Abstract

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 others 2,3 associated the illness with cereals and eventually with the gliadin fraction of wheat. 3 With the advent of intestinal biopsy techniques, Rubin et al 4 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

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