Aging Begins at 30

Diarrhea Could Indicate Celiac Sprue Disease

Stools were not greasy or foul-smelling, and she was not intolerant of dairy products. She had no childhood diarrhea, but over 20 years, she had three separate episodes of diarrhea and weight loss with red-stained excess fat in her stool. Laboratory tests only showed low carotene and vitamin A, indicating malabsorption. Biopsy of her small bowel indicated celiac sprue disease (from koilia Greek for belly and spruw Dutch for thrush mouth ulcers).

Water-soluble wheat proteins can be divided. Those that are alcohol-soluble, which we called gliadins, cause the damage in celiac sprue disease. They also are found in barley, rye and in some oat preparations. Glutens are often added to prepared food for taste and emulsification.

Yearly incidence varies, suggesting additional environmental factors. Adenovirus might help trigger an immune response in the gut damaged by gluten.

Found predominately in white populations and some patients in India, it is rare or nonexistent in native African, Japanese and Chinese populations.

Celiac disease was found in several family members in 1935. It is found in 0.2 percent of the general population and in about 10 percent of celiac patients' relatives, and in 70 percent of affected identical twins. This led to finding a genetic cause with an increased prevalence of certain genes.

Disease distribution relates to the beginning of agriculture in Iraq, where wheat-growing began. If you had celiac disease you did not live and reproduce. Celiacs survived better further north, where wheat growing arrived later.

There are pockets where the disease is common in Sweden, western Ireland and Scotland. About 25 percent of Northern Europeans have these celiac genes. Insulin-dependent diabetes and dermatitis herpetiformis (intensely itchy red rashes), and some rarer things, also occur in families with these genes, so these diseases are found together. About 10 percent of diabetes patients have celiac disease.

Host immune responses to gliadin are probably causative, and cells making immune globulins to gliadin are increased in the gut of celiac patients. Lymphocytes are increased in biopsies, and the very fine hair-like absorptive villi are damaged and often missing, producing a "flat-gut."

Dr. Willem Dicke of the Netherlands noted during food shortages in World War II that celiac disease children could eat tulip-bulb flower but could not eat any wheat products.

Symptoms vary depending on how much gut is damaged. It is primarily a disease of young children and can interfere with growth. There is diarrhea, flatulence, weight loss, fatigue and malabsorption. The effects of malabsorption can overshadow the gut symptoms and appear as iron deficiency anemia, folate (a B vitamin) deficiency, or unexplained osteoporosis (bone loss), or diarrhea in type 1 diabetics.

The best test is blood IgA antiendomysial (anti-gut, smooth muscle covering). Antibody and milder cases are now being diagnosed. Small bowel biopsy is still the gold standard. Confirmation is by unequivocal clinical improvement after gluten diet withdrawal. A repeat biopsy to show gut lining returned to normal is desirable. Serial antibodies help monitor dietary compliance. A lifetime of dietary restriction is necessary. Such a diet is a challenge to patients, dietitians, and physicians, but books of recipes help.

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See related Patient Topics Celiac Disease, Digestive System or Food, Nutrition and Metabolism.

See related Provider Topics Celiac Disease, Digestive System or Food, Nutrition and Metabolism.

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