Hu Shiqian, Rayman Margaret P
1 Department of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey , Guildford, United Kingdom .
2 Department of Endocrinology, First Affiliated Hospital of Xi'an Jiaotong University , Xi'an, Shaanxi, China .
Thyroid. 2017 May;27(5):597-610. doi: 10.1089/thy.2016.0635. Epub 2017 Apr 6.
Hashimoto's thyroiditis (HT) is considered to be the most common autoimmune disease. It is currently accepted that genetic susceptibility, environmental factors, and immune disorders contribute to its development. With regard to nutritional factors, evidence implicates high iodine intake and deficiencies of selenium and iron with a potential relevance of vitamin D status. To elucidate the role of nutritional factors in the risk, pathogenesis, and treatment of HT, PubMed and the Cochrane Library were searched for publications on iodine, iron, selenium, and vitamin D and risk/treatment of HT.
Chronic exposure to excess iodine intake induces autoimmune thyroiditis, partly because highly iodinated thyroglobulin (Tg) is more immunogenic. Recent introduction of universal salt iodization can have a similar, though transient, effect. Selenoproteins are essential to thyroid action. In particular, the glutathione peroxidases protect the thyroid by removing excessive hydrogen peroxide produced for Tg iodination. Genetic data implicate the anti-inflammatory selenoprotein S in HT risk. There is evidence from observational studies and randomized controlled trials that selenium/selenoproteins can reduce thyroid peroxidase (TPO)-antibody titers, hypothyroidism, and postpartum thyroiditis. Iron deficiency impairs thyroid metabolism. TPO, the enzyme responsible for the production of thyroid hormones, is a heme (iron-containing) enzyme which becomes active at the apical surface of thyrocytes only after binding heme. HT patients are frequently iron deficient, since autoimmune gastritis, which impairs iron absorption, is a common co-morbidity. Treatment of anemic women with impaired thyroid function with iron improves thyroid-hormone concentrations, while thyroxine and iron together are more effective in improving iron status. Lower vitamin D status has been found in HT patients than in controls, and inverse relationships of serum vitamin D with TPO/Tg antibodies have been reported. However, other data and the lack of trial evidence suggest that low vitamin D status is more likely the result of autoimmune disease processes that include vitamin D receptor dysfunction.
Clinicians should check patients' iron (particularly in menstruating women) and vitamin D status to correct any deficiency. Adequate selenium intake is vital in areas of iodine deficiency/excess, and in regions of low selenium intake a supplement of 50-100 μg/day of selenium may be appropriate.
桥本甲状腺炎（HT）被认为是最常见的自身免疫性疾病。目前认为，遗传易感性、环境因素和免疫紊乱促成了其发病。关于营养因素，有证据表明高碘摄入以及硒和铁缺乏与维生素D状态可能存在关联。为阐明营养因素在HT的风险、发病机制及治疗中的作用，我们检索了PubMed和Cochrane图书馆中有关碘、铁、硒、维生素D以及HT风险/治疗的文献。
长期暴露于过量碘摄入会诱发自身免疫性甲状腺炎，部分原因是高度碘化的甲状腺球蛋白（Tg）具有更强的免疫原性。近期普遍推行的食盐碘化也会产生类似但短暂的影响。硒蛋白对甲状腺功能至关重要。特别是谷胱甘肽过氧化物酶通过清除Tg碘化过程中产生的过量过氧化氢来保护甲状腺。遗传数据表明抗炎性硒蛋白S与HT风险有关。观察性研究和随机对照试验的证据显示，硒/硒蛋白可降低甲状腺过氧化物酶（TPO）抗体滴度、甲状腺功能减退及产后甲状腺炎的发生率。缺铁会损害甲状腺代谢。TPO是负责甲状腺激素生成的酶，它是一种血红素（含铁）酶，只有在与血红素结合后才会在甲状腺细胞的顶端表面变得活跃。HT患者常缺铁，因为损害铁吸收的自身免疫性胃炎是常见的合并症。用铁治疗甲状腺功能受损的贫血女性可提高甲状腺激素浓度，而甲状腺素和铁联合使用在改善铁状态方面更有效。已发现HT患者的维生素D水平低于对照组，并且有报道称血清维生素D与TPO/Tg抗体呈负相关。然而，其他数据以及缺乏试验证据表明，低维生素D水平更可能是包括维生素D受体功能障碍在内的自身免疫性疾病过程的结果。
临床医生应检查患者的铁（尤其是育龄女性）和维生素D水平，以纠正任何缺乏情况。在碘缺乏/过量地区以及硒摄入低的地区，充足的硒摄入至关重要，每天补充50 - 100μg的硒可能是合适的。
