The precise mechanism of mucosal damage is unclear but immunological responses to gluten play a key role . There is a strong genetic component, with around 10% of first-degree relatives of an index case affected, and there is strong (approximately 75%) concordance in monozygotic twins. There is a strong association with human leukocyte antigen (HLA)-DQ2/DQ8. Dysbiosis of the intestinal microbiota has been identified but it is unclear if this is pathological or a response to the underlying mucosal changes Clinical features Coeliac disease can present at any age. In infancy, it occurs after weaning on to cereals and typically presents with diarrhoea, malabsorption and failure to thrive. In older children, it may present with non-specific features, such as delayed growth. Features of malnutrition are found on examination and mild abdominal distension may be present. Affected children have growth and pubeal delay, leading to sho stature in adulthood. In adults, the disease usually presents during the third or fouh decade and females are affected twice as often as males. The presentation is highly variable, depending on the severity and extent of small bowel involvement. Some have florid malabsorption, while others develop non-specific symptoms, such as tiredness, weight loss, folate deficiency or iron deficiency anaemia. Other presentations include oral ulceration, dyspepsia and bloating. Unrecognised coeliac disease is associated with mild under-nutrition and osteoporosis. Coeliac disease is associated with other HLA-linked autoimmune disorders and with ceain other diseases (Box 21.42). In some centres, people at higher risk of developing coeliac disease, such as those with type 1 diabetes, may undergo periodic antibody screening. Such screening may identify people with asymptomatic or minimally symptomatic disease; there is controversy about the optimum management strategy for such individuals. Ref Davidson edition23rd pg 806