Coeliac disease, or permanent gluten sensitive enteropathy, is recognised as a public health problem worldwide that affects people of all ages . The broad spectrum of symptoms, which are often vague, is easily misinterpreted,with delayed or missed diagnosis as a consequence.Untreated, the health implications are extensive. Effective treatment is available through lifelong adherence to a strict glutenfree diet, i.e. exclusion of all foods containing wheat, rye or barley. However, the widespread use of gluten-containing foods makes compliance with treatment difficult.A multifactorial aetiology is likely . This implies that coeliac disease results from interaction between an individual’s genetic disposition and complex and lifelong environmentalexposures, which jointly shape the immunopathological processes leading to intolerance to gluten proteins.A genetic susceptibility is a prerequisite for this condition [1, 2]. Almost all coeliac disease subjects express the HLA-DQ2 molecule, and the remainder HLA-DQ8. The search for contributing non-HLA genes has been extensive, but thus far without conclusive results. Inherent in these difficulties is that each genetic risk factor, taken separately, is frequent in the general population, which suggests that it is a combinationof some of these factors and their interaction with environmental factors that induces coeliac disease.