Genetic Background of Celiac Disease and Its Clinical Implications

Victorien M. Wolters, M.D.; Cisca Wijmenga, Ph.D.


Am J Gastroenterol. 2008;103(1):190-195. 

In This Article

Possible Causal Factors

Sweden experienced a threefold increase in incidence of CD in children younger than 2-yr old in the mid-1980s.[27] This was partly explained by changing recommendations on gluten introduction in infants (in 1982) from 4 to 6 months of age; as a result more infants were introduced to gluten without ongoing breastfeeding. At the same time, the content of gluten in baby food was increased. In 1996, the Swedish authorities recommended a gradual introduction of gluten from the age of 4 months while breastfeeding, and the incidence of CD soon dropped dramatically. The current European recommendation states that breastfeeding during gluten introduction might be beneficial to children at high risk for CD, although it is unclear if breastfeeding prevents CD or simply delays the onset of disease.[46]

Interestingly, in the Swedish epidemic of CD, children born during the summer had a greater risk for CD, which might be because gluten was introduced during the winter when infections are more common.[47] Two explanations for this greater CD risk were suggested: infections might change gut permeability leading to the passage of immunogenic gluten peptides through the epithelial barrier. The other possibility implies that sequence similarities exist between proteins produced during adenovirus infections and proteins of gluten. In 1987, Kagnoff et al. suggested a role for human intestinal adenovirus.[48] Recently, a prospective study showed that multiple rotavirus infections predicted a higher risk of CD.[49]

The onset of CD has been reported during a course of treatment of hepatitis C with interferon (IFN).[50,51,52] This medication might increase epithelial permeability and proinflammatory cytokine production.[53,54] In hepatitis C patients, the activation of silent CD during IFN treatment should be suspected although symptoms subsided in almost all patients after IFN was withdrawn and without a gluten-free diet.[55] However, the histological abnormalities were still seen several months after discontinuing IFN, which means a timely diagnosis of CD after IFN.

So far there is no good animal model for CD although some experience is available with gluten-sensitive enteropathy (GSE) in Irish setter dogs.[56]


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