Abstract
Celiac disease (gluten-sensitive enteropathy, celiac sprue, nontropical sprue) is characterized by damage to the small intestinal mucosa and malabsorption of most nutrients (reviewed in Cole and Kagnoff 1985; Kagnoff 1989). The disease is activated by dietary exposure to wheat gluten and similar proteins in several other grains. Wheat gluten is a mixture of gliadin and glutenin (Kasarda 1981). It is the gliadin fraction that is responsible for activating this disease (Kasarda 1981). The symptoms commonly appear during the first 3 years of life after the introduction of cereals into the diet, with a second peak incidence occurring during the 3rd and 4th decades. Clinical manifestations predominantly reflect the consequences of malabsorption. Treatment consists of a gluten-free diet (i.e., a diet free of gluten and related, disease-associated grains) (Cole and Kagnoff 1985).
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Kagnoff, M.F. (1989). Celiac Disease: Adenovirus and Alpha Gliadin. In: Oldstone, M.B.A. (eds) Molecular Mimicry. Current Topics in Microbiology and Immunology, vol 145. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-74594-2_6
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DOI: https://doi.org/10.1007/978-3-642-74594-2_6
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