Abstract

Celiac disease, an autoimmune enteropathy triggered by the consumption of gluten, can develop in genetically predisposed children (HLA DQ2 and/or DQ8 positive) at any point from 9 months of age through adulthood. Although the incidence of celiac disease in both North America and the bulk of Europe is approximately 1 in 100, patients with a first-degree relative with celiac disease are at a much higher risk of development. For example, up to 25% of children who are homozygous for HLA-DQ2 will develop evidence of celiac autoimmunity by age 6 [1]. Additional risk factors for the development of celiac disease include type 1 diabetes, autoimmune thyroid disease, Trisomy 21, Turner syndrome, William’s syndrome, and selective IgA deficiency [2]. The celiac genes (HLA-DQ2 and DQ8) contribute 40% of the risk of developing celiac. Environmental risk factors for celiac disease include infant feeding patterns, early infections,

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