Jun 10, 2006

Gluten Sensitivity Enteropathy

Gluten sensitivity occurs in people whose immune systems react to wheat and related proteins. Because this reaction is immune-mediated, gluten sensitivity is considered an autoimmune disease, one in which the environmental trigger is clearly known. Gluten sensitivity develops in people with immune system genes (HLA antigens) that predispose them to disease development. Gluten sensitivity causes symptoms of variable degrees, with some people developing mild gastrointestinal symptoms after ingesting wheat products to people with symptoms of overt intestinal damage to the microvilli and frank celiac disease. Celiac disease, which is also known as gluten-sensitive enteropathy, celiac sprue, and nontropical sprue, affects one in every 133 Americans. Untreated, the immune changes caused by celiac disease can lead to intestinal malignancies, lymphomas and other morbidities.

Celiac disease occurs when sufficient damage to the intestinal tract is seen on biopsy. However, anyone with evidence of IgG or IgA antigliadin antibodies is considered to have gluten sensitivity even without evidence of other intestinal antibodies, such as endomysial and tissue transglutaminase antibodies. People with gluten sensitivity have immunological reactions when they ingest proteins called prolamines, including glidadin in wheat, secalin in rye, and hordein in barley. When sensitivity people ingest these compounds, these proteins react with immunologically active cells present in the gastric mucosa. In turn, these immune system cells respond by producing cellular changes and immune system chemicals that lead to the destruction of the intestinal microvilli. This interferes with nutrient absorption and leads to the stimulation and over-proliferation of intestinal B-lymphocytes.

The Celiac Iceberg

Because patients with gluten sensitivity often only have mild symptoms and do not yet show the intestinal changes associated with celiac disease, they are likely to be misdiagnosed and not advised to avoid gluten. Symptoms in gluten sensitivity are also wide-ranging and varied and may not be recognized. Gluten sensitivity causes malabsorption, which is the inability to properly absorb nutrients from food. Typical symptoms include abdominal pain, abdominal distention, weight loss, irritability, depression, muscle wasting of buttocks, thighs and arms, pale skin, peeling nails, alopecia, bloating, lactose intolerance, delayed puberty, miscarriage, arthralgia, bone pain, fatigue, gas, nausea, vomiting, increased mucus production, nasal discharge, diarrhea, increased fat in stools (steatorrhea), iron deficiency anemia, osteopenia, osteoporosis, apthous (oral) ulcerations, dental enamel defect, miscarriage, joint pain, Sjogren's syndrome, Turner's syndrome and elevated liver enzymes. Patients may also gain weight if nutrient deficiencies lead to food cravings and fatigue.

Children with celiac disease may present with failure to thrive although their abdomens may be large and distended. Disorders that may accompany gluten sensitivity include: short stature, selective IgA deficiency, dementia, Down syndrome, Williams syndrome, Addison's disease, type 1 diabetes, infertility, autoimmune thyroid disease, primary biliary cirrhosis and rheumatoid arthritis. Some researchers, such Dr. James Braly, feel that the toxic components in gluten contribute to the development of these other autoimmune diseases.

Diagnosing celiac disease is difficult. The usual approach is to order tests for gliadin and tissue transglutaminase (formerly known as endomysial) antibodies and serum IgA levels. However, many physicians fail to order tests for serum IgA levels. Because patients with gluten sensitivity often have low immunoglobulin levels, various antibody tests for IgA autoantibodies will be negative. For this reason, the presence of IgG gliadin antibodies alone in someone with a low IgA level (less than 10) should be referred to a gastroenterologist for further evaluation including intestinal biopsy if indicated. On biopsy, intestinal changes are often seen in people with gluten sensitivity, even when symptoms are mild. The ultimate confirmation for gluten sensitivity, however, is the absence of symptoms after following a gluten-free diet.

Lifelong dietary change with full removal of dietary gluten is necessary for treating gluten sensitivity. Untreated, gluten sensitivity can lead to secondary diseases resulting from disruption of the normal intestinal barrier. The presence of leaky gut, which allows for abnormal intestinal permeability, is a well-documented affect. This can lead to the ingestion of toxins and other antigens that can aggravate or cause disease in other organs. Scientists have studied the amount of gluten that can be safely ingested in patients sensitive to gluten and found that there is no safe amount. Amounts as low as 0.1 grams led to clinical relapses and changes in intestinal tissue.

Sources:

Lisa Medeiros, NP, Celiac Disease, A condition with multiple faces, Advance for Administrators of the Laboratory, June 2006.

James Braly and Ron Hogan, Dangerous Grains, Why Gluten Cereal Grains May Be Hazardous to Your Health, New York: Avery, 2002.




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Apr 7, 2009 5:20 AM
Guest :
Autoimmune diseases are the result of the body's own immune system attacking its own tissues (e.g., Myasthenia Gravis is autoimmune because self antibodies attack the ACh receptors on a person's skeletal muscle cell membrane). Since gluten is an external agent that is ingested, and the immune system is responding to gluten, this would not be considered autoimmune.

Also, I understand why anti-gluten IgA antibodies would be present in someone with a gluten sensitivity, but I am not clear on IgG. IgG is in the blood whereas IgA is in secretions (including intestinal secretions). How is gluten getting absorbed into the blood in order to elicit the formation of IgG antobodies? Maybe because of prior damage to the small intestine epithelium? I would appreciate it if anyone could explain this.
Apr 7, 2009 8:34 AM
Elaine Moore :
Hi,
gluten sensitivity enteropathy is indeed an autoimmune disorder. The external trigger is gluten. It causes the production, in sensitive people, of autoantibodies, specifically gliadin, endomysial, and tissue transglutaminase antibodies that react with the gastric mucosa, destroying villi. Both IgA and IgG antibodies are produced by the immune system and released into the blood. Many people with gluten sensitivity are deficient in IgA and their levels of IgA gliadin antibodies are too low to detect. Thus, the test for IgG gliadin antibodies is usually performed. Both alloantibodies and autoantibodies are found in the blood circulation as well as saliva. Best, Elaine
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