Author Affiliation: Division of Gastroenterology,
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass.
Celiac disease or gluten-sensitive enteropathy has emerged as a common
health problem, with an estimated prevalence of 1% in North America and Western
Europe.1,2 Although the etiology
is not fully understood, celiac disease is considered to be an autoimmune-type
disease with tissue transglutaminase (tTG) suggested as a major autoantigen.3 It is triggered in individuals who carry either HLA-DQ2
or HLA-DQ8 genes by the presence in the diet of wheat gluten and similar proteins
from rye and barley. However, the fact that only a few genetically susceptible
individuals develop celiac disease, even though virtually all individuals
are exposed to gluten, has long suggested that the etiology of celiac disease
is multifactorial and that other genetic and environmental factors play a
role in disease risk and also influence its broad clinical heterogeneity.
Farrell RJ. Infant Gluten and Celiac Disease: Too Early, Too Late, Too Much, Too Many Questions. JAMA. 2005;293(19):2410–2412. doi:10.1001/jama.293.19.2410
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