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Mortality in Celiac Disease, Intestinal Inflammation, and Gluten Sensitivity
Peter H. R. Green, MD
JAMA. 2009;302(11):1225-1226.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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Celiac disease develops in genetically predisposed individuals as a response to ingested gluten. Gluten is the term for the storage proteins of the cereal grains wheat, rye, and barley.1 While virtually 100% of the population ingests these grains in one form or another and 30% to 40% of the population carry the genetic markers of the disease (HLA-DQ2 or type 8),2 only 2% to 3% of those with genetic markers develop the disease.2 This indicates that other genetic factors and environmental precipitants are necessary for disease expression. These factors are largely unknown, although breastfeeding, timing of gluten introduction, and gastrointestinal infections in childhood have been incriminated,3-4 at least in the development of childhood celiac disease.
The diagnosis of celiac disease is dependent on finding characteristic, although not specific, pathological findings in duodenal biopsies.5 These changes include inflammatory changes within the small-intestinal epithelium (intraepithelial lymphocytosis) and . . . [Full Text of this Article]
Author Affiliation: Department of Medicine, Celiac Disease Center, Columbia University College of Physicians and Surgeons, New York, New York.
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