Rostami Rahim, Nourooz-Zadeh Sarmad, Mohammadi Afshin, Khalkhali Hamid Reza, Ferns Gordon, Nourooz-Zadeh Jaffar
Department of Clinical Biochemistry and Nutrition, Urmia University of Medical Sciences, 5714783734 Urmia, Iran.
Faculty of Medicine, University of Medical Sciences, 5714783734 Urmia, Iran.
Antioxidants (Basel). 2020 Oct 31;9(11):1070. doi: 10.3390/antiox9111070.
Selenium (Se) deficiency has been implicated in the pathogenesis of Hashimoto's thyroiditis (HT), although the available evidence is limited. The present study aimed to explore the interrelationships between serum Se status with measures of thyroid function and antioxidant defense in new cases of HT patients with hypoechogenic thyroid. HT patients ( = 49) and matched controls ( = 50) were recruited. Selenium, thyroid hormone panel, thyroid volume (TVol), glutathione (GSH), glutathione peroxidase3 (GPx3) activity, urinary iodine concentration (UIC), and urinary creatinine (Cr) were assessed. HT patients exhibited lower Se levels compared to controls ( < 0.001) with the rates of Se-deficient (<0.85 µmol/L) participants being 58.8% and 34%, respectively. Se-deficient patients exhibited higher thyroid stimulating hormone (TSH), Thyroid volume (TVol), thyroglobulin, antibody-titers, GPx3 activity and UIC/Cr compared to Se-sufficient patients (all < 0.001). In the Se-deficient patients, inverse correlations were seen between Se-levels with TSH, TVol, and Thyroid peroxidase antibody (TPO-Ab) (all < 0.001). This study is the first to uncover that coexisting Se-deficiency and elevated iodine in HT may enhance autoimmune reactions and accelerate the deterioration of thyroid function through oxidative stress. Our study also highlights the importance of optimal Se status in this disease, thus providing a rationale for the execution of intervention trials for the evaluation of the clinical benefits of antioxidant-status improvement in HT.
尽管现有证据有限，但已有研究表明硒（Se）缺乏与桥本甲状腺炎（HT）的发病机制有关。本研究旨在探讨甲状腺回声减低的HT新发病例中血清硒水平与甲状腺功能指标及抗氧化防御之间的相互关系。招募了HT患者（n = 49）和匹配的对照组（n = 50）。评估了硒、甲状腺激素指标、甲状腺体积（TVol）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶3（GPx3）活性、尿碘浓度（UIC）和尿肌酐（Cr）。与对照组相比，HT患者的硒水平较低（P < 0.001），硒缺乏（<0.85 µmol/L）参与者的比例分别为58.8%和34%。与硒充足的患者相比，硒缺乏的患者表现出更高的促甲状腺激素（TSH）、甲状腺体积（TVol）、甲状腺球蛋白、抗体滴度、GPx3活性和UIC/Cr（均P < 0.001）。在硒缺乏的患者中，硒水平与TSH、TVol和甲状腺过氧化物酶抗体（TPO-Ab）之间呈负相关（均P < 0.001）。本研究首次发现，HT患者中同时存在的硒缺乏和碘升高可能通过氧化应激增强自身免疫反应并加速甲状腺功能恶化。我们的研究还强调了最佳硒状态在这种疾病中的重要性，从而为开展干预试验以评估改善抗氧化状态对HT的临床益处提供了理论依据。
