Abstract

were EMA positive (not tested for TGA). Taken together, 13 of the 181 T1D children studied had CD, giving a prevalence of 7.18% (IC 95%: 3.8-12.3). Among the 117 siblings of T1D children studied, one with IgA deficiency and high titer of AGA IgG was found to be affected by celiac disease before screening. A total of 116 siblings were tested for EMA and 6 of these (5.17%) were positive. We performed TGA test only in 107 siblings and 6 (5.60%) were positive. Of these, 5 were also positive for EMA and 1 was EMA negative. All the 7 siblings with positive antibodies underwent jejunal biopsy; celiac disease was found in 5 subjects. Of these, 3 were EMA and TGA positive, 1 was EMA negative and TGA positive and 1 was EMA positive (not tested for TGA); 2 subjects both EMA and TGA positive, had a negative biopsy for celiac disease. Taken together 6 of 117 siblings of T1D children studied had celiac disease, giving a prevalence of 5.13% (IC 95%: 1.9-11.2). Conclusions: We found the prevalence of CD significantly higher in T1D children and their siblings than in the Italian general population (1%; IC 95% 0,6-1,3), investigated in the same period. These findings agree with figures reported from the latest population-based studies performed and should be correlated to common genetic background of T1D children and their siblings. As the prevalence of CD in siblings of T1D children is higher than the general population, the screening for CD should be extended to all first-degree relatives of patients with T1D.

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