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桥本自身免疫性甲状腺炎与维生素D缺乏。当前研究进展。

Hashimoto's autoimmune thyroiditis and vitamin D deficiency. Current aspects.

作者信息

Mazokopakis Elias E, Kotsiris Dimitrios A

机构信息

Iroon Polytechniu 38A, Chania, 73 132, Crete, Greece.

出版信息

Hell J Nucl Med. 2014 Jan-Apr;17(1):37-40. doi: 10.1967/s002449910120. Epub 2014 Feb 25.

Abstract

Hashimoto's thyroiditis (HT) is a chronic autoimmune thyroid disease caused by an interaction between genetic factors and environmental conditions, both of which are not yet completely understood. The significant association between vitamin D deficiency and HT has been investigated regarding the immune role of this hormone. In HT, an immunologic reaction is triggered when thyrocytes express major histocompatibility complex (MHC) class II surface HLA-DR antigens, a process induced by the production from T helper (Th)1 type lymphocytes, of inflammatory cytokines (especially IFN-γ), which may be inhibited by 1,25[OH]2D. Genetic polymorphism of vitamin D receptor (VDR), binding protein (DBP) and of 1α-hydroxylase (CYP1α) may also predispose to the development of HT. Considering current evidence, presented in this review, screening for vitamin D deficiency and careful vitamin D supplementation, when required, may be recommended for patients with HT. Further research is needed in patients with HT in order to investigate the mechanisms by which vitamin D affects autoimmunity and also to evaluate the cost-effectiveness of vitamin D supplementation and to suggest the possible optimal dose treatment.

摘要

桥本甲状腺炎(HT)是一种慢性自身免疫性甲状腺疾病,由遗传因素和环境因素相互作用引起,目前这两者尚未完全明确。维生素D缺乏与HT之间的显著关联已针对该激素的免疫作用进行了研究。在HT中,当甲状腺细胞表达主要组织相容性复合体(MHC)II类表面HLA - DR抗原时会引发免疫反应,这一过程由辅助性T(Th)1型淋巴细胞产生的炎性细胞因子(尤其是干扰素 - γ)诱导,而1,25[OH]2D可能会抑制该过程。维生素D受体(VDR)、结合蛋白(DBP)和1α - 羟化酶(CYP1α)的基因多态性也可能易患HT。鉴于本综述中呈现的现有证据,对于HT患者,可能建议筛查维生素D缺乏,并在必要时谨慎补充维生素D。对于HT患者还需要进一步研究,以探究维生素D影响自身免疫的机制,评估补充维生素D的成本效益,并提出可能的最佳剂量治疗方案。

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