Gluten-sensitive enteropathy or coeliac disease is a chronic condition affecting genetically-susceptible children and adults.
Their inability to digest gluten leads to chronic inflammation and damage to the small intestinal mucosa, with flattening of the
gut epithelium. The disease is caused by a pathological intolerance to gliadin, the alcohol-soluble fraction of gluten in wheat,
rye and barley. Untreated subjects affected by coeliac disease may suffer from failure to thrive, diarrhoea, gastrointestinal
disorders, anaemia, chronic fatigue, psychiatric problems, or they may be asymptomatic. Dermatitis herpetiformis is a skin
disease also associated with coeliac disease. Gluten-free diet leads to complete remission of the disease, and thus has to
be maintained for life. Consumption of gliadin will cause the symptoms to recur. The disease is HLA-associated, and may
strike at any age with peak onset in early childhood.
Coeliac disease is diagnosed by small intestinal biopsy, showing a flat mucosa. Tissue transglutaminase, a calcium-dependent
enzyme widely distributed in human organs, has been identified as the major autoantigen associated with coeliac
disease. IgA antibodies against tissue transglutaminase are a highly specific serological marker for coeliac disease and dermatitis
herpetiformis. In addition, IgA correlates with disease activity and thus is of paramount importance for diet monitoring.
Screening for tissue transglutaminase IgA in clinically suspected cases of coeliac disease in children or adults may help in
detection of untreated subclinical cases.