardness are widespread and typically appear on both sides of the body. In the more limited form, skin thickening is often restricted to the hands and face. Eventually, tissue loss occurs and the skin becomes more highly colored.

People with limited Scleroderma usually have Raynaud’s symptoms for years (often 5 to 10 years) before other signs of Scleroderma are noted. However, even the limited form can, in rare cases, present with internal organ involvement without Raynaud’s. Patients with limited Scleroderma are less likely to develop severe lung, heart, or kidney involvement than patients with diffuse disease, although all of these complications can occur late in the disease process. Most patients with limited Scleroderma eventually develop CREST symptoms. CREST is an acronym for calcinosis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly and telangiectasia. Calcinosis is the abnormal accumulation of calcium salts under the skin and in many other organs. It presents as small, localized, hard masses on fingers, forearms, or other pressure points. Raynaud's Phenomenon is characterized by the intermittent loss of blood to various parts of the body particularly the fingers, toes, nose, and/or ears after exposure to cold and causes tingling sensations, numbness, and/or pain. This can result in ulceration of the fingertips and in some severe cases, lead to amputation of the affected digits. Dysfunction of the lower esophagus results in chronic heartburn and possible esophageal scarring. If the heartburn symptoms are not well controlled, the repeated acid exposure can eventually lead to a condition know as Barrett’s esophagus, a pre-cancerous condition. The esophagus may eventually have areas that are narrowed and swallowing may become difficult. The small intestine may also lose the ability to push food through to the large intestine leading to malabsorption and increased bacterial growth in the small intestine. Sclerodactyly, a condition in which the skin becomes thin, shiny, and bright, results in decreased function of the fingers and toes. Telangiectasia, the appearance of small blood vessels near the surface of the skin, usually on the face, hands, and in the mouth, is unsightly but not debilitating. Patients with CREST Syndrome are at increased risk of developing kidney failure and lung fibrosis leading to pulmonary hypertension, but these complications usually occur at a much later date than with diffuse Scleroderma.

With diffuse Scleroderma, there is usually a short interval (weeks or months) between the development of Raynaud’s and significant additional symptoms. Relatively rapid skin changes often occur in the first few months of the disease and continue to progress over the next 2 to 3 years. This is often followed by a remission of the skin changes and the skin either thins or sometimes returns toward normal thickness. The severe fibrosis of the skin, especially in the fingers and hands, can cause significant disability. Diffuse Scleroderma can also include a wide range of potential complications including inflammation of the muscles, swelling of the fingers and/or hands, microvascular abnormalities, gastrointestinal malfunction, lung fibrosis leading to pulmonary hypertension, progressive kidney failure, and cardiovascular problems. Internal organ involvement often occurs early in diffuse Scleroderma and can be the initial presenting symptom.

Raynaud’s Phenomenon

Raynaud’s phenomenon is characterized by cold hands and feet accompanied by color changes. Upon exposure to cold or emotional stress, the fingers and/or toes (sometimes the nose), lose circulation and turn white (blanch). Once the digits are re-warmed the blood flow returns, commonly 10 to 15 minutes later. The affected portion of the digits will often turn a bluish color or will appear mottled before returning to normal appearance.

Several studies have reported that between 4% and 15% of the general adult population, primarily women, have symptoms of Raynaud’s phenomenon. These symptoms are usually quite mild and are not associated with any underlying disease. This form of Raynaud’s is known as "primary Raynaud’s". It is also associated with a negative ANA. It often first appears at a much younger age than secondary Raynaud’s, often before the age of 20. When Raynaud’s attacks are intense or long lasting or first occur after the age of 20, there is an increased likelihood that the Raynaud’s is secondary to an underlying autoimmune disorder. Note that in addition to Scleroderma, Raynaud’s can be associated with a number of other disorders, for example, lupus, mixed connective tissue disorder, polymyositis, dermatomyositis, cold aggultinin disease, hypothyroidism, etc.

With secondary Raynaud’s there can also be enlargement of the blood vessels at the base of the fingernails, although this is not always the case.

Skin Changes

In the earliest stages of Scleroderma, the skin appears mildly inflamed with swelling and often redness. The skin gradually thickens (more rapidly in the diffuse form) and the patient feels progressive "tightening" of the skin with decreased flexibility. The skin changes are more widespread in the diffuse form and the skin can become "hyperpigmented", giving the skin a salt and pepper appearance.

As the skin changes progress, the skin becomes thicker and the skin can become severely dried with intense itching. This stage can progress for a long period, up to several years. Finally, the inflammation and further thickening stops as the skin begins to thin, although the skin will usually bind with underlying structures. Painful ulcerations can occur at joints.

With the limited form of the disease (CREST), calcium deposits may form under the skin. These can appear as white spots or ulcerations and may be quite painful. Spider veins (telangiectasia) often appear on the fingers, chest, face, lips, and tongue.

Musculoskeletal (Muscles and Joints)

Nonspecific muscle pain and stiffness are often some of the earliest symptoms of Scleroderma. While arthritis can also occur, the pain and stiffness over the joints is greater than would normally be expected based on the degree of inflammation visible. Pain can also occur along tendons and into muscles of the arms and legs. This can occur with movement of the ankles, wrists, knees, or elbows. These symptoms are more common in the diffuse form of the disease.

Often, a grating sound can be heard as the inflamed tissues move over each other, particularly at and below the knees. With diffuse Scleroderma, the fingers, wrists, and elbows can become fixed in flexed positions because of the scarring of the skin. In the limited form, this is usually limited to the fingers.

In later stages of the disease, muscle loss and weakness is the main problem. In some cases, however, some of the symptoms may be caused by some of the drugs commonly used to treat Scleroderma, for example, D-penicillamine or steroids.

Pulmonary (Lungs)

Some reduction of lung functioning occurs in almost all cases of Scleroderma, both in the limited and diffuse forms. However, unless closely monitored, there can be no symptoms until later stages of the disease, at which point lung problems can become a major cause of death. The most common initial symptom is shortness of breath after exercise or other exertion. Later, a persistent non-productive cough can develop. Usually, there is no chest pain caused by the lung involvement, although chest pain can occur from other causes such as muscle pain or heartburn.

The first detectable symptom is usually impaired gas exchange, caused by progressive fibrosis of the lungs. With the diffuse form, lung fibrosis is the more common serious problem to develop, while with the limited form, isolated pulmonary hypertension is more common, although both conditions often co-exist with either form.

Pulmonary disease is best detected by a pulmonary function test (PFT) or by computerized axial tomography (CAT scan). Chest x-rays are usually normal during the early stages of lung involvement. In addition to reduced gas exchange, low lung volumes are also often detected upon testing. The most serious complications of lung disease are seen with pulmonary hypertension or a low gas exchange (less than 40% of normal).

While the course of lung involvement is highly variable, most patients have an early but limited decline in lung functioning and then either stabilize or improve. About one third of patients have a more severe progression for several years before stabilizing. While other lung problems can develop secondary to other complications, these are much less common. In addition, there is an increased risk of lung cancer with Scleroderma.

Gastrointestinal

Some of the most common symptoms of Scleroderma are various difficulties with the gastrointestinal tract. This occurs with both forms of the disease. Difficulty swallowing along with moderate to severe heartburn is common. If untreated or undertreated, this can lead to erosion of the esophagus resulting in bleeding, strictures with narrowing of the esophageal opening, and Barrett’s esophagus, a pre-cancerous condition. In addition to direct problems of the esophagus itself, delayed stomach emptying can aggravate heartburn as well as cause bloating, nausea, and vomiting.

Skin thickening on the face can lead to a small mouth opening, mouth dryness, and dental problems. This in turn can result in difficulties in chewing food, loss of teeth, and poor nutrition.

Gradual loss of small intestine functioning may initially occur with any symptoms, but it can also lead to partial obstruction of the intestines, resulting in abdominal pain and vomiting. The decrease in small bowel absorption can lead to cramping, diarrhea, weight loss, and in severe cases malnutrition.

Cardiac (Heart)

Cardiac involvement in Scleroderma can be quite variable, usually without many overt symptoms early in the disease process. In fact, overt clinical symptoms early in the course of the disease are a poor prognostic indication. Cardiac involvement tends to be more serious and more common in the diffuse form of Scleroderma. Abnormal findings, including irregular heart beats and conduction problems, are often present without any associated clinical symptoms, at least early in the course of the disease.

Renal (Kidney)

Kidney involvement is common in Scleroderma although there may no obvious clinical problems. Kidney problems tend to be more serious and more common in the diffuse form of the disease, although sudden increases in blood pressure which (if untreated) can result in kidney failure can occur early in the course of limited Scleroderma in a small percentage of cases. Approximately 80% of all major kidney problems occur within the first 4 to 5 years of the disease. For unknown reasons, serious kidney problems are more common in men and with patients with an older age of disease onset.

Other Symptoms

Recent studies have shown that about 50% of all Scleroderma patients develop moderate to major depression. However, in almost all cases the depression is responsive to treatment with medications commonly used to treat depression.

A significant number of Scleroderma patients also suffer from Sjögren’s syndrome. The primary symptoms are dry mouth and eyes. This can result in dental complications and the need to use lubricating eye drops to prevent eye problems.

Hypothyroidism (reduced function of the thyroid) has been reported because of either fibrosis of the thyroid or thyroid auto-immune disorder. Hypothyroidism causes many bodily functions to slow down. Some of the more common symptoms include: hoarse voice, slowed speech, eye and face puffiness, weight gain, cold intolerance, coarse, dry, sparse hair, dry skin and carpal tunnel syndrome.

Other symptoms that have been linked to Scleroderma include: severe chronic chilling even in the absence of hypothyroidism ,trigeminal neuralgia (sudden painful spasms in the lower portion of he face), sexual dysfunction (mostly male impotence), and liver damage.

Therapies: Standard

While there is no definitive treatment for Scleroderma, specific treatments can often relieve symptoms and improve functioning. Scleroderma patients should be under the care of a rheumatologist and may need the attention of other specialists to deal with specific symptoms. It is important to monitor blood pressure, blood counts, urinalysis, kidney, and lung function on a regular basis.

Raynaud’s Phenomenon

Raynaud's phenomenon is very common with Scleroderma. Prevention is very important - patients should dress warmly and limit outdoor activities in cold weather. If it is possible, it may make sense for patients in cold climates to move to a warmer climate! A number of medications can be prescribed to reduce Raynaud's symptoms, including calcium channel blockers such as nifedipine (Procardia). However, calcium channel blockers can reduce lower esophageal sphincter pressure and make heartburn symptoms worse. Ketanserin has also been shown to be effective. Some patients can be taught to control the temperature of their hands using biofeedback.

Intravenous Iloprost has been shown to be effective in treating Raynaud’s. However, this form of administration is not practical for general usage. Unfortunately, experimental results with an oral form of Iloprost have had mixed results.

Skin Changes

Many medications have been tried for reducing the skin thickening and delaying internal organ involvement. D-penicillamine appears to have some limited effectiveness in improving skin thickening, as well as improved 5-year survival rates. However, D-penicillamine can be quite toxic and patients receiving this treatment must be closely monitored. Steroids, for example, Prednisone, do not appear to effective in Scleroderma and are usually used only if arthritic symptoms develop.

Dryness of the skin may be reduced by frequent use of lubricating creams. Regular exercise can help to maintain flexibility of joints and pliability of skin. Fingertip ulcerations are often treated with local nitroglycerine paste or topical antibiotics; however, systemic antibiotics may be needed in some cases.

Musculoskeletal (Muscles and Joints)

Joint and tendon related pain is usually helped by nonsteroidal anti-inflammatory drugs (NSAIDS), but relief is usually more difficult to achieve than in other auto-immune disorders. In some cases, low-dose corticosteroids such as prednisone may be necessary to control musculoskeletal pain. Physical therapy with emphasis on range of motion and stretching is very important to retain as much joint movement as possible.

Pulmonary (Lungs)

Most patients with lung involvement have a mild, nonprogressive course that does not require treatment. When it occurs, lung fibrosis leasing to pulmonary hypertension is one of the major complications of Scleroderma. No medicines have proven effective in managing advanced lung fibrosis, although some success has been reported with the use of corticosteriods and cyclophosphamide. Pulmonary infections require prompt treatment with antibiotics. Supplemental oxygen may also be needed. With advanced lung fibrosis or pulmonary hypertension, the only option may be a single or double lung transplant, sometimes including a heart transplant if heart problems are severe.

Gastrointestinal

Chronic heartburn (reflux) is a common problem with Scleroderma. This can often be reduced by preventive measures such as elevation of the head of the bed, eating smaller meals more frequently, taking antacids, and avoiding eating late at night. Some foods such as alcohol, regular coffee or tea can increase heartburn and should be avoided. Foods such as chocolate or fats can reduce the pressure of the lower esophageal sphincter and should be avoided at night. If stronger measures are required, treatments of choice are drugs known as H2 blockers such as Tagamet or Pepcid. These work by reducing stomach acidity. Prilosec (omeprazole), which is significantly more effective at reducing stomach acidity may also be used. Drugs that increase the speed that the stomach empties, for example, Propulsid (cisapride) have also been shown to be beneficial. Surgical interventions may also be indicated in some cases to increase the pressure of the lower esophageal sphincter. This option has recently become more feasible because of new laparoscopic techniques that significantly reduce recovery time and reduce the risks associated with open surgery.

Bloating, diarrhea, weight loss, and malabsorption symptoms caused by bacterial overgrowth in the small intestine are usually successfully treated with broad-spectrum antibiotics such as ampicillin, tetracycline, Bactrim, metronidazole, or ciprofloxacin. The use of cisapride to increase the speed of food passage through the GI system can also be helpful.

Cardiac (Heart)

When abnormalities of the heart occur as a result of Scleroderma, the drugs nifedipine and dipyridamole may be administered. Nonsteroidal anti-inflammatory or corticosteroid drugs are typically used to treat the symptoms relating to the inflammation of the membranes of the heart (pericarditis). Generally, heart complications with Scleroderma patients are treated the same as for non-Scleroderma patients.

Renal (Kidney)

Since kidney failure can be life threatening, close monitoring of kidney function is necessary. Reduction in kidney function is often accompanied by high blood pressure. Current drugs of choice to treat kidney disease associated with Scleroderma are ACE inhibitors such as Captopril or enalapril. Other drugs to reduce blood pressure have also been used with some success. Sudden onset of high blood pressure and kidney failure is called 'Scleroderma renal crisis'. This occurs in about 20% of people with diffuse Scleroderma and can also occur with CREST. It can result in kidney failure within days to weeks. Anyone with diffuse Scleroderma should be measuring his/her own blood pressure at home every day or two. If it is elevated over a certain point (to be determined by your physician since it must be individualized) you should call your physician immediately. CREST patients should measure their blood pressure at least once a month.

Other Symptoms

Some Scleroderma patients suffer from excessive dryness of the mouth and eyes (Sjogren's Syndrome). Lubricating drops and ointments as well as artificial saliva products can relieve these symptoms. Good oral hygiene is important because gum disease is common in Scleroderma.

Scleroderma related depression seems to respond well to standard medical treatments using medications such as Prozac, Wellbutrin, Serzone, or Paxil.

Hypothyroidism is readily treated using by replacing the deficient thyroid hormone, using one of several oral medications. The preferred form is synthetic thyroid hormone, T4.

Therapies: Investigational/Alternative

A Note About Scleroderma Research

It is very difficult to do research on treatments for Scleroderma, as is the case with most rare disorders. The small number of patients means that it is difficult to locate enough patients in a single geographical area to do appropriate, well controlled research. This usually means that multi-center research is required, which is costly and difficult to coordinate.

An additional complication for doing Scleroderma research is the fact that Scleroderma appears to be a general term for a cluster of related diseases, as noted above. It is quite possible that some treatments may be effective for some forms of Scleroderma, but ineffective or less effective in other forms. And, since each subset of Scleroderma affects an even smaller population than the total Scleroderma patient population, research on subsets is even harder to do. Historically, most Scleroderma research performed over the past 20 years has not been done on specific disease subsets, but usually on a heterogeneous population which includes diffuse and limited Scleroderma patients, some of which are specific antibody positive while others are antibody negative. By mixing the patient population, results may appear to be negative overall, yet still might be positive for a subset of the patients. For example, since CREST (limited Scleroderma) generally progresses much more slowly than the diffuse form of the disease, it is quite conceivable that certain treatments which show limited results for diffuse patients may be more effective for CREST patients. Also, the slower progression means that it may take much longer to show positive results for experimental therapies than might be the case for the more rapidly progressing diffuse form. Unfortunately, little research has been done that takes this into consideration.

When considering investigational or alternative therapies, it is important to keep these limitations in mind. Since there are no generally accepted systemic treatments for Scleroderma (although specific treatments for various symptoms may be quite effective), some physicians may decide to try alternative or experimental treatment approaches on an individual basis even though there is no clear research support for these treatments. When positive results follow such treatments, it is very easy to believe that these treatments caused the improvements. In some cases this may be the case, however, it is important to realize that it is difficult to establish a cause an effect relationship between a treatment and a result with a single patient. In some cases it may be desirable to withdraw an experimental treatment from a patient to see if improved symptoms worsen. If this occurs and the symptoms again improve when the treatment is resumed, this makes it much more likely that the treatment may be causing the improvement. Nevertheless, without well controlled, double blind research, cause and effect cannot be clearly established.

Experimental Treatments

A number of experimental treatments are currently being evaluated for use in treating people with Scleroderma. More information about many of these experimental programs can be found by contacting the National Organization for Rare Disorders (NORD) (see Resource list below).

Researchers are evaluating the effects of recombinant gamma-interferon in individuals with Scleroderma. Interferon is a potential therapy for Scleroderma because of its inhibition of excessive synthesis of collagen, but side effects are common. Current research is mixed with some positive reports in the recent literature.
A treatment known as photopheresis (also called photochemotherapy) is under investigation for people with Scleroderma. During this procedure, blood in removed from the body (as in dialysis) and certain blood cells (monocytes) are "washed" with a drug (8- methoxypsoralen). The blood is then exposed to ultraviolet light (type A). It is hoped that this treatment might suppress collagen production and increase the levels of an enzyme that breaks down collagen (collagenase). Several studies have reported positive preliminary results but well controlled studies are still lacking.
Iloprost has been shown to be very effective in the treatment of Raynaud’s secondary to Scleroderma when given in IV form over a several day period with follow-up infusions done on a regular basis. However, this form of drug delivery is not practical except in severe cases of Raynaud’s. Experimental studies of an oral form of Iloprost have had mixed results.

There is also some indication that IV Iloprost can improve kidney blood flow. In addition, there are also some early reports that inhaling an aerosol form of Iloprost may be a potential treatment for certain lung problems associated with Scleroderma, including pulmonary hypertension.
Cyclosporin (Sandimmune) may be of potential benefit for treating Scleroderma, according to some uncontrolled studies. However, cyclosporine is toxic and reduces the function of the immune system, so it is generally recommended as a treatment only in the most severe cases of Scleroderma.
Scleroderma has been treated experimentally with the drug dimethyl sulfoxide (DMSO) as part of the Arthritis research program of the National Institute of Arthritis, Musculoskeletal and Skin Diseases. However, several studies have concluded that this is not an effective treatment.
Several studies have looked at the effects of methotrexate for the treatment of Scleroderma. When improvement was seen at all, it was largely confined to skin changes. A recent article concluded that Methotrexate may have about the same level of beneficial effects as recombinant gamma-interferon and Cyclosporin, but suggested that D-penicillamine might be a better choice for most patients.
Autologous stem cell transplants are now being tried in Europe for the treatment of Scleroderma and other autoimmune disorders. In this procedure, the patient’s immune system is essentially destroyed using powerful immuno-suppressive drugs. The patient then receives a transplant of his/her own previously saved hematopoietic stem cells. In essence, this procedure "restarts" the patient’s immune system. Although results are very early, it appears that the majority of Scleroderma patients treated with this approach have clinically improved or at least stabilized. In contrast with a stem cell transplant with an HLA matched individual (allogeneic), which has a transplant mortality rate of 15% to 35% in the first year, a transplant using the patient’s own stem cells (autologous) has a much better mortality rate (2% to 5% mortality in the first year).
Tissue calcification of the fingers (calcinosis), which occurs in both limited and diffuse Scleroderma, is a common problem that causes a great deal of pain and functional disability. Current treatments have been largely ineffective. One recent preliminary study evaluated the use of a carbon dioxide (CO2) laser for treatment digital calcifications. Outcomes were encouraging and suggest that this may be an effective treatment for this problem, although more studies are needed to replicate these results.
Alternative Treatments

A number of alternative treatments are also being used for treating Scleroderma. The effectiveness of these alternative approaches is based mostly on anecdotal reports, although research is underway for some of these alternative treatments.

There are several case reports indicating that Yohimbine Hydrochloride can be used as an alternative medicine for treating Raynaud's for Scleroderma patients with reflux (heartburn). A common treatment for Raynaud's is to use calcium channel blockers such as Procardia (nifedipine), however, these drugs often make the heartburn worse because they lower the lower esophageal sphincter pressure. Yohimbine does not have this side effect.
A number of case reports and research studies from Europe indicate that regular plasmapheresis treatments can be effective in treating patients with CREST, especially early in the course of the disease. Plasmapheresis is done by a continuous flow machine which removes blood from one arm, separates out the red and white blood cells by centrifuge, discards the plasma, remixes the red/white blood cells with new plasma or sterilized albumin, and returns the blood to the other arm.
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« Reply #8 on: June 28, 2006, 09:40:52 pm »

AUTOIMMUNE DISEASE IN WOMEN - THE FACTS



Autoimmune Disease

The term "autoimmune disease" refers to a varied group of more than 80 serious, chronic illnesses that involve almost every human organ system. It includes diseases of the nervous, gastrointestinal, and endocrine systems as well as skin and other connective tissues, eyes blood, and blood vessel. In all of these diseases, the underlying problem is similar--the body's immune system becomes misdirected, attacking the very organs it was designed to protect.

Table I
Female:Male Ratios
in Autoimmune Diseases
Hashimoto's disease/hypothyroiditis  50:1
Systemic lupus erythematosus  9:1 
Sjogren's syndrome  9:1 
Antiphospholipid syndrome  9:1 
Primary biliary cirrhosis  9:1 
Mixed connective tissue disease  8:1
Chronic active hepatitis  8:1
Graves' disease/hyperthyroiditis  7:1
Rheumatoid arthritis  4:1
Scleroderma  3:1
Myasthenia gravis  2:1
Multiple sclerosis  2:1
Chronic idiopathic thrombo-
cytopenic purpura 2:1



 A WOMEN'S ISSUE
For reasons we do not understand, about 75 percent of autoimmune diseases occur in women, most frequently during the childbearing years. Table I(left) lists the female-to-male ratios in autoimmune diseases. Hormones are thought to play a role, because some autoimmune illnesses occur more frequently after menopause, others suddenly improve during pregnancy, with flare-ups occurring after delivery, while still others will get worse during pregnancy.

Autoimmune diseases also seem to have a genetic component, but, mysteriously, they can cluster in families as different illnesses. For example, a mother may have lupus erythematosus; her daughter, diabetes; her grandmother, rheumatoid arthritis. Research is shedding light on genetic as well as hormonal and environmental risk factors that contribute to the causes of these diseases.

Individually, autoimmune diseases are not very common, with the exception of thyroid disease, diabetes, and systemic lupus erythematosus (SLE). However, taken as a whole, they represent the fourth-largest cause of disability among women in the United States.

A NEED FOR KNOWLEDGE
Autoimmune diseases remain among the most poorly understood and poorly recognized of any category of illnesses. Individual diseases range from the benign to the severe. Symptoms vary widely, notably from one illness to another, but even within the same disease. And because the diseases affect multiple body systems, their symptoms are often misleading, which hinders accurate diagnosis. To help women live longer, healthier lives, a better understanding of these diseases is needed, as well as providing early diagnosis and treatment.


MAJOR AUTOIMMUNE DISEASES ~ CONNECTIVE TISSUE DISEASES

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

An inflammation of the connective tissues, SLE can afflict every organ system. It is up to nine times more common in women than men and strikes black women three times as often as white women. The condition is aggravated by sunlight.

Symptoms: Fever, weight loss, hair loss, moth and nose sores, malaise, fatigue, seizures and symptoms of mental illness. Ninety percent of patients experience joint inflammation similar to rheumatoid arthritis. Fifty percent develop a classic "butterfly" rash on the nose and cheeks. Raynaud's phenomenon (extreme sensitivity to cold in the hands and feet) appears in about 20 percent of people with SLE.

Treatment: Anti-inflammatory drugs can help control arthritis symptoms; skin lesions may respond to topical treatment such as corticosteroid creams. Oral steroids, such as prednisone, are used for the systemic symptoms. Wearing protective clothing and sunscreen when outdoors is recommended.


RHEUMATOID ARTHRITIS
Rheumatoid arthritis is a systemic disorder in which immune cells attack and inflame the membrane around joints. It also can affect the heart, lungs, and eyes. Of the estimated 2.1 million Americans with rheumatoid arthritis, approximately 1.5 million (71 percent) are women.

Symptoms: Inflamed and/or deformed joints, loss of strength, swelling, pain.

Treatment: Rest and exercise; anti-inflammatory drugs when necessary.


SYSTEMIC SCLEROSIS (SCLERODERMA)
Scleroderma is an activations of immune cells which produces scar tissue in the skin, internal organs, and small blood vessels. It affects women three times more often than men overall, but increases to a rate 15 times greater for women during childbearing years, and appears to be more common among black women.

Symptoms: In most patients, the first symptoms are Raynaud's phenomenon and swelling and puffiness of the fingers or hands. Skin thickening follows a few months later. Other symptoms include skin ulcers on the fingers, joint stiffness in the hands, pain , sore throat, and diarrhea.

Treatment: The drug D-penicillamine has been shown to decrease skin thickening. Symptoms involving other organs such as the kidneys, esophagus, intestines, and blood vessels are treated individually.


SJÖGREN'S SYNDROME
Sjögren's syndrome (also called Sjögren's disease) is a chronic, slowly progressing inability to secrete saliva and tears. It can occur alone or with rheumatoid arthritis, scleroderma, or systemic lupus erythematosus. Nine out of 10 cases occur in women, most often at or around mid-life.

Symptoms: Dryness of the eyes and mouth, swollen neck glands, difficulty swallowing or talking, unusual tastes or smells, thirst, tongue ulcers, and severe dental caries.

Treatment: Interventions to keep the mouth and eyes moist include drinking a lot of fluids and using eye drops, as well as good oral hygiene and eye care.




NEUROMUSCULAR DISEASES


MULTIPLE SCLEROSIS (MS)

A disease of the central nervous system that usually first appears between the ages of 20 and 40, and affects women twice as often as men. MS is the leading cause of disability among young adults.

Symptoms: Numbness, weakness, tingling or paralysis in one or more limbs, impaired vision and eye pain, tremor, lack of coordination or unsteady gait and rapid involuntary eye movement. A history of at least two episodes of a cluster of symptoms is necessary for a diagnosis of MS. Because MS affects the central nervous system, symptoms may be misdiagnosed as mental illness.

Treatment: The drug baclofen is used to suppress muscle spasticity, and corticosteroids help reduce inflammation. Interferons also are being used to treat this disease.


MYASTHENIA GRAVIS
This is a chronic autoimmune disorder characterized by gradual muscle weakness, often appearing first in the face.

Symptoms: Drooping eyelids, double vision, and difficulty breathing, talking, chewing, and swallowing.

Treatment: The drug edrophonium along with daily rest periods can improve muscle strength.



GUILLAIN-BARRÉ SYNDROME
Guillain-Barré syndrome is an acute illness that causes severe nerve damage. Two-thirds of all cases occur after a viral infection.

Symptoms: Tingling in the fingers and toes, general muscle weakness, difficulty breathing, and, in severe cases, paralysis.

Treatment: Supportive care until the condition is stabilized, then rehabilitation therapy combined with whirlpool baths to relieve pain and facilitate retraining of movements. A process called plasmapheresis, which removes plasma and nerve-damaging antibodies from the blood, is used during the first few weeks after a severe attack and may improve the chance of a full recovery.




ENDOCRINE DISEASES



HASHIMOTO'S THYROIDITIS
Hashimoto's Thyroiditis is a type of autoimmune disease in which the immune system destroys the thyroid, the gland that helps set the rate of metabolism. It attacks women 50 times more often than men.

Symptoms: Low levels of thyroid hormone cause mental and physical slowing, greater sensitivity to cold, weight gain, coarsening of the skin, and goiter (a swelling of the neck due to an enlarged thyroid gland).

Treatment: Thyroid hormone replacement therapy.


GRAVES' DISEASE

Graves' disease is one of the most common autoimmune diseases, affecting 13 million people and targeting women seven times as often as men.. Patients with Graves' disease produce an excessive amount of thyroid hormone.

Symptoms: Weight loss due to increased energy expenditure; increased appetite, heart rate, and blood pressure; tremors, nervousness and sweating; frequent bowel movements.

Treatment: Antithyroid drug therapy or removal of the thyroid gland surgically or by radioiodine.


INSULIN-DEPENDENT (TYPE 1) DIABETES
Type 1 diabetes is caused by too little insulin production in the pancreas, and usually occurs in children and young adults, but it can occur at any age.

Symptoms: Increased thirst, increased urination, weight loss, fatigue, nausea, vomiting, frequent infections.

Treatment: Monitoring of diet and insulin.




GASTROINTESTINAL DISEASES

INFLAMMATORY BOWEL DISEASE
Inflammatory bowel disease describes two autoimmune disorder of the small intestine--Crohn's disease and ulcerative colitis.

Symptoms of Crohn's disease: Persistent diarrhea, abdominal pain, fever, and general fatigue.

Symptoms of ulcerative colitis: Bloody diarrhea, pain, urgent bowel movements, joint pains, and skin lesions.

In both diseases, there is a risk of significant weight loss and malnutrition.

Treatment: Antidiarrheal pills or bulk formers for mild cases. For more serious cases, anti-inflammatory drugs are effective. Corticosteroids are reserved for acute flare-ups of these diseases. In some cases, surgery may be required to remove obstructions or repair perforation of the colon.



OTHER AUTOIMMUNE DISEASES VASCULITIS SYNDROMES
This is a broad and heterogeneous group of diseases characterized by inflammation and damage to the blood vessels, thought to be brought on by an autoimmune response. Any type, size, and location of blood vessel may be involved. Vasculitis may occur alone or in combination with other diseases, and may be confined to one organ or involve several organ systems.


HEMATOLOGIC AUTOIMMUNE DISEASES
Blood also can be affected by autoimmune disorder. In autoimmune hemolytic anemia, red blood cells are prematurely destroyed by antibodies. Other autoimmune diseases of the blood include autoimmune thrombocytopenic purpura and autoimmune neutropenia.


AUTOIMMUNE SKIN DISEASES
The skin frequently gives the first sign that an autoimmune diseases is present. In many of the diseases mentioned, the skin is only peripherally involved, but in others, the skin is the primary site of the disease. One of the foremost is psoriasis, a common skin disease that results from a malfunction in the life cycle of skin cells. The process of skin cell production that normally takes about a month is speeded up to several days, resulting in a build-up of thick scales. [/color]
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« Reply #9 on: August 11, 2006, 05:24:55 am »

Autoimmune Disorders


Background
An autoimmune disease is perhaps one of the cruelest of all diseases.  The body's normal immune system loses its ability to recognize its own cells and attacks itself.  The result is a devastating disease process which spares no organ.  This group of diseases is sometimes referred to as collagen vascular diseases because the soft tissue supporting tissues and blood vessels are frequently attacked.

Anti-CCP
ANCA
Anti-Phospholipid Antibody Syndrome (Lupus Anticoagulant)
Autoimmune Progesterone Dermatitis
Churg-Strauss (Allergic Granulomatosis)
Eosinophilic Fasciitis
Dermatomyositis/Polymyositis
Goodpasture's Syndrome
Interstitial Granulomatous Dermatitis with Arthritis
Lupus Erythematosus (SLE, DLE, SCLE)
Mixed Connective Tissue Disease
Relapsing Polychondritis
Rheumatoid Arthritis
Sarcoidosis
Scleroderma
Sjogren's Syndrome
Skin Immunofluorescence
Vasculitis
It should be noted that this list is not complete and indeed, there are many diseases found in other body sites which are also autoimmune in nature.  A good example is pemphigus vulgaris, a devastating blistering disease of the skin and mucous membranes.  Vasculitis, or inflammation of the blood vessels, is also frequently autoimmune.  These latter diseases are found in the skin rash and blood vessel pages. 

Anti-nuclear antibodies are directed against nuclear antigens. They are one of the hallmarks of an autoimmune disease. They can be broadly grouped into four categories.
1. Antibodies to DNA
2. Antibodies to histone
3. Antibodies to nonhistone proteins bound to RNA
4. Antibodies to nucleolar antigens
These patterns are generated by employing an enzyme-linked immunoabsorbent assay (ELISA). The immunofluorescence ANA pattern is generated by the overlay of patient serum on a Hep2 cell or mouse epithelial cell-bearing glass slide. This pattern correlates with the antibody specificity and direct immunofluorescence findings in the skin biopsy material.

Five basic patterns are recognized in indirect immunofluorescence:
Pattern Ab Directed Against Associations
Homogeneous or diffuse nuclear stainingChromatin
Histones
Occasionally DS DNASLE
Drug induced SLE
Rim or peripheral stainingDS DNASLE
Fine Speckled nuclear pattern Non-DNA nuclear constituents (Extractable nuclear antigens-ENA):
Sm
Ku
U1RNP
Ro/SS-A
Ro/SS-BSCLE
Coarse Speckled nuclear patternAnti-centromereScleroderma
NucleolarNucleolar RNA Systemic sclerosis

Associations
AntigenAntibody SystemDisease % Positive
Native DNADS DNASLE 40-60%
HistonesAntihistoneDrug induced LE >95%
Core proteins of small nuclear ribonucleoprotein particles (Smith antigen) Anti-Sm SLE 20-30%
Ribonucleoprotein (U1RNP) Nuclear RNP WeakSLE in 30-40% RNP SS-A (Ro)SS-B (La) Sjogren Syndrome 70-90%
Ro/SSA antigen is a 60 kDa protein attached to small RNAs to produce a 100 kDa complex with nuclear localization in normal adult skin
If insult such as UV, viral infection, or altered cytosolic calcium milieu occurs, Ro/SSA particles manifest upregulated or displaced expression from the nucleus to the cytosol and from the cytosol to the cell surface

This may explain the photosensitivity or photoreproduceability of skin lesions in anti-Ro/SSA positive LE patients and the worsening of disease symptoms in connective tissue disease patients experiencing viral illness
DNA topoisomerase I ScI-70Systemic sclerosis 28-70%
Centromeric proteins AnticentromereCREST 90%
Histidyl-t-RNA synthetase Jo-1 Inflammatory myopathies 25%

Conditions Where ANA is intrinsic to the Diagnostic Criteria
Drug induced SLE 100%
Autoimmune hepatic disease 100%
Mixed connective tissue disease100%

Diseases where ANA is useful for monitoring or prognosis
Juvenile chronic oligoarticular arthritis with uveitis 20-50%
Raynaud phenomenon 20-60%

Diseases where ANA is not useful in diagnosis
Rheumatoid arthritis30-50%
Multiple sclerosis25%
Idiopathic thrombocytopenia purpura10-30%
Thyroid disease30-50%
Discoid lupus erythematosus5-25%
InfectionsVariable
MalignanciesVariable
Silicone breast implant patients15-25%
Fibromyalgia15-25%
Relatives of patients with autoimmune disorders5-25%

Normal Persons
Titers > than or = to Percentage
1:4020-30
1:8010-12
1:160 5
1:3203

OUTLINE
Reference Methods
Clinical Utility
Interfering Diseases or Substances that Alter Levels
Commonly Used Terms
Internet Links

REFERENCE METHODSCHARACTERIZATION
Variability between methods to determine ANA, anti-dsDNA and anti-ENA autoantibodies: a collaborative study with the biomedical industry.
Bizzaro N, Tozzoli R, Tonutti E, Piazza A, Manoni F, Ghirardello A, Bassetti D, Villalta D, Pradella M, Rizzotti P.
Laboratorio di Patologia Clinica, Ospedale Civile, S. Dona di Piave (VE), Italy. J Immunol Methods 1998 Oct 1;219(1-2):99-107 Abstract quote

This study was performed by the Italian Society of Laboratory Medicine (SIMeL) in order to establish the variability between the different analytical systems currently used in clinical laboratories for the detection of autoantibodies diagnostic of systemic autoimmune disease.
Sixteen industrial, and two university laboratories participated in this study which entailed the determination of anti-nuclear (ANA), anti-dsDNA and anti-ENA antibodies in 11 sera from patients with clinically diagnosed systemic rheumatic disease, using reagents produced by these companies and different methodologies (indirect immunofluorescence, immunoenzymatic assay, counterimmunolectrophoresis, immuno and western blotting). We found 93.5% agreement between the methods used for the detection of ANA, 85.2% for anti-dsDNA antibodies, and 86.9% for anti-ENA antibodies. Among the anti-ENA antibodies, regardless of the method used, detection percentages were excellent for anti-RNP and anti-SSB/La (100%), good for anti-SSA/Ro (93%), but unacceptable for the anti-Jo-1 (67%), anti-Scl70 and anti-Sm (47%) antibodies.

This further stresses the need for rigorous standardisation of commercial reagents and analytical procedures, as well as the introduction of external quality assessment (EQA) programs, and a complete definition of operative protocols adjusted to the sensitivity and specificity of the various methods.
Comparison of an enzyme immunoassay to an indirect fluorescent immunoassay for the detection of antinuclear antibodies.
Reisner BS, DiBlasi J, Goel N.
University of Texas Medical Branch, Galveston, USA. Am J Clin Pathol 1999 Apr;111(4):503-6 Abstract quote
The standard method for detecting antinuclear antibodies (ANAs) is by immunofluorescence assay (IFA), a method that is labor intensive and subjective. In an attempt to overcome these limitations, several commercial enzyme immunoassays (EIAs) have been developed.
We report the results of our evaluation of the ANA Microplate EIA (Sanofi Diagnostics Pasteur, Chaska, MN). For the evaluation, 808 serum samples were tested by EIA and IFA; 52 specimens were positive by both assays, 561 were negative by both assays, 91 were positive by EIA only, and 3 were positive by IFA only. Borderline results (not positive or negative) were obtained for 101 specimens, which were excluded when calculating the sensitivity, specificity, and positive and negative predictive values of this assay, which were 94.6%, 86.0%, 36.4%, and 99.5%, respectively.
Because of its high negative predictive value, this assay can be used reliably to detect ANA-negative samples; however, the low positive predictive value indicates that EIA-positive specimens should be retested by an IFA to determine the final result.
Guidelines for the Laboratory Use of Autoantibody Tests in the Diagnosis and Monitoring of Autoimmune Rheumatic Diseases
Renato Tozzoli, MD
Nicola Bizzaro, MD
Elio Tonutti, MD
Danilo Villalta, MD
Danila Bassetti, MD
Fabio Manoni, MD
Anna Piazza, MD
Marco Pradella, MD
and Paolo Rizzotti, MDAm J Clin Pathol 2002;117:316-324 Abstract quote
The Italian Society of Laboratory Medicine Study Group on the Diagnosis of Autoimmune Diseases has generated a series of guidelines for the laboratory diagnosis and monitoring of systemic autoimmune rheumatic diseases intended for the use of clinical pathologists and laboratory physicians.
These guidelines are based on a systematic review of published works and expert panel discussion and consist of 13 recommendations for antinuclear antibodies, anti–double-stranded native DNA, and antinuclear specific antibodies.
To improve analytic performances and help select the most appropriate test for specific autoantibodies, as well as provide education and guidance in the use of these tests, special emphasis is placed on laboratory methods.

CLINICAL UTILITYCHARACTERIZATION
EARLY ONSET OF ANTI-dsDNA
Development of anti-dsDNA autoantibodies prior to clinical diagnosis of systemic lupus erythematosus.
Arbuckle MR, James JA, Kohlhase KF, Rubertone MV, Dennis GJ, Harley JB.
Arthritis and Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA. Scand J Immunol 2001 Jul-Aug;54(1-2):211-9 Abstract quote
Anti-double stranded (dsDNA) antibodies are of considerable diagnostic value and are thought to be involved in the pathogenesis of systemic lupus erythematosus (SLE). Fluctuations in anti-dsDNA antibody levels are also used as markers for disease activity and exacerbations.
In this study we sought to evaluate the anti-dsDNA antibody level in serum samples collected before the onset of SLE diagnosis. A total of 130 SLE patients were identified with stored serum samples available prior to diagnosis within the US Department of Defense serum repository. All 633 sera available from these patients were screened for anti-dsDNA antibodies using an enzyme linked immunosorbant assay (ELISA). Within this cohort 55% of cases had detectable anti-dsDNA antibodies prior to SLE diagnosis. The onset of anti-dsDNA antibodies ranged from 9.3 years before to within the same month as diagnosis (with a mean onset 2.7 years before diagnosis).
In order to assess for fluctuations in anti-dsDNA levels relative to diagnosis, cases were selected with at least two positive samples, one within 6 months and a second greater than 6 months prior to diagnosis (n = 26). Seven of these cases also had samples available shortly after diagnosis (< or = 6 months) for comparison. Fifty-eight percent of the 26 cases developed a significant rise in anti-dsDNA antibody levels within 6 months of diagnosis. A significant decline in anti-dsDNA levels ensued after diagnosis (and following treatment with corticosteroids) in all seven cases with samples available. Patients with a significant rise in anti-dsDNA antibodies at diagnosis were more likely to have renal disease than those who did not (66.7% compared to 27.3%, chi2 =3.94, P<0.05).
These data suggest that anti-dsDNA antibodies are present in SLE patient sera much earlier than previously suspected. In addition, the data are consistent with increases in anti-dsDNA levels contributing to the onset of clinical illness in some patients with SLE.


INTERFERING DISEASES OR SUBSTANCES THAT ALTER LEVELSCHARACTERIZATION
GENERAL
Complete saturation of protamine sulphate by dsDNA is necessary in order to obtain a highly sensitive and specific anti-dsDNA ELISA.
Rupin A, de Jong W, Degenne D, Bardos P.
Laboratory of Immunology, Faculte de Medecine, Tours, France. J Immunol Methods 1993 Apr 2;160(2):245-52 Abstract quote
A protamine sulphate (PS) pretreated solid phase coated with different amounts of dsDNA has been used to develop a sensitive, specific and reproducible anti-dsDNA ELISA.
Using low concentrations of a dsDNA coat 50% of SLE sera were found to be positive and false positive reactivity due to anti-PS reactivity was found in 3/40 patients with other auto-immune diseases (OAID). In contrast, when PS was saturated with higher concentrations of dsDNA 80% of SLE sera were detected, the reproducibility of the results was better and anti-PS reactivity of OAID patients with an anti-PS reactivity disappeared. The sera of three other OAID patients contained low avidity anti-dsDNA, measured after a salt elution step in the ELISA procedure, and 2/60 patients with non-auto-immune disease exhibited a false positive anti-dsDNA reactivity since they reacted with the solid phase even in the absence of PS and dsDNA.
Thus an ELISA procedure using a PS pretreated solid phase permits the sensitive, specific and reproducible measurement of anti-dsDNA antibodies only if a high concentration of dsDNA is coated on the PS and appropriate controls are performed.
Differences in clinical sensitivity of ELISA tests for autoantibodies with human and bovine extractable nuclear antigens.
Kapogiannis B, Gussin HA, Teodorescu MR, Teodorescu M.
University of Illinois College of Medicine, Department of Pediatrics, Chicago 60612, USA.Lupus 2000;9(5):343-52 Abstract quote
Bovine antigens are routinely used in indirect ELISA tests to detect autoantibodies against extractable nuclear antigens (ENA).
Here we investigate the difference in clinical sensitivity between ELISA tests prepared with native human and bovine antigens. SSA and SSB were obtained from spleen and nRNP/Sm complex from thymus. Each antigen was extracted with the same immunoaffinity column. ELISA tests with human and bovine antigens were set up under the same conditions of clinical specificity established on 50 blood bank donors.
Of 109 random SLE and Sjogren's syndrome sera 49% and 35% were positive, respectively, for human and bovine SSA, 26% and 16% for SSB. Of 98 random SLE sera 52% and 41% were positive for human and bovine nRNP/Sm, respectively. A few specimens reacted only with bovine antigens, probably false positive reactions. The relative clinical sensitivity for all specimens identified as positive by human and/or bovine antigens was significantly higher with human than with bovine SSA, (93% vs 67%; P<0.001, chi2), SSB (93% vs 50%; P<0.001), and for nRNP/Sm (96% vs 75%; P<0.01). However, for values that exceeded 2.5-4 times the upper normal limit, the levels were similar for human and bovine antigens.
We concluded that native human antigens offer clinical sensitivity superior to native bovine antigens for the measurement of anti-ENA antibodies by ELISA.

AGE
Anti-double-stranded DNA antibodies in the healthy elderly: prevalence and characteristics.
Ruffatti A, Calligaro A, Del Ross T, Bertoli MT, Doria A, Rossi L, Todesco S.
Division of Rheumatology, University of Padova, Italy. J Clin Immunol 1990 Nov;10(6):300-3 Abstract quote
Using Crithidia luciliae fluorescent assay a significant prevalence (7.6%; P less than 0.006) of anti-double-stranded DNA antibodies was found in a healthy old population. A negative enzyme-linked immunosorbent assay for anti-total histone antibodies excluded a false-positive reaction.
Anti-double-stranded DNA antibodies in the aged differed from those found in patients with systemic lupus erythematosus and were characterized by a low titer (95.6% of cases), belonging to the IgA class alone (95.6%), no complement-fixing ability (100%), and negativity to Farr assay (100%).
It is concluded that, in elderly subjects without signs and symptoms of disease, including systemic lupus erythematosus, such a peculiar anti-double-stranded DNA antibody may be detected.

HIV INFECTION
Anti-nuclear, anti-neutrophil cytoplasmic and anti-glomerular basement membrane antibodies in HIV-infected individuals.
Savige JA, Chang L, Horn S, Crowe SM.
University Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australia. Autoimmunity 1994;18(3):205-11 Abstract quote
Many autoantibodies have been described in HIV-infected individuals.
We have examined the incidence, associations and prognostic significance of anti-nuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA) and anti-glomerular basement membrane (GBM) antibodies in individuals with HIV infections.
One hundred and five patients, with asymptomatic infections (n = 37), AIDS-related complex (n = 32) or AIDS (n = 36) were studied.
Plasma from 24 of these (23%) were positive for ANA: most demonstrated speckled fluorescence (n = 21) and were of low titre (1+ in 18). ANCA were demonstrated by IIF in 18 individuals (17%) and all fluorescent patterns were seen; 6 of these plasma were also positive in the ELISAs for antibodies to proteinase 3, myeloperoxidase or elastase. Thirteen plasma were positive for ANCA in the neutrophil cytoplasm ELISA; 10 of these were also positive in the specific ELISAs. A total of 30 plasma bound to proteinase 3, myeloperoxidase or elastase in specific ELISAs, in 6 cases with 2 specificities. Finally, 18 plasma (17%) contained anti-GBM antibodies by ELISA, but none of 4 plasma tested in inhibition assays was specific.
ANA, ANCA and anti-GBM antibodies were not uncommon in HIV-infected individuals but the presence of these antibodies was not associated with the clinical manifestations of the corresponding autoimmune diseases. In addition, there was no correlation between the demonstration of these antibodies and the immunological status of the individual (apart from a correlation between CD4 counts less than 400/microliters with anti-GBM antibodies), the presence of an opportunistic infection, the development of malignancy or reduced survival. Some of these antibodies may arise from polyclonal activation, or be due to "sticky" serum since we have shown that the presence of anti-GBM antibodies correlated with the demonstration of ANCA by ELISA. These antibodies are not more common in hypergammaglobulinemic plasma but some may be due to heat-treatment of the plasma.
The clinician caring for HIV-infected individuals needs to be aware of these "false-positive" antibody results.

LOW DENSITY LIPOPROTEINS
Specificity of the Crithidia luciliae method for detecting anti-DNA antibodies. Effect of absorption for lipoproteins.
Kumar V, Krasny S, Beutner EH. Immunol Invest 1985 Jun;14(3):199-210 Abstract quote
Using the immunofluorescent (IF) assay with Crithidia luciliae smears, anti-native (n) DNA antibodies were detected in the sera of 12 of 20 systemic lupus erythematosus (SLE) patients, in 1 of 6 mixed connective tissue disease cases, in 2 of 38 patients with systemic sclerosis but in none of the sera from 96 normal subjects. All anti-nDNA antibodies were associated with antinuclear antibodies (ANA). However, occasionally sera were encountered in routine screening which appear to be positive for anti-DNA antibodies but negative for ANA.
Studies of such sera indicate that this is a nonspecific reaction which can be abolished by treating sera with dextran sulfate or heparin. Treatment of SLE sera with these agents had no effect on their anti-nDNA antibody activity. Absorption of sera with Aerosil eliminated the false positive reactions with C. luciliae; however, this treatment also removed immunoglobulins, ANA and anti-nDNA antibodies.
Evidence is reviewed which points to a role of complexes of low density lipoprotein and IgG in the nonspecific binding reactions with C. luciliae which is seen as false positive reactions for anti-nDNA antibodies.

MALARIA, ACUTE INFECTION
Autoantibodies, immunoglobulins, complement and circulating immune complexes in acute malaria.
Jhaveri KN, Ghosh K, Mohanty D, Parmar BD, Surati RR, Camoens HM, Joshi SH, Iyer YS, Desai A, Badakere SS.
Government Medical College and New Civil Hospital, Surat, Gujarat, India. Natl Med J India 1997 Jan-Feb;10(1):5-7 Abstract quote

BACKGROUND: Malaria caused by Plasmodium vivax and Plasmodium falciparum is common in the Indian subcontinent. Studies conducted elsewhere have suggested that malarial infection causes intense immunostimulation. We screened patients with malarial infection for autoantibodies and measured the immunoglobulin, circulating immune complex and complement levels to determine the extent of immunological alterations in these patients.

METHODS: One hundred adults with acute malarial infection confirmed by examination of the peripheral blood smear and 25 age- and sex-matched controls were studied. An autoantibody screen and serum immunoglobulin complement (C3 and C4) and circulating immune complex levels were measured at the time of admission and 4 weeks after they became afebrile. A direct Coomb's test was also done.

RESULTS: Anti-ssDNA, anti-dsDNA and rheumatoid factor were positive at the time of admission in 51, 30 and 38 patients respectively. None of the controls were positive for these autoantibodies except for one who was positive for rheumatoid factor. The IgM, IgG and IgA levels were raised in 16, 25 and 36 patients respectively. Circulating immune complex levels were raised in 32 patients and complement C3 and C4 were low in 8 and 31 patients. Follow up studies at 4 weeks in 19 patients showed that the autoantibodies were negative. However, the immunoglobulin, C4 and circulating immune complex levels remained elevated. Six per cent of patients had a positive direct Coomb's test with reticulocytosis at the time of presentation.

CONCLUSION: Acute malarial infection can cause false-positive results for anti-ssDNA, anti-dsDNA and rheumatoid factor and may also cause a rise in the serum immunoglobulin, complement and circulating immune complex levels.

J Cutan Pathol 2001;28:1-23.
Henry JB. Clinical Diagnosis and Management by Laboratory Methods. Twentieth Edition. WB Saunders. 2001.
Rosai J. Ackerman's Surgical Pathology. Ninth Edition. Mosby 2004.
Sternberg S. Diagnostic Surgical Pathology. Fourth Edition. Lipincott Williams and Wilkins 2004.
Robbins Pathologic Basis of Disease. Seventh Edition. WB Saunders 2005.
DeMay RM. The Art and Science of Cytopathology. Volume 1 and 2. ASCP Press. 1996.
Weedon D. Weedon's Skin Pathology Second Edition. Churchill Livingstone. 2002
Fitzpatrick's Dermatology in General Medicine. 5th Edition. McGraw-Hill. 1999.
Weiss SW and Goldblum JR. Enzinger and Weiss's Soft Tissue Tumors. Fourth Edition. Mosby 2001.



Commonly Used Terms
HLA-Human Leukocyte Antigen.   These are a group of proteins present on the majority of cells.  They interact with the body's immune system, the T lymphocytes and involved in the induction and regulation of the system.  The antigens are involved in transplant rejection as well as processing and eventual elimination of foreign proteins.  Many diseases, including autoimmune disorders, are associated with these disease states.

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« Reply #10 on: August 11, 2006, 05:32:25 am »


Autoimmune Disorders

What is the immune system?
The immune system is the body's means of protection against germs and other "foreign" substances. The immune system is composed of two major parts. One component is the production of antibodies, proteins that attack "foreign" substances and cause them to be removed from the body; this is sometimes called the humoral immune system. The other component is composed of special blood cells, called T lymphocytes, that can attack "foreign" substances directly; this is sometimes called the cellular immune system. At birth, the only protection we have are antibodies that come to the baby from its mother before birth; antibodies and T lymphocytes become protective only after they are exposed to a "foreign" substance for the first time. This is the reason that we use vaccinations: to allow our immune system to recognize weakened or inactivated forms of bacteria and viruses that can cause disease, so that we will be protected if we actually come in contact with them.

Normally, the immune system recognizes that the tissues in the body are not "foreign" and does not attack them. If a transplant is performed, however, the immune system usually recognizes that the organs that are transplanted are different and attacks them, a process called rejection.

 Drugs that reduce the activity of the immune system (immunosuppressants) are typically given to persons who have received transplants, unless the donor is an identical twin. Cancer cells are sometimes different enough from normal cells that the immune system attacks them, but the immune response alone is usually not enough to keep a cancer from spreading.

What are autoimmune disorders?
Autoimmune disorders are diseases caused by the body producing an immune response against its own tissues. The cause of autoimmune diseases is unknown, but it appears that there is an inherited predisposition to develop autoimmune disease in many cases.
In a few types of autoimmune disease (such as rheumatic fever), a bacteria or virus triggers an immune response, and the antibodies or T-cells attack normal cells because they have some part of their structure that resembles a part of the structure of the infecting germ.

Autoimmune disorders fall into two general types: those that damage many organs (systemic autoimmune diseases), and those where only a single organ or tissue is directly damaged by the autoimmune process (localized). The effect of localized autoimmune disorders, however, can be systemic as they frequently have an indirect effect other body organs and system

Some of the most common types of autoimmune disorders include:
Systemic Autoimmune Diseases
Localized Autoimmune Diseases
Rheumatoid arthritis (joints; less commonly lung, skin)
Type 1 Diabetes Mellitus (pancreas islets)
Lupus [Systemic Lupus Erythematosus] (skin, joints, kidneys, heart, brain, red blood cells, other)
Hashimoto's thyroiditis,
Graves' disease (thyroid)
Scleroderma (skin, intestine, less commonly lung)
Celiac disease, Crohn's disease, Ulcerative colitis (GI tract)
Sjogren's syndrome (salivary glands, tear glands, joints)
Multiple sclerosis*,
Guillain-Barre syndrome (central nervous system)
Goodpasture's syndrome (lungs, kidneys)
Adisease (adrenal)

Wegener's granulomatosis (sinuses, lungs, kidneys)
Primary biliary sclerosis,
Sclerosing cholangitis,
Autoimmune hepatitis (liver)
Polymyalgia Rheumatica (large muscle groups)Raynaud’s phenomenon (fingers, toes, nose, ears)
Temporal Arteritis / Giant Cell Arteritis (arteries of the head and neck)

* There is still some debate as to whether MS is an autoimmune disease


In some cases, a person may have more than one autoimmune disease; for example, persons with Addison's disease often have type 1 diabetes, while persons with sclerosing cholangitis often have either ulcerative colitis or Crohn's disease.
In some cases, the antibodies may not be directed at a specific tissue ororgan; for example, antiphospholipid antibodies can react with clotting proteins in the blood, leading to formation of blood clots within the blood vessels (thrombosis).




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« Reply #11 on: September 19, 2006, 09:04:55 am »

In an autoimmune disorder, antibodies or cells produced by the body attack the body's own tissues ...Many autoimmune disorders affect connective tissue in a variety of organs. Connective tissue is the structural tissue that gives strength to joints, tendons, ligaments, and blood vessels

In autoimmune disorders, inflammation and the immune response may result in connective tissue damage, not only in and around joints but also in other tissues, including vital organs, such as the kidneys and brain.

 The sac that surrounds the heart (pericardium), the membrane that covers the lungs (pleura), and even the brain can be affected. The type and severity of symptoms depend on which organs are affected.

An autoimmune disorder of connective tissue is diagnosed on the basis of its particular symptom pattern, the findings during a physical examination, and the results of laboratory tests.

 Sometimes the symptoms of one disease overlap with those of another so much that doctors cannot make a distinction; in this case, the disorder may be called undifferentiated connective tissue disease or overlap disease.

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« Reply #12 on: October 09, 2006, 06:00:34 pm »

Breakthrough in Autoimmune Disease Research
Stem Cell Research Gives New Hope to Patients

April 10, 2006— - Before seeking out Dr. Richard Burt of Northwestern Memorial Hospital, Kathy Hammons could barely care for her children as a result of the effects of lupus, an autoimmune disease in which the body attacks itself.

She had been on oxygen for two years, was constantly fatigued, and was overweight from the steroids used to control her disease.

"I would say before this option, they [lupus patients] hit a brick wall," Burt said. "They had nothing more, no further treatments."

Burt's pioneering research, however, offered a new option. His breakthrough procedure uses a patient's stem cells to treat extremely severe cases of lupus and other autoimmune diseases.

"We bring the patient in, and we give them chemo to destroy their immune system," Burt said. "And then right after the chemotherapy, we infuse the stems cells to make a brand-new immune system."

Since undergoing Burt's stem cell procedure, Hammons' lupus has been in remission. She's off the oxygen, and she's lost 120 pounds.

"The thing I enjoy most is just being a mom again," Hammons said. "It's the best."

Hammons was part of Burt's initial stem cell transplant study conducted on 50 lupus patients. After five years, half are disease-free. Now, his work is giving hope to those suffering from other autoimmune diseases.

One of those people is Bethany Pappalardo.

A little more than a year ago, Pappalardo could not walk around the block and had no idea whether she would be able to get out of bed on any given morning.

"I woke up one morning, and my legs were numb," Pappalardo said. "By the end of the day, I was numb from the neck down."


Pappalardo was diagnosed with multiple sclerosis when she was 18 years old, and, like most MS sufferers, her symptoms manifested at any time.


"The most frustrating thing for me was I was in my freshman year in college," Pappalardo said. "I was away from home, and I had to learn to give myself injections."

Last year, Pappalardo contacted Burt.

"I thought maybe this can be different," Pappalardo said. "Maybe this can go away. Maybe I can be a typical 25-year-old."

She underwent the stem cell treatment and said the most difficult part was losing her hair. The results so far have made it worth it.

"Since the procedure, she's had not only no more attacks but she had marked improvements and she's functioning normally," Burt said.

Burt's treatment could prove to be the first effective new treatment for lupus and other autoimmune diseases in nearly 40 years.

"I never use the word 'cure,' I say it's promising," Burt said. "If I use the word 'cure,' God will humble me."

From GMA interview
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« Reply #13 on: November 10, 2006, 10:00:40 am »

Autoimmune Hepatitis


   Autoimmune hepatitis is a disease in which the body's immune system attacks liver cells. This causes the liver to become inflamed (hepatitis). Researchers think a genetic factor may predispose some people to autoimmune diseases. About 70 percent of those with autoimmune hepatitis are women, most between the ages of 15 and 40.

The disease is usually quite serious and, if not treated, gets worse over time. It's usually chronic, meaning it can last for years, and can lead to cirrhosis (scarring and hardening) of the liver and eventually liver failure.

Autoimmune hepatitis is classified as either type I or II. Type I is the most common form in North America. It occurs at any age and is more common among women than men. About half of those with type I have other autoimmune disorders, such as type 1 diabetes, proliferative glomerulonephritis, thyroiditis, Graves' disease, Sjögren's syndrome, autoimmune anemia, and ulcerative colitis. Type II autoimmune hepatitis is less common, typically affecting girls ages 2 to 14, although adults can have it too.



Autoimmune Disease
One job of the immune system is to protect the body from viruses, bacteria, and other living organisms. Usually, the immune system does not react against the body's own cells. However, sometimes it mistakenly attacks the cells it is supposed to protect. This response is called autoimmunity. Researchers speculate that certain bacteria, viruses, toxins, and drugs trigger an autoimmune response in people who are genetically susceptible to developing an autoimmune disorder.



Symptoms
Fatigue is probably the most common symptom of autoimmune hepatitis. Other symptoms include

enlarged liver


jaundice


itching


skin rashes


joint pain


abdominal discomfort


fatigue
 spider angiomas (abnormal blood vessels) on the skin


nausea


vomiting


loss of appetite


dark urine


pale or gray colored stools
 

People in advanced stages of the disease are more likely to have symptoms such as fluid in the abdomen (ascites) or mental confusion. Women may stop having menstrual periods.

Symptoms of autoimmune hepatitis range from mild to severe. Because severe viral hepatitis or hepatitis caused by a drug—for example, certain antibiotics—has the same symptoms, tests may be needed for an exact diagnosis. Your doctor should also review and rule out all your medicines before diagnosing autoimmune hepatitis.



Diagnosis
Your doctor will make a diagnosis based on your symptoms, blood tests, and liver biopsy.

Blood tests. A routine blood test for liver enzymes can help reveal a pattern typical of hepatitis, but further tests, especially for autoantibodies, are needed to diagnose autoimmune hepatitis. Antibodies are proteins made by the immune system to fight off bacteria and viruses. In autoimmune hepatitis, the immune system makes antinuclear antibodies (ANA), antibodies against smooth muscle cells (SMA), or liver and kidney microsomes (anti-LKM). The pattern and level of these antibodies help define the type of autoimmune hepatitis (type I or type II).

Blood tests also help distinguish autoimmune hepatitis from viral hepatitis (such as hepatitis B or C) or a metabolic disease (such as Wilson's disease).


Liver biopsy. A tiny sample of your liver tissue, examined under a microscope, can help your doctor accurately diagnose autoimmune hepatitis and tell how serious it is. You will go to a hospital or outpatient surgical facility for this procedure.


Treatment
Treatment works best when autoimmune hepatitis is diagnosed early. With proper treatment, autoimmune hepatitis can usually be controlled. In fact, recent studies show that sustained response to treatment not only stops the disease from getting worse, but also may actually reverse some of the damage.

The primary treatment is medicine to suppress (slow down) an overactive immune system.

Both types of autoimmune hepatitis are treated with daily doses of a corticosteroid called prednisone. Your doctor may start you on a high dose (20 to 60 mg per day) and lower the dose to 5 to 15 mg/day as the disease is controlled. The goal is to find the lowest possible dose that will control your disease.

Another medicine, azathioprine (Imuran) is also used to treat autoimmune hepatitis. Like prednisone, azathioprine suppresses the immune system, but in a different way. It helps lower the dose of prednisone needed, thereby reducing its side effects. Your doctor may prescribe azathioprine, in addition to prednisone, once your disease is under control.

Most people will need to take prednisone, with or without azathioprine, for years. Some people take it for life. Corticosteroids may slow down the disease, but everyone is different. In about one out of every three people, treatment can eventually be stopped. After stopping, it is important to carefully monitor your condition and promptly report any new symptoms to your doctor because the disease may return and be even more severe, especially during the first few months after stopping treatment.

In about 7 out of 10 people, the disease goes into remission, with a lessening of severity of symptoms, within 2 years of starting treatment. A portion of persons with a remission will see the disease return within 3 years, so treatment may be necessary on and off for years, if not for life.



Side Effects
Both prednisone and azathioprine have side effects. Because high doses of prednisone are needed to control autoimmune hepatitis, managing side effects is very important. However, most side effects appear only after a long period of time.

Some possible side effects of prednisone are

weight gain


anxiety and confusion


thinning of the bones (osteoporosis)


thinning of the hair and skin


diabetes


high blood pressure


cataracts


glaucoma
Azathioprine can lower your white blood cell count and sometimes causes nausea and poor appetite. Rare side effects are allergic reaction, liver damage, and pancreatitis (inflammation of the pancreas gland with severe stomach pain).



Other Treatments
People who do not respond to standard immune therapy or who have severe side effects may benefit from other immunosuppressive agents like mycophenylate mofetil, cyclosporine or tacrolimus. People who progress to end stage liver disease (liver failure) and/or cirrhosis may need a liver transplant. Transplantation has a 1-year survival rate of 90 percent and a 5-year survival rate of 70 to 80 percent.



Hope Through Research
Scientists are studying various aspects of autoimmune hepatitis to find out who gets it and why and to discover better ways to treat it. Basic research on the immune system will expand knowledge of autoimmune diseases in general. Epidemiologic research will help doctors understand what triggers autoimmune hepatitis in some people. Research on different steroids, alternatives to steroids, and other immunosuppressants will eventually lead to more effective treatments.



Points to Remember
Autoimmune hepatitis is a long-term disease in which your body's immune system attacks liver cells.


The disease is diagnosed using various blood tests and a liver biopsy.


With proper treatment, autoimmune hepatitis can usually be controlled. The main treatment is medicine that suppresses the body's overactive immune system.


For More Information

American Liver Foundation (ALF)
75 Maiden Lane, Suite 603
New York, NY 10038–4810
Phone: 1–800–GO–LIVER (465–4837),
1–888–4HEP–USA (443–7872),
or 212–668–1000
Fax: 212–483–8179
Email: info@liverfoundation.org
Internet: www.liverfoundation.org

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« Reply #14 on: November 13, 2006, 08:44:34 am »

Autoimmune Diseases
Facts
Approximately 75% of those affected with an autoimmune disease are woman.
Autoimmune diseases are not contagious.
It is estimated that one in every 5 people are affected by some form of an autoimmune disease.
Because all autoimmune diseases have the same root cause, it is common to have symptoms from more than then just one disease.
It is often hard to diagnose autoimmune diseases.
Autoimmunity and autoimmune diseases were finally accepted by most doctors in the 1950s and 1960s.


~What Is An Autoimmune Disease?
The term "autoimmune disease" refers to a varied group of more than 80 serious, chronic illnesses that involve almost every human organ system. The human immune system is designed to protect our bodies from invading organisms such as bacteria, viruses, fungi, and parasites. However, in all autoimmune diseases, the underlying problem is similar--the body's immune system becomes misdirected and unbalanced, attacking the very organs it was designed to protect.

The systems in the body which are most often affected by an autoimmune disease are: blood, digestive tract, eyes, glands, heart, joints, kidneys, lungs, muscles, nerves, brain and skin. Autoimmune diseases can also affect connective tissue. (This is the tissue which binds together various tissues and organs.)



~How Are Autoimmune Diseases Diagnosed?
Autoimmune diseases often don't show a clear pattern of symptoms at first. So diagnosing them can be hard. But with time, a diagnosis can usually be made by using:

Medical history What type of symptoms there are and how long someone has had them. A family history of any autoimmune disease makes someone more likely to have one.

Physical exam During an exam, the doctor checks for any signs. Inflamed joints, swollen lymph nodes, or discolored skin might give clues.

Medical tests No one test will show that you have an autoimmune disease. But doctors may find clues in a blood sample. For example, people with lupus or rheumatoid arthritis often have certain autoantibodies in their blood. Autoantibodies are blood proteins formed against the body's own parts.

Not all people with these diseases have these autoantibodies. And some people without autoimmune disease do have them. So blood tests alone may not always help. But if a person has disease symptoms and autoantibodies, the doctor can be more sure of a diagnosis.



~What Types of Doctors Treat Autoimmune Diseases?
Treatments for autoimmune diseases vary. So do the types of doctors who provide them.

For some people, one doctor will be enough to manage their disease. Others may require a team approach. One doctor might coordinate and give care, and others would treat specific organ problems. For example, a person with lupus might be seen by a rheumatologist. But that person might also see a nephrologist for related kidney problems and a dermatologist for skin problems.

Specialists you may need to see include:

A rheumatologist, who treats arthritis and other rheumatic diseases. These include scleroderma and systemic lupus erythematosus (lupus or SLE).

An endocrinologist, who treats gland and hormone problems. These include diabetes and thyroid disease.

A neurologist, who treats nerve problems. These include multiple sclerosis and myasthenia gravis.

A hematologist, who treats diseases that affect the blood. These include pernicious anemia and autoimmune hemolytic anemia.

A gastroenterologist, who treats problems with the digestive system. These include Crohn's disease and ulcerative colitis.

A dermatologist, who treats problems of the skin, hair, and nails. These include psoriasis, pemphigus/pemphigoid, alopecia areata and discoid lupus.

A nephrologist, who treats kidney problems. These include glomerulonephritis, inflamed kidneys associated with lupus.



~Glossary of Diseases

Here are brief descriptions of some of the many diseases in which autoimmunity may be involved.
Note: Because the specific causes of many diseases are unknown, there is debate among scientists about whether some of these are truly autoimmune diseases.

Alopecia areata--A disorder in which the immune system attacks the hair follicles, causing loss of hair on the scalp, face, and other parts of the body.

Ankylosing spondylitis--A rheumatic disease that causes inflamed joints in the spine and sacroiliac (the joints that connect the spine and the pelvis) and, in some people, inflamed eyes and heart valves.

Arthritis--A general term for more than 100 different diseases that affect the joints. Many forms of arthritis and related conditions are believed to have an autoimmune component.

Autoimmune hemolytic anemia--A condition in which immune system proteins attack the red blood cells, resulting in fewer of these oxygen-transporting cells.

Autoimmune hepatitis--A disease in which the body's immune system attacks liver cells, causing inflammation. If not stopped, inflammation can lead to cirrhosis (scarring and hardening) of the liver and eventually liver failure.

Behçet's disease--A condition characterized by sores in the mouth and on the genitals and by inflammation in parts of the eye. In some people, the disease also results in inflammation of the joints, digestive tract, brain, and spinal cord.

Celiacs disease--When individuals with CD ingest gluten, the villi, tiny hair-like projections in the small intestine that absorb nutrients from food are damaged. This is due to an immunological reaction to gluten. Damaged villi interferes with the body's ability to absorb basic nutrients -- proteins, carbohydrates, fats, vitamins, minerals, and, in some cases, water and bile salts. If CD is left untreated, damage to the small bowel can be chronic and life threatening, causing an increased risk of associated disorders -- both nutritional and immune related.


Crohn's disease--An inflammatory disease of the small intestine or colon that causes diarrhea, cramps, and excessive weight loss.

Dermatomyositis--A rare autoimmune disease that causes patchy red rashes around the knuckles, eyes, and other parts of the body along with chronic inflammation of the muscles. It may occur along with other autoimmune diseases such as rheumatoid arthritis or systemic lupus erythematosus.

Diabetes mellitus, type 1--A condition in which the immune system destroys insulin-producing cells of the pancreas, making it impossible for the body to use glucose (blood sugar) for energy. Type 1 diabetes usually occurs in children and young adults.

Glomerulonephritis--Inflammation of the kidney's tiny filtering units, which in severe cases can lead to kidney failure.

Graves' disease--An autoimmune disease of the thyroid gland that results in the overproduction of thyroid hormone. This causes such symptoms as nervousness, heat intolerance, heart palpitations, and unexplained weight loss.

Guillain-Barré syndrome--A disorder in which the body's immune system attacks part of the nervous system, leading to numb, weak limbs and, in severe cases, paralysis.

Inflammatory bowel disease--The general name for diseases that cause inflammation in the intestine, the most common of which are ulcerative colitis and Crohn's disease.

Lupus nephritis--Damaging inflammation of the kidneys that can occur in people with lupus. If not controlled, it may lead to total kidney failure.

Multiple sclerosis--A disease in which the immune system attacks the protective coating called myeline around the nerves. The damage affects the brain and/or spinal cord and interferes with the nerve pathways, causing muscular weakness, loss of coordination, and visual and speech problems.

Myasthenia gravis--A disease in which the immune system attacks the nerves and muscles in the neck, causing weakness and problems with seeing, chewing, and/or talking.

Myocarditis--Inflamed and degenerating muscle tissue of the heart that can cause chest pain and shortness of breath. This can lead to congestive heart failure.

Pemphigus/pemphigoid--An autoimmune disease of the skin characterized by itching and blisters.

Pernicious anemia--A deficiency of the oxygen-carrying red blood cells that often occurs in people with autoimmune diseases of the thyroid gland.

Polyarteritis nodosa--An autoimmune disease that causes inflammation of the small and medium-sized arteries. This leads to problems in the muscles, joints, intestines, nerves, kidney, and skin.

Polymyositis--A rare autoimmune disease characterized by inflamed and tender muscles throughout the body, particularly those of the shoulder and hip girdles.

Primary biliary cirrhosis--A disease that slowly destroys the bile ducts in the liver. When the ducts are damaged, bile (a substance that helps digest fat) builds up in the liver and damages liver tissue.

Psoriasis--A chronic skin disease that occurs when cells in the outer layer of the skin reproduce faster than normal and pile up on the skin's surface. This results in scaling and inflammation. An estimated 10 to 30 percent of people with psoriasis develop an associated arthritis called psoriatic arthritis.

Rheumatic fever--A disease that can occur following untreated streptococcus (strep) infection. It most often affects children, causing painful, inflamed joints and, in some cases, permanent damage to heart valves.

Rheumatoid arthritis--A disease in which the immune system is believed to attack the linings of the joints. This results in joint pain, stiffness, swelling, and destruction.

Sarcoidosis--A disease characterized by granulomas (small growths of blood vessels, cells, and connective tissue) that can lead to problems in the skin, lungs, eyes, joints, and muscles.

Scleroderma--An autoimmune disease characterized by abnormal growth of connective tissue in the skin and blood vessels. In more severe forms, connective tissue can build up in the kidneys, lungs, heart, and gastrointestinal tract, leading in some cases to organ failure.

Sjögren's syndrome--A condition in which the immune system targets the body's moisture-producing glands, leading to dryness of the eyes, mouth, and other body tissues.

Systemic lupus erythematosus--An autoimmune disease, primarily of young women, that can affect many parts of the body, including the joints, skin, kidneys, heart, lungs, blood vessels, and brain.

Thyroiditis--An inflammation of the thyroid gland that causes the gland to become underactive. This results in symptoms such as fatigue, weakness, weight gain, cold intolerance, and muscle aches.

Ulcerative colitis--A disease that causes ulcers in the top layers of the lining of the large intestine. This leads to abdominal pain and diarrhea.

Uveitis--The inflammation of structures of the inner eye, including the iris (the colored tissue that holds the lens of the eye) and the choroid plexus (a network of blood vessels around the eyeball). Uveitis occurs with some rheumatic diseases, including ankylosing spondylitis and juvenile rheumatoid arthritis.

Vitiligo--A disorder in which the immune system destroys pigment-making cells called melanocytes. This results in white patches of skin on different parts of the body.

Wegener's granulomatosis--An autoimmune disease that damages the small and medium-sized blood vessels throughout the body, resulting in disease in the lungs, upper respiratory tract, and kidneys.
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« Reply #15 on: November 21, 2006, 09:00:48 am »

Autoimmune Diseases Threaten The Body's Natural Defense For Fighting Disease

Lupus can be difficult to identify and to treat.
Transcript of radio broadcast: 20 November 2006
 

http://128.11.143.113/mediaassets/specialenglish/2006_11/Audio/mp3/se-sin-lupus-autoimmune.mp3




VOICE ONE:

This is SCIENCE IN THE NEWS, in VOA Special English.  I’m Bob Doughty.

VOICE TWO:

And I’m Faith Lapidus.  On our program this week, we talk about a sickness called lupus and other autoimmune diseases.  Autoimmune diseases affect the immune system – the body’s natural defense for fighting disease.

(MUSIC)

VOICE ONE:

The immune system normally protects the body against foreign materials, such as viruses and bacteria.  Autoimmune diseases result from a failure of the body’s own defenses against disease.  The immune system loses its ability to tell the difference between foreign materials and its own cells.  So, the body starts attacking its own organs and tissues.

VOICE TWO:

 
The hands of of a lupus patient
There are three kinds of lupus.  Discoid lupus affects only the skin and can be identified by red marks on the face or neck.  These marks on the skin can also be a sign of another form of lupus called systemic lupus.  Systemic lupus can affect almost any organ or organ system in the body.  When people talk about lupus, they usually mean the systemic form of the disease.

Some kinds of medicines can cause what is called drug-induced lupus.  This form of lupus usually goes away when the patient stops using the medicines.

VOICE ONE:

High body temperature and pain in the elbows or knees are common signs of lupus.  Other signs are red marks on the skin, feelings of extreme tiredness and lack of iron in the body.

At different times, the effects of lupus can be either mild or serious.  The signs of the disease can come and go.  This makes identifying the disease difficult.  There is no one laboratory test to tell is someone has lupus.  Many people with lupus also suffer from depression.

Lupus can also lead to other health problems.  Women with lupus are at greater risk of developing heart disease.  And between thirty and fifty percent of lupus patients will develop lupus-related kidney disease, known as lupus nephritis.

(MUSIC)

VOICE TWO:

Experts are not sure what causes lupus.  Genetics or environmental influences seem to be involved.  Lupus has been known to attack members of the same family.  Yet, the genes responsible have yet to be identified.  Also, many women with lupus give birth to healthy babies.

Many scientists believe infections may cause lupus.  So can extreme bodily or mental tension, commonly known as stress.  Two other suspected causes are antibiotic drugs and hormones produced by the body.

In fact, hormones might explain why lupus affects women far more often then men.  The Lupus Foundation of America says ninety percent of the people with lupus are women.  Persons of African American, American Indian or Asian ancestry become infected more often than white women.

Scientists do not know why women are more at risk than men.  They think it might have to do with female hormones, like estrogen.  Another idea is that is could involve the foreign cells left in a woman’s body after a pregnancy.

VOICE ONE:

There is currently no cure for lupus.  Yet doctors have developed ways of treating the disease.  Treatments are based on the condition and needs of each patient.  No two individuals have the exact same problems.  A treatment could include a combination of stress-reduction methods and drugs such as painkillers and steroids.  Anti-malaria drugs also have been effective.  Recent research also suggests that supervised exercise training can improve the quality of life for lupus patients.

It has been forty years since the United States Food and Drug Administration approved a drug especially for treating lupus.  Several companies are working to make drugs that can help lupus patients.  Organizations like the Lupus Foundation of America are working to increase public understanding of the disease.  Early recognition of lupus and treatment can often prevent serious heath problems.

Lupus can be life threatening if left untreated.  Yet, many patients can lead a normal and healthy life if they follow their doctor’s advice.  Patients must take their medicines and keep looking for side effects or new signs of the disease.

(MUSIC)

VOICE TWO:

Lupus is not the only autoimmune disease.  Doctors and scientists have identified at least eighty other such diseases in which the body attacks its own organs and cells.  Some of the diseases attack just one area of the body, like the skin, eyes or muscles.  Others affect an organ system or even the whole body. 

Some of the diseases are well known, such as rheumatoid arthritis, multiple sclerosis and type-one diabetes.  Others are less well known and more difficult to identify.

For example, celiac disease is difficult to identify because the signs of the disease are so common.  Patients may have low iron levels and experience stomach pain.  The uncontrolled release of bodily wastes is also a problem. 

Doctors might treat those signs and not know they are caused by celiac disease.  Some people develop celiac disease after eating gluten, a protein found in all wheat products.  It is not always clear that eating something as harmless as wheat can be bad for a person’s health.  For some patients, it can be years before the problem is correctly identified.

VOICE ONE:

The United States National Institutes of Health says autoimmune diseases affect an estimated five to eight percent of the country’s population.  That represents between fourteen million and twenty-two million Americans.

The physical, emotional and financial cost of autoimmune diseases is huge.  Most of those affected are women.  While people of all ages are affected, women who are old enough to have children are especially at risk. 

Some autoimmune diseases like lupus and scleroderma are more common in African Americans.  Diseases such as multiple sclerosis and type-one diabetes are more common among whites.  Doctors do not yet know why this is true.

(MUSIC)

VOICE TWO:

New drugs are being tested to help treat autoimmune diseases.  Some drugs can be a problem because they suppress the immune system.  This means the body is less able to defend itself against infections.  As a result, the side effects of the drugs can be as dangerous as the disease itself.

Newer drugs attempt to suppress only one small part of the immune system, not all of it.  For example, drugs like Enbrel and Remicade block tumor necrosis factor.  This is a protein that causes inflammation, a physical reaction to infection, injury or other causes.  These drugs have been useful in treating autoimmune diseases like rheumatoid arthritis, psoriasis, and Crohn’s disease.  However, the drugs are very costly.  The drugs have also been found to increase the risk of cancer. 

VOICE ONE:

Scientists continue searching for other methods of treatment.  For example, some scientists hope to use stem cells to replace tissues damaged by disease.  Stem cells have the ability to grow other cells, such as heart, nerve or brain cells.

Medical experts also are working together to improve the way autoimmune diseases are identified and treated.  A few years ago, the Johns Hopkins Autoimmune Disease Research Center was formed in the American state of Maryland.  The aim of the center is to bring together experts to improve the study of autoimmune diseases.

Private groups like the center show how important it is for scientists to share information about such diseases.  Because each disease often affects different organs, many experts might be needed to treat the disorder.  Experts need to know about the most recent medical research and technology.  By sharing information about their patients, doctors also can learn from other cases.

VOICE TWO:

Government agencies also are working with to increase knowledge about autoimmune diseases.  In the United States, the National Institutes of Health created an autoimmune disease research plan three years ago.  The plan urges agencies from different areas to work together. 

Both private and government organizations are working to increase public understanding of such diseases.  This can help individuals better understand what to do should they develop a health problem.  At the same time, medical researchers continue working to help patients have a better quality of life.

(MUSIC)

 

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« Reply #16 on: November 24, 2006, 06:46:09 pm »

Novel Drug Boosts Platelet Production, Reversing Chronic Immune Thrombocytopenic Purpura

AMG 531 Appears Safe, Effective Against the Autoimmune Disease

NEW YORK, NY -- November 14, 2006 -- Attacking a platelet-depleting autoimmune disease in a whole new way, an experimental drug is helping patients with immune thrombocytopenic purpura (ITP) once again produce healthy amounts of platelets -- with no major side effects.

That's the conclusion of a new, multicenter study led by Dr. James B. Bussel, professor of pediatrics at Weill Cornell Medical College, attending pediatrician at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, and director of the Hospital's Program for Platelet Disorders.

His team's findings appear in The New England Journal of Medicine.

The new drug, a novel protein called AMG 531, successfully boosted platelet production in patents with chronic ITP, a serious autoimmune disorder that affects more than 16,000 adult Americans, and perhaps as many children, each year.

In ITP, immune system antibodies mysteriously begin to attack and destroy blood platelet cells. In some cases, the disease goes into spontaneous remission, but for many patients it remains a chronic condition. Impaired clotting leaves many patients, especially the elderly, vulnerable to serious or fatal hemorrhage.

Up till now, ITP patients have typically turned to powerful drugs such as corticosteroids or intravenous immune globulin, which work by inhibiting platelet destruction. These drug therapies can have limited success, but they also have serious side effects. For some ITP patients splenectomy (surgical removal of the spleen) is another treatment option.

AMG 531 fights ITP in a totally different way.

"Experts have long realized that ITP not only destroys platelets, it also inhibits platelet production in the marrow," explains Dr. Bussel.

In fact, prior work in the 1990s had focused on a type of recombinant thrombopoietin, called PEG-MGDF, that researchers hoped would stimulate platelet production.

The drug did have success. "However, Dr. David Kuter at Massachusetts General Hospital showed that some patients -- and even healthy volunteers -- developed antibodies to the drug, and these antibodies cross-reacted with their own natural thrombopoietin. The result was chronic low platelet counts in people who, in many cases, had never had such problems before," Dr. Bussel says.

The trick, then, was to find a platelet-stimulating agent that avoided this dangerous immune-system response.

"Luckily, Amgen, the company that has funded this research, didn't throw in the towel," Dr. Bussel says.

The company, under the guidance of the study's senior author, Dr. Janet Nichol, eventually developed AMG 531 -- a novel protein with no structural similarity to human thrombopoietin. This dissimilarity and other features mean AMG 531 is largely ignored by the immune system.

The new, two-phase trial was led by Dr. Bussel and conducted at nine centers across the United States.

In the Phase 1 part of the study, doctors first gave six groups of four ITP patients (24 total) two subcutaneous injections of AMG 531 delivered at least two weeks apart. Depending on the group they were in, patients received anywhere from 0.2 to 10 micrograms of the drug per kilogram of body weight.

In the Phase 2 part of the trial, 21 patients were randomized to receive six weekly injections of either a harmless placebo, or AMG 531 at doses of 1, 3, or 6 micrograms per kilogram of body weight.

The Phase 1 results showed the drug to be safe, with no major adverse events attributed to AMG 531 during the treatment period. Four of a total of 41 patients did show some temporary post-treatment lowering of their platelet counts, but this later resolved.

The drug's efficacy impressed the researchers.

"We were very pleased," says Dr. Bussel. Hoping to boost platelet counts to between 50,000 to 450,000 per cubic millimeter, the researchers report that seven of 12 patients given higher doses of AMG 531 (3, 6 or 10 micrograms/kilogram) fell within that range after six weeks on the therapy.

"In fact, three of these patients saw their counts rise to over 450,000 per cubic millimeter," Dr. Bussel notes.

Platelet counts increased in treated patients in a dose-dependent fashion, with mean peak counts of 163,000, 309,000 and 746,000 per cubic millimeter for doses of 3, 6 and 10 micrograms/kilogram, respectively.

"This was a relatively small trial, so more study is needed. However, the results point to a new, effective and safe way of letting people receive an injection once a week that stimulates them to increase their platelets," Dr. Bussel says.

How does AMG 531 work? According to the researchers, the drug acts much like natural thrombopoietin, stimulating the production of platelets from their earliest stages of development within the marrow, straight through to their appearance in the bloodstream.

Based on the findings, Dr. Bussel is optimistic that ITP patients everywhere will soon have a potent new weapon against the disease.

"Further clinical trials in AMG 531 are well under way," he says, "and the next step, we hope, will be to license the compound. Then, maybe, we can begin to broaden its use to other illnesses, where boosting platelets might help the many other patients with low platelets fight disease."

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« Reply #17 on: December 02, 2006, 02:01:11 pm »



Facing fatigue from an immune system disease such as lupus, multiple sclerosis (MS), or rheumatoid arthritis (RA)?

You're not alone. Fatigue is common with those conditions. But walking, biking, or other low-impact aerobic exercise may reduce your fatigue, Australian researchers report.

Jane Neill, Ph.D., R.N., and colleagues reviewed 11 studies on exercise and fatigue. Their review appears in the Journal of Advanced Nursing. The studies included more than 400 patients with lupus, MS, or RA. Those are autoimmune diseases, in which the immune system attacks the body instead of defending it.

Patients first got a thorough checkup to make sure they were healthy enough to exercise. The studies used various exercise programs for three months, on average. Patients typically worked out for 30 to 60 minutes, three times per week. Some patients took low-impact aerobics classes. Others walked, biked, or swam on their own.

In six studies, patients' fatigue improved to a degree that likely wasn't due to chance.

Inspired to give exercise a try for fatigue? You may want to consider these tips from the study:


Get your doctor's permission first.

Consider your preferences — would you rather exercise on your own at home or with others at a gym?

Start exercise early in the course of the disease or following disease flare.

Begin with low-intensity activities and avoid provoking symptoms.

Combine aerobic and resistance training where possible.

Gradually increase exercise intensity.

Exercise at least three times weekly for 15 to 30 minutes as tolerated.
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« Reply #18 on: December 06, 2006, 10:03:11 am »


Low Impact Aerobic Exercise Reduces Fatigue In Auto-immune Conditions Says Multi-study Review
Low impact aerobic exercise, such as walking and cycling, can effectively reduce fatigue in adults with chronic auto-immune conditions, according to a research review in the latest issue of the UK-based Journal of Advanced Nursing.


A team led by nurse researcher Dr Jane Neill from Flinders University in Adelaide, examined 162 research studies published between 1987 and 2006, analysing 36 in detail.

They discovered that there was evidence that people with conditions like multiple sclerosis, rheumatoid arthritis and systemic lupus erythematosus could benefit from exercise that gradually increased in intensity, duration and frequency.

"Fatigue is a major symptom in all three conditions and can cause a range of physical, psychological and social problems" says Dr Neill.

"Our review showed that aerobic exercise can significantly reduce fatigue and that some behavioural, nutritional and physiological interventions are also very effective."

Studies reviewed by the team tested 38 interventions on more than 1,700 patients. 24 resulted in statistically reduced fatigue or increased vitality levels.

The effective aerobic exercise programmes lasted an average of 12 weeks, with participants exercising for 30 to 60 minutes, three times a week.

Group interventions involved supervised exercise classes, including warm up, low impact aerobic activity and strengthening or stretching exercises before cool down.

Home-based programmes made use of exercise bicycles, walking, cycling, jogging or swimming.

"There is good evidence that people experiencing fatigue from chronic auto-immune conditions can benefit from a range of non-medicinal interventions" concludes Dr Neill.

"Other effective strategies, apart from aerobic exercise, include health education and cognitive behavioural therapy.

"Cooling techniques and nutritional supplements such as acetyl-L-carnitine and fish oil showed a number of benefits, but need to be looked at in more detail."

The authors suggest electro-magnetic field devices also warrant further investigation, due to promising results.

But they add that low-cost, low technology interventions that promote self-management of fatigue are probably more appropriate and feasible than those requiring specialised equipment or professional expertise.

They stress that any exercise programmes must be suitable for each individual and take account of issues that affect how people manage their conditions, like reduced mobility, pain, nausea and stress.

"Healthcare professionals should ask people about their fatigue and assess each person's symptoms" adds Dr Neill. "People with fatigue should be encouraged to design their own exercise routines based on awareness of their individual fatigue patterns and daily priorities, while group activities must take account of the changing nature of fatigue over time."

Previous research suggests that 70 per cent of people with multiple sclerosis suffer daily fatigue, 57 per cent of people with rheumatoid arthritis experience fatigue and 81 per cent of those with system lupus erythematosus find fatigue moderately to severely disabling.

"Any measures that can reduce people's fatigue and improve their quality of life are to be welcomed. Our review shows that some interventions have great potential, particularly in the short term, but that more research is needed to measure their long-term effectiveness" says Dr Neill.

Thank you Karyl, as always smiley
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« Reply #19 on: February 15, 2007, 12:56:06 pm »

Cracking Open The Black Box Of Autoimmune Disease
   

Autoimmune diseases such as type 1 diabetes, lupus and rheumatoid arthritis occur when the immune system fails to regulate itself. But researchers have not known precisely where the molecular breakdowns responsible for such failures occur. Now, a team of scientists from the Whitehead Institute and the Dana-Farber Cancer Institute have identified a key set of genes that lie at the core of autoimmune disease, findings that may help scientists develop new methods for manipulating immune system activity.

"This may shorten the path to new therapies for autoimmune disease," says Whitehead Member and MIT professor of biology Richard Young, senior author on the paper that will appear January 21 online in Nature. "With this new list of genes, we can now look for possible therapies with far greater precision."

The immune system is often described as a kind of military unit, a defense network that guards the body from invaders. Seen in this way, a group of white blood cells called T cells are the frontline soldiers of immune defense, engaging invading pathogens head on.

These T cells are commanded by a second group of cells called regulatory T cells. Regulatory T cells prevent biological "friendly fire" by ensuring that the T cells do not attack the body's own tissues. Failure of the regulatory T cells to control the frontline fighters leads to autoimmune disease.

Scientists previously discovered that regulatory T cells are themselves controlled by a master gene regulator called Foxp3. Master gene regulators bind to specific genes and control their level of activity, which in turn affects the behavior of cells. In fact, when Foxp3 stops functioning, the body can no longer produce working regulatory T cells.
When this happens, the frontline T cells damage multiple organs and cause symptoms of type 1 diabetes and Crohn's disease. However, until now, scientists have barely understood how Foxp3 controls regulatory T cells because they knew almost nothing about the actual genes under Foxp3's purview.

Researchers in Richard Young's Whitehead lab, working closely with immunologist Harald von Boehmer of the Dana-Farber Cancer Institute, used a DNA microarray technology developed by Young to scan the entire genome of T cells and locate the genes controlled by Foxp3. There were roughly 30 genes found to be directly controlled by Foxp3 and one, called Ptpn22, showed a particularly strong affinity.

"This relation was striking because Ptpn22 is strongly associated with type 1 diabetes, rheumatoid arthritis, lupus and Graves' disease, but the gene had not been previously linked to regulatory T-cell function," says Alexander Marson, a MD/PhD student in the Young lab and lead author on the paper. "Discovering this correlation was a big moment for us. It verified that we were on the right track for identifying autoimmune related genes."

The researchers still don't know exactly how Foxp3 enables regulatory T cells to prevent autoimmunity. But the list of the genes that Foxp3 targets provides an initial map of the circuitry of these cells, which is important for understanding how they control a healthy immune response.

"Autoimmune diseases take a tremendous toll on human health, but on a strictly molecular level, autoimmunity is a black box," says Young. "When we discover the molecular mechanisms that drive these conditions, we can migrate from treating symptoms to developing treatments for the disease itself."

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« Reply #20 on: June 02, 2007, 09:24:11 am »

High rates of autoimmune and endocrine disorders, fibromyalgia, chronic fatigue syndrome and atopic diseases
Open PDF file to read
*Thank you Holly (Weasellover)


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« Reply #21 on: June 06, 2007, 03:44:03 pm »

Antiphospholipid Syndrome


Antiphospholipid syndrome (APS) is characterized by the following:


venous or arterial thrombosis--a condition where clots, called thrombi, form in the blood vessels;

recurrent miscarriages--the repeated loss of the fetus in pregnancies; and

thrombocytopenia--a low number of blood platelets that can lead to bleeding, seen as bruising and tiny red dots on the skin.

Patients with APS also may experience symptoms of stroke such as transient ischemic attacks (TIAs).

APS is diagnosed based on the above clinical manifestations and on laboratory test results. A blood sample is analyzed for the presence of antibodies that react with naturally occurring proteins complexed (bound together) with phospholipids. These are called antiphospholipid antibodies or anticardiolipin antibodies (cardiolipin is one type of phospholipid used in lab tests). Sometimes these antibodies are called lupus anticoagulants when clotting assays (a testing method) are used for their detection.

The way in which these antibodies cause clinical problems is not well understood. Patients with APS may develop systemic lupus erythematosus, an autoimmune disorder (where antibodies fight against the body's own tissue); these patients should be followed periodically by a doctor who specializes in rheumatology. However, not all APS patients develop lupus. The tendency to have autoimmune disorders is inherited, but APS is not necessarily inherited. It is anticipated that continuing research will reveal more about the disease and lead to a greater understanding of all aspects of APS.

Treatment of APS is directed at the clinical manifestations of the disease. Warfarin and aspirin are anticoagulants used to treat thrombosis. Prompt treatment is necessary because thrombi can break away from the emboli (blood vessel walls) and travel to the lungs and lodge there. Frequent followup visits are needed to evaluate the effectiveness of these anticoagulants.

For pregnant patients, heparin and aspirin are usually used to prevent thrombosis and miscarriage. Corticosteroid therapy using prednisone, along with aspirin, is sometimes used instead of heparin. Heparin and aspirin also are recommended to treat patients undergoing surgery.


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« Reply #22 on: June 14, 2007, 09:28:37 am »


Autoimmune disorders

~Definition

Autoimmune disorders are conditions caused by an immune response against the body's own tissues.



~Causes, incidence, and risk factors

The immune system protects the body from potentially harmful substances (antigens) such as microorganisms, toxins , cancer cells, and foreign blood or tissues from another person or species. Antigens are destroyed by the immune response, which includes production of antibodies (molecules that attach to the antigen and make it more susceptible to destruction) and sensitized lymphocytes (specialized white blood cells that recognize and destroy particular antigens).

Immune system disorders occur when the immune response is inappropriate, excessive, or lacking. Autoimmune disorders develop when the immune system destroys normal body tissues. This is caused by a hypersensitivity reaction similar to allergies , where the immune system reacts to a substance that it normally would ignore. In allergies, the immune system reacts to an external substance that would normally be harmless. With autoimmune disorders, the immune system reacts to normal "self" body tissues.

Normally, the immune system is capable of differentiating "self" from "non-self" tissue. Some immune system cells (lymphocytes) become sensitized against "self" tissue cells, but these faulty lymphocytes are usually controlled (suppressed) by other lymphocytes. Autoimmune disorders occur when the normal control process is disrupted. They may also occur if normal body tissue is altered so that it is no longer recognized as "self." The mechanisms that cause disrupted control or tissue changes are not known. One theory holds that various microorganisms and drugs may trigger some of these changes, particularly in people with a genetic predisposition to an autoimmune disorder.

Autoimmune disorders result in destruction of one or more types of body tissues, abnormal growth of an organ, or changes in organ function. The disorder may affect only one organ or tissue type or may affect multiple organs and tissues. Organs and tissues commonly affected by autoimmune disorders include blood components such as red blood cells, blood vessels, connective tissues, endocrine glands such as the thyroid or pancreas, muscles, joints, and skin.

A person may experience more than one autoimmune disorder at the same time. Examples of autoimmune (or autoimmune-related) disorders include:

Hashimoto's thyroiditis
pernicious anemia
Addison's disease
type I diabetes
rheumatoid arthritis
systemic lupus erythematosus
dermatomyositis
Sjogren's syndrome
lupus erythematosus
multiple sclerosis
myasthenia gravis
Reiter's syndrome
Grave's disease
Celiac disease - sprue
~Symptoms

Symptoms of autoimmune disease vary widely depending on the type of disease. A group of very nonspecific symptoms often accompany autoimmune diseases especially of the collagen vascular type and include:

fatigue
dizziness
malaise (nonspecific feeling of not being well)
fever, low-grade temperature elevations
~Specific autoimmune disease results in:

destruction of an organ or tissue resulting in decreased functioning of an organ or tissue (for example, the islet cells of the pancreas are destroyed in diabetes )
increase in size of an organ or tissue (for example, thyroid enlargement in Grave's Disease)
Note: Symptoms vary with the specific disorder and the organ or tissue affected.

~Signs and tests

Signs vary according to the specific disorder. This disease may also alter the results of the following tests:

erythrocyte sedimentation rate (ESR)
C-reactive protein (CRP)
~Treatment

The goals of treatment are to reduce symptoms and control the autoimmune process while maintaining the ability to fight disease. The symptoms are treated according to the type and severity.

Hormones or other substances normally produced by the affected organ may need to be supplemented. This may include thyroid supplements, vitamins, insulin injections, or other supplements. Disorders that affect the blood components may require blood transfusions.

Measures to assist mobility or other functions may be needed for disorders that affect the bones, joints, or muscles.

Autoimmunity is controlled through balanced suppression of the immune system. The goal is to reduce?the immune response?against normal body tissue while leaving intact the immune response against micro-organisms and abnormal tissues. Corticosteroids and immunosuppressant medications (including cyclophosphamide or azathioprine) are used to reduce the immune response.




~Expectations (prognosis)

The outcome varies with the specific disorder. Most are chronic , but many can be controlled with treatment. Side effects of medications used to suppress the immune system can be severe.

~Complications

destruction or lack of function of body tissues
side effects of medications
~Calling your health care provider

Call your health care provider if illness or symptoms of any autoimmune disorder develop

~Prevention

Prevention may not be possible at this time for most autoimmune disorders.



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« Reply #23 on: June 24, 2007, 01:20:20 pm »

AutoImmunity
http://www.niams.nih.gov/hi/topics/autoimmune/autoimmunity.htm



~What Is AutoImmunity?

When your body is attacked—perhaps by a virus or germs on a nail you
stepped on—your immune system defends you. It sees and kills the germs
that might hurt you.

But when the system doesn’t work right, this process can cause harm.
Immune cells can mistake your body’s own cells as invaders and attack
them. This “friendly fire” can affect almost any part of the body. It
can sometimes affect many parts of the body at once. This is called
autoimmunity (meaning self-immunity).

~What Causes AutoImmunity?

No one knows why the immune system treats some body parts like germs. We
do know that you can’t catch autoimmune diseases from another person.

Most scientists think that our genes and things in the environment are
involved. If you have a certain gene or combination of genes, you may be
at higher risk for autoimmune disease. But you won’t get the disease
until something around you turns on your immune system. This may include
the sun, infections, drugs, or, in some women, pregnancy.

~What Kinds of Problems Are Caused by AutoImmunity?

AutoImmunity can affect almost any organ or body system. The exact
problems one has with autoimmunity (or its diseases) depends on which
tissues are targeted.

If the skin is the target, you may have skin rashes, blisters, or color
changes. If it’s the thyroid gland, you may be tired, gain weight, be
more sensitive to cold, and have muscle aches. If it’s the joints, you
may have joint pain, stiffness, and loss of function.

You may know which organ or system is affected from the start. But you
may not know the site of the attack. In many people, the first symptoms
are fatigue, muscle aches, and low fever.

~Where Does AutoImmunity Strike?

Because autoimmune diseases can affect almost any organ or system of the
body, one way to group them is by the body system(s) they attack. The
following is a list (not inclusive) of body systems and the autoimmune
diseases that can affect them.

~Blood and Blood Vessels

· AutoImmune Hemolytic Anemia

· Pernicious Anemia

· Polyarteritis Nodosa

· Systemic Lupus Erythematosus

· Wegener’s Granulomatosis

~Digestive Tract (including the mouth)

· Autoimmune Hepatitis

· Behçet’s Disease

· Crohn’s Disease

· Primary Bilary Cirrhosis

· Scleroderma

· Ulcerative Colitis

~Eyes

· Sjögren’s Syndrome

· Type 1 Diabetes Mellitus

· Uveitis

~Glands

· Graves’ Disease

· Thyroiditis

· Type 1 Diabetes Mellitus

~Heart

· MyoCarditis

· Rheumatic fever

· Scleroderma

· Systemic Lupus Erythematosus

~Joints

· Ankylosing Spondylitis

· Rheumatoid Arthritis

· Systemic Lupus Erythematosus

~Kidneys

· GlomeruloNephritis

· Systemic Lupus Erythematosus

· Type 1 Diabetes Mellitus

~Lungs

· Rheumatoid Arthritis

· Sarcoidosis

· Scleroderma

· Systemic Lupus Erythematosus

~Muscles

· Dermatomyositis

· Myasthenia Gravis

· Polymyositis

~Nerves and brain

· Guillain-Barré Syndrome

· Multiple Sclerosis

· Systemic Lupus Erythematosus

~Skin

· Alopecia Areata

· Pemphigus/Pemphigoid

· Psoriasis

· Scleroderma

· Systemic Lupus Erythematosus

· Vitiligo

~How Are Autoimmune Diseases Diagnosed?

AutoImmune Diseases often don’t show a clear pattern of symptoms at
first. So diagnosing them can be hard. But with time, a diagnosis can
usually be made by using:

· Medical History—The doctor will ask about your symptoms and how long
you have had them. Your symptoms may not point to one disease. But they
can be a starting point for your doctor. You should tell your doctor if
you have a family member with autoimmune disease. You may not have the
same disease as your family member. But having a family history of any
autoimmune disease makes you more likely to have one.

· Physical Exam—During the exam, the doctor will check for any signs.
Inflamed joints, swollen lymph nodes, or discolored skin might give clues.

· Medical Tests—No one test will show that you have an autoimmune
disease. But doctors may find clues in a blood sample. For example,
people with lupus or rheumatoid arthritis often have certain
autoantibodies in their blood. AutoAntibodies are blood proteins formed
against the body’s own parts.

Not all people with these diseases have these autoantibodies. And some
people without autoimmune disease do have them. So blood tests alone may
not always help. But if a person has disease symptoms and
autoantibodies, the doctor can be more sure of a diagnosis.

The key is patience. Your doctor may be able to diagnose your condition
quickly based on your history, exam, and test results. But the process
often takes time. It may take several visits to find out exactly what’s
wrong and the best way to treat it.

~How Are Autoimmune Diseases Treated?

Autoimmunity takes many forms. There are also many treatments for it.
Treatment depends on the type of disease, how severe it is, and its
symptoms. Generally, treatments have one of three goals:

· Relieving Symptoms—If your symptoms bother you, your doctor may
suggest treatments that give some relief. Relieving symptoms may be as
simple as taking a drug for pain relief. It may also be as involved as
having surgery.

· Preserving Organ Function—When autoimmune diseases threaten organs,
treatment may be needed to prevent damage. Such treatments may include
drugs to control an inflamed kidney in people with lupus. Insulin
injections can regulate blood sugar in people with diabetes. These
treatments don’t stop the disease. But they can save organ function.
They can also help people live with disease complications.

· Targeting Disease Mechanisms—Some drugs may also be used to target how
the disease works. In other words, they can suppress the immune system.
These drugs include Cyclophosphamide (Cytoxan*
<http://www.niams.nih.gov/hi/topics/autoimmune/autoimmunity.htm#star>)
and cyclosporine (Neoral and Sandimmune). The same immune-suppressing
drug may be used for many diseases.

Your doctor may not prescribe a treatment. If your symptoms are mild,
the risks of treatment may be worse than the symptoms. You may choose to
put off treatment for now. But you should watch for signs that your
disease is progressing. Visit your doctor regularly. You need to catch
changes before they lead to serious damage.

* Brand Names included in this booklet are provided as examples only,
and their inclusion does not mean that these products are endorsed by
the National Institutes of Health or any other Government agency. Also,
if a particular brand name is not mentioned, this does not mean or imply
that the product is unsatisfactory.

~What Types of Doctors Treat AutoImmune Diseases?

Treatments for autoimmune diseases vary. So do the types of doctors who
provide them.

For some people, one doctor will be enough to manage their disease.
Others may require a team approach. One doctor might coordinate and give
care, and others would treat specific organ problems. For example, a
person with lupus might be seen by a rheumatologist. But that person
might also see a Nephrologist for related kidney problems and a
Dermatologist for skin problems.

~Specialists you may need to see include:

· A Rheumatologist, who treats arthritis and other rheumatic diseases.
These include Scleroderma and Systemic Lupus Erythematosus (Lupus or SLE).

· An Endocrinologist, who treats gland and hormone problems. These
include Diabetes and Thyroid Disease.

· A Neurologist, who treats nerve problems. These include Multiple
Sclerosis and Myasthenia Gravis.

· A Hematologist, who treats diseases that affect the blood. These
include Pernicious Anemia and AutoImmune Hemolytic Anemia.

· A Gastroenterologist, who treats problems with the digestive system.
These include Crohn’s Disease and Ulcerative Colitis.

· A Dermatologist, who treats problems of the skin, hair, and nails.
These include Psoriasis, Pemphigus/Pemphigoid, and Alopecia Areata.

· A Nephrologist, who treats kidney problems. These include
GlomeruloNephritis, inflamed kidneys associated with Lupus.

What Are Some Other Problems Related to AutoImmune Diseases?

Having a chronic disease can affect almost every part of your life. The
problems you might have with an autoimmune disease vary. They may include:

· How you look and your self-esteem—Depending on your disease, you may
have discolored or damaged skin or hair loss. Your joints may look
different. These can all affect how you look and your selfesteem. Such
problems can’t always be prevented. But their effects can be reduced
with treatment. Cosmetics, for example, can hide a skin rash. Surgery
can correct a malformed joint.

· Caring for yourself—Painful joints or weak muscles can make it hard to
do simple tasks. You may have trouble climbing stairs, making your bed,
or brushing your hair. If doing daily tasks is hard, talk with a
physical therapist. The therapist can teach you exercises to improve
strength and function. An occupational therapist can show you new ways
to do things or tools to make tasks easier. Sometimes regular exercise
or simple devices can help you do more things on your own.

· Family relationships—Family members may not understand why you don’t
have energy to do things you used to do. They may even think you are
just being lazy. But they may also be overly concerned and eager to help
you. They may not let you do the things you can do. They may even give
up their own interests to be with you. Learn as much as you can about
your disease. Share what you learn with your family. Involve them in
counseling or a support group. It may help them better understand the
disease and how they can help.

· Sexual relations—Sexual relationships can also be affected. For men,
diseases that affect blood vessels can lead to problems with erection.
In women, damage to glands that produce moisture can lead to vaginal
dryness. This makes intercourse painful. In both men and women, pain,
weakness, or stiff joints may make it hard for them to move the way they
once did. They may not be sure about how they look. Or they may be
afraid that their partner will no longer find them attractive. With
communication, good medical care, and perhaps counseling, many of these
issues can be overcome or at least worked around.

· Pregnancy and childbearing—In the past, women with some autoimmune
diseases were told not to have children. But better treatments and
understanding have changed that advice. Autoimmune diseases can affect
pregnancy, and pregnancy can affect autoimmune diseases. But women with
many such diseases can safely have children. How a pregnancy turns out
can vary by disease and disease severity. If you have an autoimmune
disease, you should consult your doctor about having children.

~What Research Is Being Conducted To Help People With Autoimmune Diseases?

The National Institutes of Health (NIH) supports research in autoimmune
diseases. Here are a few examples:

· Rheumatoid Arthritis—The National Institute of Arthritis and
Musculoskeletal and Skin Diseases (NIAMS) and the North American
Rheumatoid Arthritis Consortium will study 1,000 siblings with
rheumatoid arthritis. Scientists will look at gene material to find and
identify parts of DNA involved in the disease. They will test for
proteins called rheumatoid factor in the blood. And they will look at x
rays of the joints. This work will provide basic facts about the
genetics of the disease.

· Systemic Lupus Erythematosus (SLE)—NIAMS-supported scientists are
studying whether women with lupus can safely take oral contraceptives or
hormone replacement therapy. Previous research suggests that female
hormones may contribute to the disease or make it worse.

· Lupus Nephritis—One NIAMS project is testing a drug that may be less
toxic than the drugs now used for lupus nephritis (kidney disease caused
by lupus).

· Vitiligo—With NIAMS support, scientists are studying genes from pairs
of siblings affected by this skin pigmentation disorder. They hope to
find genes that may cause vitiligo and learn how they affect the skin.

· Type 1 Diabetes—Researchers supported by the National Institute of
Diabetes and Digestive and Kidney Diseases have found a way to identify
people who are likely to get type 1 diabetes (formerly known as juvenile
diabetes). They are now testing ways to prevent these people from
getting the disease.

· Multiple Sclerosis—Scientists supported by the National Institute of
Neurological Disorders and Stroke are looking at the autoimmune system,
infectious agents, and genes as culprits in multiple sclerosis (MS).
Such studies strengthen the theory that MS comes from a number of
factors rather than a single one. Studies use magnetic resonance imaging
to see how MS lesions evolve in the brain’s white matter. Research has
shown that MS has no bad effects on pregnancy, labor, or delivery. In
fact, the stabilizing or remission of symptoms during pregnancy may be
due to changes in a woman’s immune system that allow her to carry a baby.

· Multiple AutoImmune Diseases—The National Institute of Allergy and
Infectious Diseases is supporting clinical trials of drugs that prevent
the immune system from attacking healthy cells. The Institute wants to
see if they are safe and useful. Such drugs may prove helpful for
treating a number of autoimmune diseases.

~Where Can People Find More Information About AutoImmunity?

Various parts of the NIH provide information on different aspects of
autoimmune diseases. Many nonprofit organizations have patient
resources, local chapters, and support groups. Your own doctor can best
tell you about your own medical condition.


~National Institutes of Health

§ National Institute of Arthritis and Musculoskeletal and Skin Diseases
(NIAMS)
1 AMS Circle
Bethesda, MD 20892-3675
Phone: 301-495-4484 or
877-22-NIAMS (226-4267) (free of charge)
TTY: 301-565-2966
Fax: 301-718-6366
www.niams.nih.gov

National Institute of Allergy and Infectious Diseases
Office of Communications
Building 31, Room 7A25
31 Center Drive, MSC 2520
Bethesda, MD 20892-2520
Phone: 301-496-5717
www.niaid.nih.gov/publications
and
www.niaid.nih.gov/clintrials/default.htm


National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
National Diabetes Information Clearinghouse (NDIC)
1 Information Way
Bethesda, MD 20892-3560
Phone: 301-654-3327 or 800-860-8747 (free of charge)
E-mail: ndic@info.niddk.nih.gov
www.niddk.nih.gov

National Institute of Neurological Disorders and Stroke
Office of Communication and Public Liaison
P.O. Box 5801
Bethesda, MD 20824
Phone: 301-496-5751 or 800-352-9424 (free of charge)
E-mail: braininfo@ninds.nih.gov
www.ninds.nih.gov

NIH Clinical Center
Patient Recruitment Office
Phone: 800-411-1222 (free of charge)
TTY: 866-411-1010
E-mail: prpl@mail.cc.nih.gov
http://clinicalstudies.info.nih.gov/

Office of Rare Diseases
6100 Executive Boulevard
Room 3B01, MSC 7518
Bethesda, MD 20892-7518
Phone: 301-402-4336
http://rarediseases.info.nih.gov

~Other Resources Sponsored by the U.S. Department of Health and Human
Services

Combined Health Information Database
http://chid.nih.gov

National Health Information Center
Phone: 301-565-4167 or 800-336-4797 (free of charge)
Health Finder: www.healthfinder.gov

Other Organizations

American Academy of Dermatology
P.O. Box 4014
Schaumburg, IL 60168-4014
Phone: 847-330-0230 or
888-462-DERM (3376) (free of charge)
Fax: 847-330-0050
www.aad.org
or
1350 Eye Street, N.W., Suite 880
Washington, DC 20005-4355
Phone: 202-842-3555
Fax: 202-842-4355



American Academy of Orthopaedic Surgeons
P.O. Box 1998
Des Plaines, IL 60017-1998
Phone: 800-824-BONE (2663) (free of charge)
www.aaos.org



American College of Rheumatology
1800 Century Place, Suite 250
Atlanta, GA 30345
Phone: 404-633-3777
Fax: 404-633-1870
E-mail: acr@rheumatology.org
www.rheumatology.org


American Autoimmune Related Diseases Association
22100 Gratiot Avenue
East Detroit, MI 48021
Literature requests: 800-598-4668 (free of charge)
Phone: 586-776-3900
Fax: 586-776-3903
E-mail: aarda@aol.com
www.aarda.org

American Behçet’s Disease Association
P.O. Box 19952
Amarillo, TX 79114
Phone: 800-7-BEHCET (723-4238) (free of charge)
www.behcets.com <http://www.behcets.com/>

American Diabetes Association
Attn: National Call Center
1701 N. Beauregard Street
Alexandria, VA 22311
Phone: 800-DIABETES (342-2383) (free of charge)
www.diabetes.org



American Liver Foundation
75 Maiden Lane, Suite 603
New York, NY 10038
Phone: 800-GO-LIVER (465-4837) (free of charge) or
800-4HEP-USA (443-7872) (free of charge)
E-mail: info@liverfoundation.org
www.liverfoundation.org


Arthritis Foundation
P.O. Box 7669
Atlanta, GA 30357
Phone: 404-872-7100 or 800-568-4045 (free of charge)
www.arthritis.org



Crohn’s and Colitis Foundation of America
National Headquarters
386 Park Avenue South, 17th Floor
New York, NY 10016-8804
Phone: 800-932-2423 (free of charge)
www.ccfa.org


Guillain-Barré Syndrome Foundation International
P.O. Box 262
Wynnewood, PA 19096
Phone: 610-667-0131
Fax: 610-667-7036
E-mail: info@gbsfi.com
www.guillain-barre.com



Juvenile Diabetes Research Foundation International
120 Wall Street
New York, NY 10005-4001
Phone: 212-785-9500 or
800-JDF-CURE (533-2873) (free of charge)
Fax: 212-785-9595
E-mail: info@jdrf.org
www.jdf.org

Lupus Mixed Connective Tissue Disorders
921 Pasadena Lane
Modesto, Ca
Fax: 209-524-4680
Email: LupusMCTD@aol.com
www.LupusMCTD.com
www.LupusMCTD.org
www.LupusMCTD.info
www.LupusMCTD.net
www.LupusMCTD.ning.com


Lupus Foundation of America, Inc.
2000 L Street, N.W., Suite 710
Washington, DC 20036
Phone: 202-349-1155 or 800-558-0121 (free of charge)
E-mail: info@lupus.org
www.lupus.org


Myasthenia Gravis Foundation of America
1821 University Avenue W., Suite S256
St. Paul, MN 55104
Phone: 651-917-6256 or 800-541-5454 (free of charge)
Fax: 651-917-1835
E-mail: mgfa@myasthenia.org
www.myasthenia.org



The Myositis Association
1233 20th Street, N.W., Suite 402
Washington, DC, 20036
Phone: 202-887-0088
Fax: 202-466-8940
E-mail: tma@myositis.org
www.myositis.org


National Adrenal Diseases Foundation
505 Northern Boulevard
Great Neck, NY 11021
Phone: 516-487-4992
E-mail: nadfmail@aol.com
www.medhelp.org/nadf


National Alopecia Areata Foundation
14 Mitchell Boulevard
San Rafael, CA 94903
or
P.O. Box 150760
San Rafael, CA 94915-0760
Phone: 415-472-3780
Fax: 415-472-5343
E-mail: info@naaf.org
www.naaf.org


National Multiple Sclerosis Society
733 Third Avenue, 6th Floor
New York, NY 10017-3288
Phone: 212-986-3240 or 800-344-4867 (free of charge)
Fax: 212-986-7981
E-mail: info@nmss.org
www.nmss.org


National Organization for Rare Disorders
P.O. Box 1968
Danbury, CT 06813-1968
Phone: 203-744-0100 or 800-999-6673 (free of charge)
TDD: 203-797-9590
E-mail: orphan@rarediseases.org
www.rarediseases.org


International Pemphigus Foundation
1540 River Park Drive, Suite 208
Sacramento, CA 95815
Phone: 916-922-1298
Fax: 510-527-8497
E-mail: pemphigus@pemphigus.org
www.pemphigus.org


National Psoriasis Foundation
6600 SW 92nd Avenue, Suite 300
Portland, OR 97223-7195
Phone: 503-244-7404 or 800-723-9166 (free of charge)
Fax: 503-245-0626
E-mail: getinfo@psoriasis.org
www.psoriasis.org


National Vitiligo Foundation
700 Olympic Plaza Circle, Suite 404
Tyler, TX 75701
Phone: 903-595-3713
Fax: 903-593-1545
E-mail: info@nvfi.org
www.nvfi.org


Scleroderma Foundation
300 Rosewood Drive, Suite 105
Danvers, MA 01923
Phone: 978-463-5843
Info line: 800-722-HOPE (4673) (free of charge)
Fax: 978-463-5809
E-mail: sfinfo@scleroderma.org
www.scleroderma.org


Scleroderma Research Foundation
220 Montgomery Street, Suite 1411
San Francisco, CA 94104
Phone: 415-834-9444 or
800-441-CURE (2873) (free of charge)
Fax: 415-834-9177
E-mail: info@sclerodermaresearch.org
www.sclerodermaresearch.org

Sjögren’s Syndrome Foundation
6707 Democracy Blvd Ste 325
Bethesda, MD 20817
Phone: 301-530-4420 or
800-475-6473 (free of charge)
Fax: 301-530-4415
E-mail: ssf@sjogrens.org
www.sjogrens.org



Spondylitis Association of America
P.O. Box 5872
Sherman Oaks, CA 91413
Phone: 800-777-8189 (free of charge)
E-mail: info@spondylitis.org
www.spondylitis.org


S.L.E. Lupus Foundation
330 Seventh Avenue, Suite 1701
New York, NY 10001
Phone: 212-685-4118 or 800-74-LUPUS (745-8787) (free of charge)
Fax: 212-545-1843
E-mail: lupus@lupusny.org
www.lupusny.org


Thyroid Foundation of America, Inc.
One Longfellow Place, Suite 1518
Boston, MA 02114
Phone: 800-832-8321 (free of charge)
Fax: 617-534-1515
E-mail: info@allthyroid.org
www.allthyroid.org

 
Vasculitis Foundation
P.O. Box 28660
Kansas City, MO 64188-8660
Phone: 800-277-9474 (free of charge)
Phone/Fax: 816-436-8211
E-mail: vf@vasculitisfoundation.org
www.vasculitisfoundation.org

Appendix I: Glossary of Terms

Antibodies—Special proteins produced by the body’s immune system that
help fight and destroy viruses, bacteria, and other foreign substances
that invade the body.

Antigen—A substance (usually foreign) that stimulates the immune
response. In people with autoimmune disease, the body’s own cells may be
seen as antigens.

AutoAntibodies—Abnormal antibodies that attack parts of the body,
causing autoimmune disease.

AutoImmune Disease—A disease that occurs when the immune system turns
against parts of the body it is designed to protect.

Fever—A rise in body temperature caused by the immune system’s response
to infection or disease.

Immune Response—The reaction of the immune system against foreign
substances. When the reaction occurs against the body’s own cells or
tissues, it is called an autoimmune reaction.

Immune System—A complex system that normally protects the body from
infections. The immune system consists of a group of cells, the
chemicals that control those cells, and the chemicals that those cells
release.

ImmunoSuppressive Drugs—Drugs that suppress the immune response and can
be used to treat autoimmune disease. Unfortunately, because normal
immunity is also suppressed with these drugs, they leave the body at
risk for infection.

Infection—Invasion of the body tissues by bacteria or other tiny
organisms that cause illness.

Inflammation—A reaction of tissues to injury or disease, typically
marked by four signs: swelling, redness, heat, and pain.

Trigger—Something that either sets off a disease in people who are
genetically predisposed to developing the disease, or that causes a
certain symptom to occur in a person who has a disease. For example,
sunlight can trigger rashes in people with lupus.

Appendix II: Glossary of Diseases

Autoimmunity plays a role in more than 80 diseases. Following are brief
descriptions of some of the many diseases in which autoimmunity may be
involved.

Note: Because the specific causes of many diseases are unknown, there is
debate among scientists about whether some of these are truly autoimmune
diseases. Your own doctor may classify some of these diseases differently.

Alopecia Areata—A disorder in which the immune system attacks the hair
follicles, causing loss of hair on the scalp, face, and other parts of
the body.

Ankylosing Spondylitis—A rheumatic disease that causes inflamed joints
in the spine and sacroiliac (the joints that connect the spine and the
pelvis) and, in some people, inflamed eyes and heart valves.

Arthritis—A general term for more than 100 different diseases that
affect the joints. Many forms of arthritis and related conditions are
believed to have an autoimmune component.

AutoImmune Hemolytic Anemia—A condition in which immune system proteins
attack the red blood cells, resulting in fewer of these
oxygen-transporting cells.

AutoImmune Hepatitis—A disease in which the body’s immune system attacks
liver cells, causing inflammation. If not stopped, inflammation can lead
to cirrhosis (scarring and hardening) of the liver and eventually liver
failure.

Behçet’s Disease—A condition characterized by sores in the mouth and on
the genitals and by inflammation in parts of the eye. In some people,
the disease also results in inflammation of the joints, digestive tract,
brain, and spinal cord.

Crohn’s Disease—An inflammatory disease of the small intestine or colon
that causes diarrhea, cramps, and excessive weight loss.

DermatoMyositis—A rare autoimmune disease that causes patchy red rashes
around the knuckles, eyes, and other parts of the body along with
chronic inflammation of the muscles. It may occur along with other
autoimmune diseases such as Rheumatoid Arthritis or Systemic Lupus
Erythematosus.

Diabetes Mellitus, Type 1—A condition in which the immune system
destroys insulin-producing cells of the pancreas, making it impossible
for the body to use glucose (blood sugar) for energy. Type 1 diabetes
usually occurs in children and young adults.

GlomeruloNephritis—Inflammation of the kidney’s tiny filtering units,
which in severe cases can lead to kidney failure.

Graves’ Disease—An autoimmune disease of the thyroid gland that results
in the overproduction of thyroid hormone. This causes such symptoms as
nervousness, heat intolerance, heart palpitations, and unexplained
weight loss.

Guillain-Barré Syndrome—A disorder in which the body’s immune system
attacks part of the nervous system, leading to numb, weak limbs and, in
severe cases, paralysis.

Inflammatory Bowel Disease—The general name for diseases that cause
inflammation in the intestine, the most common of which are Ulcerative
Colitis and Crohn’s disease.

Lupus Nephritis—Damaging inflammation of the kidneys that can occur in
people with lupus. If not controlled, it may lead to total kidney failure.

Multiple Sclerosis—A disease in which the immune system attacks the
protective coating called myelin around the nerves. The damage affects
the brain and/or spinal cord and interferes with the nerve pathways,
causing muscular weakness, loss of coordination, and visual and speech
problems.

Myasthenia Gravis—A disease in which the immune system attacks the
nerves and muscles in the neck, causing weakness and problems with
seeing, chewing, and/or talking.

Myocarditis—Inflamed and degenerating muscle tissue of the heart that
can cause chest pain and shortness of breath. This can lead to
Congestive Heart Failure.

Pemphigus/Pemphigoid—An autoimmune disease of the skin characterized by
itching and blisters.

Pernicious Anemia—A deficiency of the oxygen-carrying red blood cells
that often occurs in people with autoimmune diseases of the thyroid gland.

Polyarteritis Nodosa—An autoimmune disease that causes inflammation of
the small and medium-sized arteries. This leads to problems in the
muscles, joints, intestines, nerves, kidney, and skin.

Polymyositis—A rare autoimmune disease characterized by inflamed and
tender muscles throughout the body, particularly those of the shoulder
and hip girdles.

Primary Biliary Cirrhosis—A disease that slowly destroys the bile ducts
in the liver. When the ducts are damaged, bile (a substance that helps
digest fat) builds up in the liver and damages liver tissue.

Psoriasis—A chronic skin disease that occurs when cells in the outer
layer of the skin reproduce faster than normal and pile up on the skin’s
surface. This results in scaling and inflammation. An estimated 10 to 30
percent of people with psoriasis develop an associated arthritis called
Psoriatic Arthritis.

Rheumatic Fever—A disease that can occur following untreated
streptococcus (strep) infection. It most often affects children, causing
painful, inflamed joints and, in some cases, permanent damage to heart
valves.

Rheumatoid Arthritis—A disease in which the immune system is believed to
attack the linings of the joints. This results in joint pain, stiffness,
swelling, and destruction.

Sarcoidosis—A disease characterized by granulomas (small growths of
blood vessels, cells, and connective tissue) that can lead to problems
in the skin, lungs, eyes, joints, and muscles.

Scleroderma—An autoimmune disease characterized by abnormal growth of
connective tissue in the skin and blood vessels. In more severe forms,
connective tissue can build up in the kidneys, lungs, heart, and
gastrointestinal tract, leading in some cases to organ failure.

Sjögren’s Syndrome—A condition in which the immune system targets the
body’s moisture-producing glands, leading to dryness of the eyes, mouth,
and other body tissues.

Systemic Lupus Erythematosus—An autoimmune disease, primarily of young
women, that can affect many parts of the body, including the joints,
skin, kidneys, heart, lungs, blood vessels, and brain.

Thyroiditis—An inflammation of the thyroid gland that causes the gland
to become underactive. This results in symptoms such as fatigue,
weakness, weight gain, cold intolerance, and muscle aches.

Ulcerative Colitis—A disease that causes ulcers in the top layers of the
lining of the large intestine. This leads to abdominal pain and diarrhea.

Uveitis—The inflammation of structures of the inner eye, including the
iris (the colored tissue that holds the lens of the eye) and the choroid
plexus (a network of blood vessels around the eyeball). Uveitis occurs
with some rheumatic diseases, including Ankylosing Spondylitis and
Juvenile Rheumatoid Arthritis.

Vitiligo—A disorder in which the immune system destroys pigment-making
cells called Melanocytes. This results in white patches of skin on
different parts of the body.

Wegener’s Granulomatosis—An autoimmune disease that damages the small
and medium-sized blood vessels throughout the body, resulting in disease
in the lungs, upper respiratory tract, and kidneys.[/size]


For Your Information

For updates and for any questions about any medications you are taking,
please contact the U.S. Food and Drug Administration at 1-888-INFO-FDA
(1-888-463-6332, a toll-free call) or visit their Web site at
www.fda.gov <http://www.fda.gov>.


National Institute of Arthritis and Musculoskeletal and Skin Diseases
NIAMS/National Institutes of Health
1 AMS Circle
Bethesda, MD 20892-3675

You can also find this booklet on the NIAMS Web site at
www.niams.nih.gov <http://www.niams.nih.gov>.

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« Reply #24 on: August 21, 2007, 08:31:19 am »

Autoimmunity, Part D: Autoimmune Disease, Annus Mirabilis


 
Edited by: Yehuda Shoenfeld, Center for Autoimmune Diseases, Sheba Medical Center, Tel Hashomer, Israel; M. Eric Gershwin, University of California, Davis, California

The incidence of autoimmune diseases is increasing worldwide, and the search for better management of these diseases and even for a cure is being pursued by scientists from many disciplines. Tools from the areas of genetics, neuroscience, cell biology, virology, and infectious disease are being applied to the problem and are yielding useful results.

This is the fourth and final volume of a series on autoimmunity, and findings related to particular clinical manifestations are presented, particularly systemic lupus erythematosus, scleroderma, rheumatoid arthritis, Sjogren's syndrome, antiphospholipid antibodies, and infections and autoantibodies.

Part A presents new principles in autoimmunity and new diagnostic tools; Part B focuses on genetics and advances in treatment; and Part C begins the focus on the clinical venue.

We could read this in it's entirty if were are members for $15.00. Non-Members are $145.00
This is from NY Academy of Science..
Anyone have a Dad, Uncle or a  Cousin who is a doctor and can look it up for us?
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« Reply #25 on: November 13, 2007, 12:09:15 am »

DO YOU KNOW YOUR FAMILY AQ?

 AQ is a play on IQ and stands for Autoimmune Quotient
.


It’s about knowing how likely you or a loved one is to develop an autoimmune disease, based on the prevalence of these diseases and your family history.



1. Understand that autoimmune diseases constitute a major U.S. health crisis. According to the National Institutes of Health (NIH), there are 23.5 million Americans who suffer from autoimmune diseases and the prevalence of these diseases is rising. In comparison, cancer affects up to 9 million and heart disease up to 22 million. Collectively, autoimmune disease is one of the top 10 leading causes of death in children and women under 65 and represents some $100 billion in annual direct health care costs.


There are more than 80 known autoimmune diseases and an additional 40 diseases that are suspected to be autoimmune-related. The diseases themselves can affect almost any part of the body, including the kidneys, skin, heart, liver, lymph nodes, thyroid and the central nervous system. As a result, they cut across various medical specialties, such as endocrinology, neurology, dermatology, rheumatology, gastroenterology and hematology, among others. Autoimmune diseases include multiple sclerosis, myasthenia gravis, scleroderma, polymyositis, vasculitis, lupus, Sjögren's disease, idiopathic thrombocytopenic purpura (ITP), type 1 or juvenile diabetes, Crohn’s disease and Graves’ disease.

Autoimmunity is the underlying cause of these diseases. It is the process whereby the immune system mistakenly recognizes the body's own proteins as foreign invaders and begins producing antibodies that attack healthy cells and tissues, causing a variety of diseases.



3. Be aware that autoimmune diseases target women.
Women are more likely than men to be affected; some estimates say that 75 percent of those affected are women. These women are usually in the childbearing years. In the past several years, autoimmunity has begun to be recognized as a major women’s health issue, with the Office of Research on Women’s Health at NIH recognizing it as such and the Society for Advancement of Women’s Health Research naming it as one of 10 diseases that most disproportionately affect women.


4. Know that autoimmune diseases run in families.
Current research points to a genetic component in autoimmune diseases. However, autoimmune diseases are not typical genetic diseases like, for instance, sickle cell anemia, where there is a specific gene mutation. With autoimmune diseases, multiple genes are involved that collectively increase vulnerability or susceptibility. Thus, what is inherited is not one specific gene but several genes that increase risk. As a result, autoimmune diseases tend to “cluster” in families - not as one particular disease, but as a general tendency to the autoimmune process and, consequently, different autoimmune diseases. For example, one family member may have autoimmune hepatitis; another, celiac disease; another, rheumatoid arthritis.

5. Do your own family medical history.
Given the family connection, knowing the health histories of other family members is critical. For example, if your grandmother or father or sister or uncle has an autoimmune disease, you could be more susceptible to developing one yourself. Take an inventory of your family health problems, expanding your research beyond your immediate family to include grandparents, aunts, uncles, cousins and other relatives. Once you know your family history, share it with other family members and your doctor who can then assess the possibilities with a degree of accuracy and order appropriate tests.

6. Keep a "symptoms" list.
People with autoimmune diseases often suffer from a number of symptoms that, on the surface, seem unrelated. In addition, they may have suffered from other seemingly unrelated symptoms throughout their lives. It is important, therefore, to make a list of every major symptom you’ve experienced so that you can present it clearly to your doctor. List the symptoms in the order of concern to you.

7. Realize that getting an autoimmune disease diagnosis is often challenging.
A study of autoimmune patients found that the average time for diagnosis of a serious autoimmune disease is 4.6 years. During that period, the patient typically has seen 4.8 doctors; and 46 percent of the patients were told initially that they were too concerned about their health or that they were chronic complainers.

One of the factors that makes getting a correct autoimmune disease diagnosis so difficult is that symptoms can vary widely, notably from one disease to another, but even within the same disease. Also, because autoimmune diseases affect multiple systems, their symptoms can often be misleading.

The medical community’s lack of knowledge of autoimmune disease compounds the problem. Even though these diseases share a genetic background and tend to run in families, most health questionnaires at doctors’ offices do not ask whether there is a family history of autoimmune disease.

8. Hold the power to protect your family’s future health and well-being in your hands.
By working through these steps and doing your homework, you now have the knowledge to determine whether you or your loved ones could be at risk for developing an autoimmune disease.
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« Reply #26 on: November 29, 2007, 08:05:42 pm »

Staying Army Strong

Nicole Lillis (left) in May 2001 after she graduated from basic training and Military Police school at Fort Leonard Wood, Mo.

Junior Nicole Lillis (left) with friends on Water Street in October 2006. Lillis is a U.S. Army veteran who says she is sick from vaccines given to her during basic training.


Junior Nicole Lillis' disdain for the U.S. Army and the government that controls it all comes down to a preventative measure that many in the United States and throughout the world take for granted nowadays.

It all comes down to a technological advancement that helps children ward off the flu and chicken pox.

It all comes down to a series of elixirs intended to protect soldiers in the event of a biological weapon - vaccines.

"I'm not going to tell you the fluffy story of the military," she often tells people when they ask her about her time in the service.

Lillis suffers from painful symptoms that are typically associated with autoimmune disorders. Lillis said she and doctors believe the vaccines the Army gave her to take at the beginning of her military career caused her immune system to become hyperactive.

Leading researchers agree and have shown a link between military vaccines and autoimmune disorders, claims and connections that the U.S. government emphatically denies.

~Basic training

Lillis, 29, began her college education at UW-Eau Claire in 1998 as a criminal justice major. In January 2001, she decided to join the military, something she said she knew she wanted do since she was 16.

"I really wanted to see the world and travel," she said. "Everyone has their own reasons for joining. Some do it for money; some really want to do it. I just wanted to do it."

In high school, Lillis wanted to join the Air Force, but instead chose the Army, initially enlisting in the Airborne program, where she could "jump out of a perfectly good airplane."

She began her military service by reporting to Fort Leonard Wood, Mo., for basic training.

She said she remembers getting onto trucks and traveling to the Military Entrance Processing Station, which prepared her and the rest of the incoming recruits for the weeks ahead. There, soldiers got haircuts, purchased toiletries and got medical examinations, which included receiving the vaccines. Lillis said she and the other soldiers received 12 vaccines that day, one of which was experimental.

She said the soldiers then got back on to the trucks and went to their basic training units where the "drill sergeants were lined up waiting."

The sergeants screamed at the soldiers the moment the soldiers stepped off the trucks, she said, immediately making the recruits "get down and push."

Two months into the program, the symptoms began, she said. She began having extreme pain in her pelvis and joints, but kept telling herself that it was just the training catching up with her and that she wasn't going to be one of those who didn't finish.

After eight weeks of the physical gauntlet and excruciating pain, Lillis graduated from basic training. Immediately after she began training to be a military police officer.

"When you're going through it you're like, 'this is hell,'" she said. "But basic training was a riot. When you're done, you look back and say to yourself, 'I did that.'"

Once the programs were complete, she said the drill sergeants acknowledged the soldiers' hard work and gave them all advice.

Despite the stress fracture in her pelvis keeping her from heading to Fort Benning, Ga., for airborne training, one drill sergeant told her not to not pursue the training for other reasons.

"My drill sergeant looked me in the eye and said, 'The Army will never be worth your health,'" she said. "I will never forget that."

~Pain continues

The completion of basic training and military police training was bittersweet for Lillis whose complications got worse shortly after finishing the programs.

She went to a civilian physician who was unable to find anything wrong with her body.

"I remember being so tired and in so much pain, but I just figured that it all had to do with the physical demand of basic training," she said. "So, I just pushed through it."

Lillis reported to Fort Hood, Texas, in June 2001 for her duty assignment where she worked for some time as a patrol officer and then moved to being a 911 dispatcher. There, she said her unit gave her a lot of flak for not being able to run like them due to the extreme pain she was in.

One night while at Fort Hood, Lillis said she woke up to go to the restroom when she collapsed onto the floor and vomited continually. A doctor at the military hospital examined her and diagnosed her with bursitis, joint inflammation and gave her high doses of ibuprofen for the pain.

~Dead ends

Lillis said her pain worsened through her time at Fort Hood, and she continued receiving the same diagnosis each time doctors examined her at the military hospital and received the same treatment of ibuprofen and cortisone injections. One doctor went as far to give her Zoloft, an anti-depressant, even after Lillis repeatedly told the doctor she was not depressed.

Finally, a breakthrough came in January 2002 when the doctor diagnosed Lillis, 23, with fibromyalgia, a disease that causes severe muscle, joint and bone pain.

The diagnosis led to the military honorably discharging her in May 2003. She remained in Texas until January 2006, when she moved back to Wisconsin and began her own research into vaccines causing autoimmune disorders, which took her into diseases such as Gulf War Syndrome and lupus. This included research that Dr. Pamela Asa conducted, who discovered the connection between the anthrax vaccine and autoimmune disorders.

Lillis said insurance companies view soldiers as having a pre-existing condition, making them ineligible for affordable insurance after their time in the service. So the only affordable health care is through Veterans Affairs hospitals. Lillis initially went to the VA hospital in Tomah for treatment but said doctors attempted to treat "the symptoms and not the problem."

When she would ask doctors about the possibility of vaccines causing her ailments and noting the experimental one she received, the doctors would ignore the comment or deny it. She said one doctor even went as far as asking if she had an appointment with the psychiatric ward that day after she brought up the vaccine question.

Her luck changed when a Tomah VA doctor referred her to a doctor at the Madison VA hospital who, in the summer of 2006 told her she was on the borderline for lupus and that there was no doubt the vaccines "kicked her immune system into overdrive."

~The vaccines

When Lillis and the other recruits rolled up their sleeves for vaccinations during basic training, they got stuck with 12 needles. Soldiers had to sign an informed consent document before receiving one of the vaccines. She said when soldiers asked why they needed to sign the form, the doctors and drill sergeants told them it was for a pneumonia vaccine.

"We were given the one page to sign without any information on it," she said, showing the piece of paper she signed that day. "The drill instructors screamed at us to sign the consent document and told us if we didn't, they would be sure our lives were a living hell. They intimidated us into signing it."

Under U.S. Code Title 10, Section 1107, when the Secretary of Defense requires or requests soldiers to take an experimental or non-Food and Drug Administration approved vaccine, the Department of Defense must inform the soldiers in writing of the purpose of the drug, the fact that it is investigative or unapproved and its potential side effects before they give it to them. The soldiers must also provide informed consent before receiving the vaccine.

Lillis later found three more pages to her consent form after reviewing her medical records after her time in the service. She said she never saw the pages before getting the vaccine.

The vaccine Lillis received was an investigative pneumonia vaccine that the Department of Defense said the elderly have used successfully for years, saying soldiers should not worry about taking it, according to the consent form. Lillis said she is skeptical if that was really what the vaccine was.

"If the elderly have been taking it for years and it has been effective, then why did we have to sign a consent document?" Lillis asked.

If Lillis or the other soldiers refused to sign the form and take the vaccine, they could have faced a court-martial or a dishonorable discharge for refusing a direct order, according to the Army handbook.

~Connections are made

In 1994, Asa, an immunologist, said the path to discovering the connection between vaccines and autoimmune disorders started when Gulf War veterans came to her with rashes, severe pain, headaches and memory lapses.

"It sounded like these people had lupus," Asa said. "This was uncommon because most of them were men," noting lupus typically affects women.

Soldiers who served in the United States during the war were experiencing the same symptoms as those serving abroad, so Asa looked to determine what both groups had in common. She said she thought the answer lay in vaccines.

"I said to myself, 'Oh my God, somebody spiked the punch with an adjuvant," she said, explaining that adjuvants are added to vaccines to increase their effectiveness.

The daunting task of determining what the adjuvant was and what vaccine it was in began.

Asa had help from a former colleague at Tulane University in Louisiana, Dr. Bob Garry, a leading researcher in creating an AIDS vaccine, who developed a test that showed the presence of squalene, an oil-based adjuvant, in blood in 1997. The test detected anti-squalene antibodies.

She said she sent Garry blood samples from soldiers that came to her with symptoms to have him test for the anti-squalene antibodies.

"When my samples popped hot with anti-squalene antibodies, I just cried," she said. "My theory was right."

She said initially the anthrax vaccine wasn't on the table until the mandatory Anthrax Vaccine Immunization Program started in 1998. Asa said that was when soldiers began coming to her with symptoms again.

They too tested positive for anti-squalene antibodies, she said.

The AVIP ran through June of 2001 when the Department of Defense temporarily stopped using the vaccine due to non-FDA-approved production methods, according to program records.

The program used Anthrax Vaccine Absorbed, which the FDA approved in the 1970s to protect against skin contact with anthrax spores, not inhalation as the military was using it during AVIP, according to the vaccine's history explained in a U.S. District Court opinion. The FDA eventually labeled the vaccine as an investigative experimental vaccine in the use against inhalation of anthrax spores, according to the opinion, which would place it under Title 10 Section 1107 of the U.S. Code.

Asa tracked the lot numbers of the vaccine, determining that six anthrax vaccine lots had some levels of squalene in them. Later, an independent FDA test confirmed these lot numbers.

"I can't put into words the look of horror on (the soldiers') faces and how difficult it was to tell them that the country and the government they were willing to die for had done this to them," Asa said. "It makes me sick to tell these kids they are positive for anti-squalene antibodies. I hope like hell they're negative."

Lillis said she isn't sure if she received the AVA during basic training because her immunization records were not with her medical records, however, AVIP was still in progress in January 2001.

~Court steps in

Several soldiers took their cases to Congress and ultimately brought a lawsuit against the Department of Defense in the form of Doe v. Rumsfeld. As a result, the U.S. District Court issued a temporary injunction on AVIP on Dec. 22, 2003, according to AVIP policy records, which later became permanent in October of 2004, according to the court order.

In February 2007, the Department of Defense reinstituted mandatory anthrax vaccinations for soldiers. AVIP has inoculated nearly 1.8 million soldiers and defense workers since 1998, according to AVIP records.

~Government reaction

Both Asa and Lillis said they, along with other soldiers affected by unknown sickness, have been trying to get the government to acknowledge the harm caused by vaccines, but both said they have gotten nowhere.

"I've been fighting this since 1994," Asa said. "I have been receiving hell for it the entire time."

She said certain officials in the government have accused her and Garry of having an anti-military agenda.

"We don't have an anti-military agenda," she said. "I got into this because I am indebted to military personnel who will take a bullet for one of my kids."

The government's reaction to Lillis has been the same to most soldiers experiencing problems, Asa said, noting the military would blame the symptoms on things other than the vaccines or would call the soldiers "crazy" and argued that they suffered from Post Traumatic Stress Disorder.

"Crazy doesn't cause rashes. Crazy doesn't cause arthritis. Crazy doesn't cause these symptoms," Asa said.

A representative from the Military Vaccine Agency, the Department of Defense body that oversees military vaccine policies, refused to give his name due to Department protocol. He said that protecting soldier health is the No. 1 priority of the agency and the Department and said that all vaccines administered are "safe and effective."

"Absolutely all of the vaccines are FDA approved," he said. "There have never been experimental vaccines given to any service members. All service members are given licensed, proven safe and effective vaccines that are approved by the FDA and are administered under the guidance of the American Council of Immune Practices."

Susan Walker, the Midwest regional analyst for the agency, as well as clinical and communication specialists within the agency, did not comment on questions asked of them.

~Pressing forward

Lillis, now an organizational communications major, said her symptoms are ongoing six years later. She recalled an incident that happened during this summer in which she had a severe migraine and began vomiting continually - an event she has experienced in the past. She said the distance to the nearest VA hospital in Tomah, apart from the Chippewa Falls hospital which she said doesn't accept walk-in appointments, makes it very scary when she does get severely sick.

She said that the muscle, joint and bone pains have gotten worse, noting that at times her back and neck muscles spasm, causing migraines. She also said she started taking the prescribed muscle relaxants again, adding it is sometimes difficult for her to get out of bed in the morning.

Despite her complications Lillis said she doesn't let it get her down and said she has a support network of family and friends who help her through the struggles. She said she doesn't want people to feel sorry for her because she doesn't feel sorry for herself.

"It is just something that I live with," she said.

She said she doesn't regret the experiences of the Army. Although she said she would rather have her health, the events of the last six years have shaped her into the person she is today.

Lillis also said she won't give up the battle for people to acknowledge that what is happening to her is real.

"I don't let it get me down," she said. "I'm so stubborn and I will fight this until the end."

And I hope and wish you the best, continue that fight!
Kathy  CandleSmilie 
« Last Edit: November 29, 2007, 08:07:54 pm by Admin » Logged


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« Reply #27 on: March 02, 2009, 07:29:06 pm »

Vitamin A Signals Offer Clues To Treating Autoimmunity

Mar. 1, 2009

 Dendritic cells, the microbe-sensing alarms of the immune system, can send out a "red alert" to stimulate immunity, or a "calm down" message that tones down excessive immunity that might damage the host.  The "calm down" message makes use of vitamin A, providing an explanation for the link between vitamin A deficiency and autoimmune diseases.

Bacteria and viruses that cause chronic infections, such as tuberculosis, hepatitis C and HIV, may have evolved strategies that skew this balance of signals in their favor.

Distributed around the body, dendritic cells act as the security alarms of the immune system. After sensing the presence of intruders, dendritic cells can transmit the alarm to white blood cells or tell them to relax, depending on the signals they send out.

Researchers at the Emory Vaccine Center and Yerkes National Primate Research Center have discovered that dendritic cells can respond to the same compound, through two different receptors, by sending out both stimulatory and calming messages at once.

The compound is zymosan, a component of yeast cell walls. However, the finding could guide scientists in designing vaccines against many infectious agents since the calming receptor is known to respond to bacteria and viruses as well as yeast. In addition, silencing the calming receptor's messages might boost the immune system's ability to fight a chronic infection.

The results are published in the March 2009 issue of Nature Medicine.

The calming receptor, known as TLR2 (Toll-like receptor 2), uses vitamin A to transmit its signals, which provides an explanation for the connection between vitamin A deficiency and autoimmune diseases. Vitamin A deficiency has been linked to diseases such as rheumatoid arthritis, lupus and type I diabetes.

This "two signals at once" feature of the immune system can be viewed as the result of an evolutionary tug of war, says senior author Bali Pulendran, PhD, professor of pathology and laboratory medicine at Emory University School of Medicine and Yerkes National Primate Research Center.

"The immune system has to provide a defense against infection, while avoiding the destruction of too much of the body along the way," he says. "At the same time, pathogens have evolved strategies to manipulate the immune system for their own purposes."

Working with Pulendran, postdoctoral fellow Santhakumar Manicassamy, PhD, examined which genes are turned on in dendritic cells by zymosan in cell culture. They were surprised to find that both zymosan and live Candida albicans, which causes yeast infections, turned on genes involved in converting vitamin A to its active form, retinoic acid.

"Others have seen that these genes are turned on constitutively in the gut, but seeing how they can be induced elsewhere is new," Pulendran says.

Manicassamy and colleagues found that dendritic cells use retinoic acid along with other chemical messengers to steer white blood cells into a regulatory mode, rather than an attack mode. For dendritic cells to do so, they need TLR2, since zymosan also activates another receptor called dectin-1, which sends out stimulatory signals.

The effects of zymosan and TLR2 can deter white blood cells from attacking nerve tissue in a mouse model of multiple sclerosis, the authors found.

In the model, mice are immunized against myelin, which forms a protective sheath around nerves. Injecting the mice with zymosan at the same time as immunization reduced the damage to their nerves.

The research was supported by the National Institutes of Health.

SOURCE: Science Daily
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« Reply #28 on: March 03, 2009, 01:15:03 pm »

Antibody titers predict clinical features of autoimmune autonomic ganglionopathy



Abstract
Autoimmune autonomic ganglionopathy is a disorder of isolated autonomic failure associated with antibodies to the nicotinic acetylcholine receptor of the autonomic ganglia resulting in severe orthostatic intolerance, syncope, constipation, gastroparesis, urinary retention, dry mouth, dry eyes, blurred vision and anhidrosis. We report the autonomic test results, antibody titers and clinical findings in 8 patients with antibodies to the nicotinic acetylcholine receptor of the autonomic ganglia. There was a sigmoidal relation between the antibody titers and the fall in systolic blood pressure (r2=0.84). The threshold occurred with antibody titers of ~1 nmol/l. Over the linear portion of the sigmoid curve, with antibody titers in the 1–3 nmol/l range, increasing antibody titers resulted in more severe orthostatic hypotension (r=0.94, P<0.001). The saturation point of the sigmoidal relation occurred at ~3 nmol/l with drops in systolic blood pressure of ~100 mmHg during upright tilt. The antibody titers correlated inversely with the Valsalva ratio (r=−0.87, P<0.001), the 30:15 ratio (r=−0.84, P<0.001) and the expiratory to inspiratory ratio (r=−0.67, P<0.01). Patients with orthostatic intolerance, anhidrosis, constipation, urinary dysfunction, sicca syndrome and pupillary dysfunction had higher antibody titers than subjects that did not (P<0.01 in all cases). Autoimmune autonomic ganglionopathy is a clinically heterogeneous disease with variable presentation, particularly in subjects with lower antibody titers. Our data suggest that patients with higher antibody titers have wide spread dysautonomia while those with lower antibody levels may present with, or evolve into, more focal or restricted presentations.

Keywords: Autoimmune autonomic ganglionopathy, Autonomic testing, Autonomic failure


Corresponding author. Autonomic and Peripheral Nerve Laboratory, Department of Neurology, Beth Israel Deaconess Medical Center, 1 Deaconess Road, Boston, MA 02215, USA
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« Reply #29 on: January 30, 2011, 09:19:40 am »

Does vitamin D affect risk of developing autoimmune disease?: A systematic review

Cross-sectional data point to a potential role of vitamin D in autoimmune disease prevention, but prospective interventional evidence in humans is still lacking.

Methods
PubMed, limited to English from inception through April 2010, searched using keywords: “vitamin D,” “autoimmune,” and autoimmune disease names
Summarized in vitro, animal, and genetic association studies of vitamin D in autoimmune disease pathogenesis
Sorted epidemiologic studies by design and disease and performed systematic review of (a) cross-sectional data concerning vitamin D level and autoimmune disease; (b) interventional data on vitamin D supplementation in autoimmune diseases; and (c) prospective data linking vitamin D level or intake to autoimmune disease risk

Results
Vitamin D has effects on innate and acquired immune systems, and vitamin D receptor polymorphisms have been associated with various autoimmune diseases
In experimental animal models, vitamin D supplementation can prevent or forestall autoimmune disease
Of 1446 studies identified and screened, 76 studies examined vitamin D levels in autoimmune disease patients, particularly with active disease, and compared with controls
19 observational or interventional studies assessed effect of vitamin D supplementation as therapy for various autoimmune diseases (excluding psoriasis and vitiligo) with range of study approaches and results
Few prospective human studies performed conflict as to whether vitamin D level or intake is associated with autoimmune disease risk
No interventional trials investigated whether vitamin D affects human autoimmune disease risk
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