Gluten intolerance (coeliac disease).

Coeliac disease is a permanent condition of gluten intolerance associated with characteristic gluten-sensitive changes in the jejunal mucosa. In Edinburgh and the Lothians Region of Scotland, the prevalence of the disease is one in 1637 (61/100,000) with considerable variation in age, and sex-specific prevalence and incidence. Several lines of evidence indicate an immunologic basis for the gluten-sensitive enteropathy in coeliac disease. Animal models of intestinal T cell-mediated reactions in the gut have shown pathologic features similar to those of coeliac disease. These include changes in villus and crypt architecture with crypt hyperplasia, and increased numbers of intraepithelial lymphocytes and of intraepithelial lymphocyte mitosis. Experimental CMI reactions also influence differentiation of goblet cells and expression of Ia antigen on epithelial cells, but these factors have not yet been reported for the coeliac mucosa. In addition to this circumstantial evidence, based on animal work, other factors which suggest that CMI reactions rather than antibodies are relevant to coeliac disease include the findings of antigliadin antibodies in a proportion of normal individuals, patients without gastrointestinal disease (seen in hospital), and patients with jejunal Crohn's disease. In addition, there is a well documented patient with adult onset primary hypogammaglobulinaemia and coeliac disease. The underlying pathogenesis in coeliac disease can be envisaged as failure of the normal inhibition of immune responses to this particular food antigen in the gut. Manipulation of immunoregulatory mechanisms would provide a new approach to treatment or cure of this disease and of other food protein-sensitive enteropathies.