Around one in 100 people suffers from coeliac disease, a condition in which the small INTESTINE fails to digest and absorb food adequately, but many have no or few symptoms and remain undiagnosed. The intestinal lining is permanently sensitive to the protein gliadin (an insoluble and potentially toxic PEPTIDE) which is contained in GLUTEN, a constituent of the germ of wheat, barley and rye. As bread or other grain-based foods are a regular part of most people's diet, the constant presence of gluten in the intestine of sufferers of coeliac disease causes atrophy of the digestive and absorptive cells of the intestine. Children are usually diagnosed when they develop symptoms such as diarrhoea, swollen abdomen and pale, frothy, foul-smelling faeces with failure to thrive, lethargy and ANAEMIA. The diagnosis is usually made by a positive blood antibody test such as the level of antiendomysial antibodies. However, because there may be an occasional false positive result, the ‘gold standard’ is to obtain a biopsy of the JEJUNUM through a tiny metal capsule that can be swallowed, a specimen taken, and the capsule retrieved. Though coeliac disease was long thought to occur in childhood, a second peak of the disorder has been identified among people in their 50s.

Not all sufferers from coeliac disease present with gastrointestinal symptoms: doctors, using screening techniques, have increasingly identified large numbers of such people. This is important because researchers have discovered that untreated, overt and silent coeliac disease increases the risk of developing OSTEOPOROSIS and lymphoma. The key treatment is a strict, lifelong diet free from gluten. As well as returning the bowel lining to normal, this diet results in a return to normal bone density. (See also GLUTEN; MALABSORPTION SYNDROME; SPRUE.)