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Multiple nutritional factors and thyroid disease, with particular reference to autoimmune thyroid disease

机译:多种营养因子和甲状腺疾病,特别是自身免疫性甲状腺疾病

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Hashimoto's thyroiditis (HT) and Graves’ disease (GD) are examples of autoimmune thyroid disease (AITD), the commonest autoimmune condition. Antibodies to thyroid peroxidase (TPO), the enzyme that catalyses thyroid-hormone production and antibodies to the receptor for the thyroid-stimulating hormone, are characteristic of HT and GD, respectively. It is presently accepted that genetic susceptibility, environmental factors, including nutritional factors and immune disorders contribute to the development of AITD. Aiming to investigate the effect of iodine, iron and selenium in the risk, pathogenesis and treatment of thyroid disease, PubMed and the Cochrane Library were searched for relevant publications to provide a narrative review. Iodine: chronic exposure to excess iodine intake induces autoimmune thyroiditis, partly because highly-iodinated thyroglobulin (Tg) is more immunogenic. The recent introduction of universal salt iodisation can have a similar, although transient, effect. Iron: iron deficiency impairs thyroid metabolism. TPO is a haem enzyme that becomes active only after binding haem. AITD patients are frequently iron-deficient since autoimmune gastritis, which reduces iron absorption and coeliac disease which causes iron loss, are frequent co-morbidities. In two-thirds of women with persistent symptoms of hypothyroidism despite appropriate levothyroxine therapy, restoration of serum ferritin above 100 μg/l ameliorated symptoms. Selenium: selenoproteins are essential to thyroid action. In particular, the glutathione peroxidases remove excessive hydrogen peroxide produced there for the iodination of Tg to form thyroid hormones. There is evidence from observational studies and randomised controlled trials that selenium, probably as selenoproteins, can reduce TPO-antibody concentration, hypothyroidism and postpartum thyroiditis. Appropriate status of iodine, iron and selenium is crucial to thyroid health.
机译:Hashimoto的甲状腺炎(HT)和Graves疾病(GD)是自身免疫性甲状腺疾病(AITD),最常见的自身免疫病症的例子。对甲状腺过氧化物酶(TPO)的抗体,将甲状腺激素产生的酶和对甲状腺刺激激素的受体抗体的酶分别是HT和GD的特征。目前已接受遗传易感性,环境因素,包括营养因素和免疫障碍有助于发展AITD。旨在探讨碘,钢和硒的影响,在甲状腺疾病的风险,发病机制和治疗中,搜查了有关出版物,以提供叙事审查的相关出版物。碘:慢性暴露于过量的碘摄入量诱导自身免疫性甲状腺炎,部分原因是高碘化甲状腺球蛋白(Tg)更加免疫原性。最近引入的通用盐碘化可以具有相似的,尽管瞬态,效果。铁:铁缺乏损害甲状腺代谢。 TPO是一种纯种酶,其仅在结合哈格中变得活跃。由于自身免疫性胃炎,AITD患者经常是耐铁缺乏症,这减少了导致铁损失的铁吸收和乳糜泻,是频繁的共同病态。在三分之二的女性中,尽管有适当的左甲喹氏疗法,但仍然有适当的左甲肾上腺素治疗,血清铁蛋白恢复以上100μg/升改善症状。硒:Selenoproteins对甲状腺作用至关重要。特别地,谷胱甘肽过氧化物酶除去在那里制备过量的过氧化氢以形成TG的碘化以形成甲状腺激素。有证据来自观察性研究和随机对照试验,即硒,可能是硒蛋白,可以降低TPO-抗体浓度,甲状腺功能亢进和产后甲状腺炎。碘,铁和硒的适当状态对于甲状腺健康至关重要。

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