Evaluation of thyroid antibodies and benign disease prevalence among young adults exposed to (131)I more than 25 years after the accident at the Chernobyl Nuclear Power Plant

切尔诺贝利核电站事故发生25年后,对暴露于碘-131的年轻成年人进行甲状腺抗体和良性疾病患病率的评估

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Abstract

Background. The Chernobyl Nuclear Power Plant (CNPP) accident exposed a large number of inhabitants to internal (131)I radiation. The associations between internal (131)I exposure and thyroid autoimmunity and benign thyroid diseases remain controversial in the population living in the contaminated area around the CNNP. In this study, we evaluate the association of (131)I with benign thyroid diseases. Methods. We compared the prevalence of Anti-Thyroid Autoantibodies (ATAs), thyroid function, and prevalence of thyroid ultrasound finding outcomes in 300 residents of the contaminated area of Ukraine who were 0-5 years of age at the time of the CNPP accident (group 1) and 300 sex-matched residents who were born after the accident (group 2). Results. We did not find any differences of the prevalence of Antithyroglobulin Antibodies (TGAb) positive, Antithyroid Peroxidase Antibodies (TPOAb) positive, and TGAb and/or TPOAb positive between the study groups. (11.7% vs 10.3%; p = 0.602, 17.3% vs 13.0%; p = 0.136, 21.0% vs 17.3%; p = 0.254, respectively); after adjusting for age and sex, the prevalence was not associated with the (131)I exposure status in the study groups. The prevalence of subclinical and overt hypothyroidism cases was not significantly different (p = 0.093 and p = 0.320) in the two groups, nor was the prevalence of goiter (p = 0.482). On the other hand, the prevalence of nodules was significantly higher in group 1 (p = 0.003), though not significantly so after adjustment for age and sex. Discussion. Working 26-27 years after the CNNP accident, we found no increased prevalence of ATAs or benign thyroid diseases in young adults exposed to (131)I fallout during early childhood in the contaminated area of Ukraine. Long-term follow-up is needed to clarify the effects of radiation exposure on autoimmunity reaction in the thyroid.

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