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微量元素诱导桥本甲状腺炎发生发展的研究进展
Research progress on the incidence and progression of Hashimoto's thyroiditis induced by trace elements
桥本甲状腺炎(HT)是在遗传易感性的基础上,由环境因素触发的一种自身免疫性疾病。微量元素是环境因素的重要组成部分,其中碘过量、硒缺乏、镁缺乏和维生素D缺乏是诱导HT发生发展的危险因素。这些微量元素诱导HT发生发展的机制与甲状腺自身免疫反应、氧化应激反应和炎症反应的激活有关。对于HT易感人群及HT患者,要给予合理的饮食指导,从而延缓HT的发生发展。
Hashimoto's thyroiditis (HT) is an autoimmune disease triggered by environmental factors on the basis of genetic susceptibility. Trace elements are an important part of environmental factors, among which iodine excess, selenium deficiency, magnesium deficiency and vitamin D deficiency are the risk factors inducing the incidence and progression of HT. The mechanism of HT induced by these nutritional factors is related to the activation of thyroid autoimmune response, oxidative stress response and inflammatory response. For HT susceptible population and HT patients, rational dietary guidance should be given, and corresponding nutritional supplements should be delivered when necessary, aiming to delay the incidence and progression of HT.
桥本甲状腺炎 / 碘 / 硒 / 镁 / 维生素D {{custom_keyword}} /
Hashimoto's thyroiditis / Iodine / Selenium / Magnesium / Vitamin D {{custom_keyword}} /

| [1] |
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| [2] |
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| [3] |
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| [4] |
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| [5] |
李红岩, 王翠翠, 曹婷婷, 等. 不同碘营养状况桥本甲状腺炎患者甲状腺功能与自身抗体的相关性分析. 第十四届全国免疫学学术大会论文摘要汇编. 成都, 2021: 473.
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| [6] |
曹晓晓, 徐菁, 王海燕, 等. 碘过量对NOD•H-2h4小鼠甲状腺转录组影响的分析. 中国食物与营养, 2020, 26(5): 75-79.
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| [7] |
The global effort to prevent iodine deficiency disorders through iodine supplementation, such as universal salt iodization, has achieved impressive progress during the last few decades. However, iodine excess, due to extensive environmental iodine exposure in addition to poor monitoring, is currently a more frequent occurrence than iodine deficiency. Iodine excess is a precipitating environmental factor in the development of autoimmune thyroid disease. Excessive amounts of iodide have been linked to the development of autoimmune thyroiditis in humans and animals, while intrathyroidal depletion of iodine prevents disease in animal strains susceptible to severe thyroiditis. Although the mechanisms by which iodide induces thyroiditis are still unclear, several mechanisms have been proposed: (1) excess iodine induces the production of cytokines and chemokines that can recruit immunocompetent cells to the thyroid; (2) processing excess iodine in thyroid epithelial cells may result in elevated levels of oxidative stress, leading to harmful lipid oxidation and thyroid tissue injuries; and (3) iodine incorporation in the protein chain of thyroglobulin may augment the antigenicity of this molecule. This review will summarize the current knowledge regarding excess iodide as an environmental toxicant and relate it to the development of autoimmune thyroid disease.
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| [8] |
刘方, 张熙冰, 牛玲, 等. 成年人尿碘水平与甲状腺疾病的相关性. 昆明医科大学学报, 2021, 42(3): 104-108.
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| [9] |
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| [10] |
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| [11] |
Selenium (Se) can be found in the molecular structure of selenoproteins; including thioredoxin reductase and glutathione peroxidase and also in Type I and II deiodinases. Previous studies have shown that Se deficiency has been linked to autoimmune thyroid disease (AITD). In the present study, we investigated the serum Se levels of patients with Graves' disease (GD), Hashimoto's thyroiditis (HT), and euthyroid individuals as a control group.The present study was performed on patients with newly diagnosed AITD (GD and HT). The control group was matched with the case group in terms of parameters such as age and sex. Free thyroxine, free triiodothyronine, thyroid-stimulating hormone, antithyroid peroxidase, antithyroglobulin, and serum Se levels were measured in all participants. These parameters were compared between groups.Data from 132 patients with HT, 120 patients with GD, and 120 healthy euthyroid patients as a control group were analyzed. The Se level in patients with HT (104.36 μg/l) and GD (97.68 μg/l) was significantly lower than in the control group (122.63 μg/l) (< 0.001). The incidence of Se deficiency in patients with HT, GD, and in the control group was 15.2%, 2.5%, and 2.5%, respectively (< 0.001). In patients with GD, 34 patients (28.33%) had Graves' orbitopathy. Se levels in patients with orbitopathy were significantly lower than in patients without orbitopathy.The serum Se level was significantly lower in newly diagnosed patients with GD and HT than in the control group. Overall, Se deficiency can be considered a risk factor for AITDs.Copyright: © 2022 Journal of Research in Medical Sciences.
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| [12] |
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| [13] |
韩夏, 刘喆隆. 硒酵母片治疗甲状腺功能正常的桥本甲状腺炎的真实世界研究. 医药导报, 2021, 40(8): 1065-1069.
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| [14] |
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| [15] |
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| [16] |
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| [17] |
The aims of this study were to evaluate: (1) associations of vitamin D with the presence/severity of Hashimoto's thyroiditis (HT) and (2) correlations of vitamin D with thyroid-related phenotypes. Total 25(OH)D (vitamin D in the text) was measured from stored serum samples of 461 HT patients and 176 controls from a Croatian Biobank of HT patients (CROHT). (1) Vitamin D levels, and proportions of vitamin D deficiency, were compared between HT cases and controls. HT patients were additionally divided into two groups (MILD and OVERT) to take into account HT severity. (2) Correlations between vitamin D and 10 clinical phenotypes in all HT patients and two subgroups of HT patients were tested using the Spearman correlation test. Our analyses were adjusted for age, gender, BMI, smoking status and seasonality of blood sampling. (1) No significant differences in vitamin D levels, or proportions of vitamin D deficiency, were detected between HT patients of all disease stages and controls. However, a nominally significant difference in vitamin D levels between MILD and OVERT subgroups (OR = 1.038, p = 0.023) was observed. Proportions of individuals with vitamin D deficiency during winter–spring were high: all HT cases (64.69%), MILD (60.64%), OVERT (68.7%), controls (60.79%). (2) A nominally significant negative correlation between vitamin D and TSH in all HT patients (r = −0.113, p = 0.029) and a positive correlation between vitamin D and systolic blood pressure in OVERT HT patients (r = 0.205, p = 0.025) were identified. Our study indicates that there is no association between vitamin D and HT; however, there may be a subtle decrease in vitamin D levels associated with overt hypothyroidism.
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| [19] |
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| [20] |
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| [21] |
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