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“We found a significant association between exposure to enterovirus and subsequent risk of celiac disease,” wrote lead author Christian R. Kahrs of the University of Oslo and his coauthors, adding that “adenovirus was not associated with celiac disease.” The study was published in the BMJ.
From 2001 to 2007, 46,939 newborns in Norway were screened for the HLA-DQ2/DQ8 genotype, which is associated with an increased risk of celiac disease. The genotype was identified in 912 children, and blood and stool sample collection began at 3 months. Children who were still contributing blood samples by 2014-2016 were invited to be screened for celiac disease.
Of the 220 children screened, 25 were diagnosed with celiac disease. Enterovirus was detected in 370 (17%) of the 2,135 stool samples and was more frequent in children who developed celiac disease antibodies than in matched controls (adjusted odds ratio, 1.49; 95% confidence interval, 1.07-2.06; P = .02). There was a significant association between later development of celiac disease and the commonly identified enterovirus A (aOR, 1.62; 95% CI, 1.04-2.53; P = .03) and enterovirus B (aOR, 2.27; 95% CI, 1.33-3.88; P = .003). No adenovirus types were associated with development of celiac disease.
The authors acknowledged their study’s limitations, including the possibility that children might be diagnosed with celiac disease later than the study’s roughly 10-year follow-up and the limited number of children with the disease despite a large number of analyzed samples. They noted that, “given the limited number of cases, we call for corroboration in similar studies and preferably interventional studies to reach conclusions about causality.”
The study was funded by the Research Council of Norway, the Project for the Conceptual Development of Research Organization, and the Norwegian Coeliac Society. Two authors reported grant support from trusts and foundations in Norway and Switzerland; no conflicts of interest were reported.
SOURCE: Kahrs CR et al. BMJ. 2019 Feb 13. doi: 10.1136/bmj.l231.