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An inverse association between history of childhood eczema and subsequent risk of type 1 diabetes that is not likely to be explained by HLA‐DQ, PTPN22 , or CTLA4 polymorphisms
Author(s) -
Stene Lars C,
Rønningen Kjersti S,
Bjørnvold Marit,
Undlien Dag E,
Joner Geir
Publication year - 2010
Publication title -
pediatric diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.678
H-Index - 75
eISSN - 1399-5448
pISSN - 1399-543X
DOI - 10.1111/j.1399-5448.2009.00605.x
Subject(s) - ptpn22 , medicine , odds ratio , type 1 diabetes , type 2 diabetes , case control study , confidence interval , human leukocyte antigen , diabetes mellitus , population , immunology , genotype , genetics , endocrinology , single nucleotide polymorphism , biology , environmental health , gene , antigen
Stene LC, Rønningen KS, Bjørnvold M, Undlien DE, Joner G. An inverse association between history of childhood eczema and subsequent risk of type 1 diabetes that is not likely to be explained by HLA‐DQ, PTPN22 , or CTLA4 polymorphisms. Background: Established genetic susceptibility loci for type 1 diabetes are important in immune regulation and may play a role also in atopic disorders, potentially explaining the inverse association between childhood eczema and subsequent risk for type 1 diabetes previously reported. Objective: We aimed to directly assess whether HLA‐DQ, CTLA4 , and PTPN22 genes could explain the putative association between childhood eczema and lower subsequent risk of type 1 diabetes observed in several case–control studies. Methods: We designed a case–control study with 339 incident cases of type 1 diabetes identified in the Norwegian childhood diabetes registry, and 985 population‐based control children. DNA was collected, and physician‐diagnosed childhood eczema was ascertained by a questionnaire administered to the parents of children with and without type 1 diabetes. Results: The previously reported association between childhood eczema and lower risk of type 1 diabetes was confirmed (odds ratio,OR, 0.61, 95% confidence interval, CI, 0.40–0.95] and this was consistent in subgroups defined by HLA‐DQ, CTLA4 , and PTPN22 genotypes. The OR was essentially not influenced by adjustment for genetic variation at these loci (OR simultaneously adjusted for the three genetic loci: 0.55, 95% CI: 0.32–0.92). The ratio of the unadjusted to adjusted OR was 1.12, with a corresponding 95% CI from 0.84 to 1.50. Conclusion: In this first study of its kind, we demonstrated directly that the observed inverse association between childhood eczema and type 1 diabetes is not likely to be explained by the established diabetes susceptibility genes HLA‐DQ , CTLA4 , or PTPN22 .