Celiac disease, more appropriately termed gluten-sensitive enteropathy (GSE), was originally described in 1888 by Gee,1 but it was only after World War II that Dicke and others2,3 associated the illness with cereals and eventually with the gliadin fraction of wheat.3 With the advent of intestinal biopsy techniques, Rubin et al4 demonstrated the direct toxic effect of wheat instillation in the proximal ileum of patients whose conditions were in remission. Toxicity is related to peptic-tryptic digests of gliadin as well as the whole gliadin fraction, with the greatest toxicity residing in fraction 9 (separated by column chromatography). Removal of the carbohydrate side chains of gluten has been shown to eliminate its toxicity.
Several theories have been proposed for the etiology of GSE.5 A specific peptidase deficiency was considered, but no single enzyme deficiency has been identified. During the acute stage of the disease, all of