[Endemic sprue].

Coeliac disease or Gluten enteropathy is a well-defined, but in its pathogenesis poorly understood syndrome. Diarrhoea, steatoroea and malnutrition due to damage and transformation of the small intestinal mucosa are induced by cereal proteins (gliadin) in genetically predisposed children and adults. Local interactions between immunocompetent cells and structural elements of the small intestinal mucosa have been investigated by immunochemical, ultrastructural and cell biological methods. In this review we discuss the events produced by defined gliadin derivates in vivo and in vitro. They suggest a complex mucosal reaction pattern, involving inflammatory and hyperergic manifestations. The cytotoxicity of gliadin is discussed in the context of defined mediators of lymphocyte and inflammatory cell interactions. The importance of structural elements of the lamina propria and the epithelium as target tissues of the immunological attack and its impact on the local environment is elucidated. Gliadin hypersensitivity is regarded as a genetically determined disposition which can be correlated to the HLA system. The distribution of HLA class I and II antigens with respect to T- and B-lymphocyte functions is described. The diagnosis of coeliac disease and the scientific exploration of cell culture techniques have been greatly improved by modern endoscopy. However, the specificity and sensitivity of laboratory tests for coeliac disease are still controversial The value of determining autoantibodies and antigliadin antibodies is evaluated. Clinical syndromes associated with coeliac disease typically involve immunological phenomena and a comprehensive review of the relevant experiences will be presented. Finally, the general prognosis of coeliac disease and the risk of developing malignancies with respect to the necessity and feasibility of a stringent, lifelong gluten-free diet and patient compliance are discussed.