LAUSR

Background/Aims: Hashimoto thyroiditis, characterized by positive thyroid peroxidase antibodies (TPOAbs), is caused by the interaction of genetic and environment factors. The aim of this study was to clarify the interaction of gene polymorphisms and iodine intake in the incidence of TPOAb positivity. Methods: 1,733 subjects were included in this study. Genomic DNA was extracted from peripheral blood white cells. Four SNPs (rs11675434 [TPO], rs3094228 [HCP5], rs9277555 [HLA-DPB1], and rs301799 [RERE]) were selected for genotyping. Weighted TPOAb genetic risk score (GRS) was calculated based on these 4 SNPs. Thyroid hormones and autoimmune antibodies (TPOAb and thyroglobulin antibody) were determined using the electrochemiluminescence immunoassay method. Results: The mean serum thyrotropin level in TPOAb-positive subjects was higher than in TPOAb-negative subjects (p < 0.01). Genotype GG of rs9277555 was associated with an increased risk of TPOAb positivity (OR = 1.64, 5–95% CI 1.09, 2.47, p = 0.02). Genotype TT of rs11675434 showed marginal increased risk of TPOAb positivity (OR = 1.57, 5–95% CI 1.01, 2.43, p = 0.048). Logistic regression analysis showed TPOAb-GRS and rs9277555 were associated with TPOAb positivity (OR = 5.09, 5–95% CI 1.30, 19.91, p = 0.02 and OR = 1.30, 5–95% CI 1.05, 1.61, p = 0.02). Subjects with a high TPOAb-GRS had a 52% increased risk of TPOAb positivity compared to subjects with a low TPOAb-GRS (OR 1.52, 5–95% CI 1.05, 2.21, p = 0.03). Conclusion: TPOAb-GRS was associated with an increased risk of TPOAb positivity in a Chinese Han population. This effect might be attribute to rs9277555.