Adequate iodine intake is necessary for normal thyroid function. Iodine deficiency is associated with serious complications, but also iodine excess can lead to thyroid dysfunction, and iodine supplementation aimed to prevent iodine deficiency disorders has been associated with development of thyroid autoimmunity. The epidemiology of thyroid diseases has undergone profound changes since the implementation of iodoprophylaxis, notably by means of iodine-enriched salt, specifically resulting in decreased prevalence of goiter and neonatal hypothyroidism, improved cognitive function development in infancy, and reduced incidence of more aggressive forms of thyroid cancer. The main question we address with this review is the clinical relevance of the possible effect on autoimmunity exerted by the use of iodine-enriched salt to correct iodine deficiency. In animal models, exogenous iodine is able to trigger or exacerbate thyroid autoimmunity, but it is still not clear whether the observed immunological changes are due to a direct effect of iodine on immune response, or whether they represent a secondary response to a toxic effect of iodine on thyroid tissue. Previous iodine status of a population seems to influence the functional thyroid response to increased iodine intake and possibly the development of thyroid autoimmunity. Moreover, the prevalence of thyroid antibodies, regarded as hallmark of autoimmune thyroid disease, varies between populations under the influence of genetic and environmental factors, and the presence of thyroid antibodies does not always coincide with the presence of thyroid disease or its future development. In addition, the incidence of autoimmune diseases shows a general increasing trend in the last decades. For all these reasons, available data are quite heterogeneous and difficult to analyze and compare. In conclusion, available data from long-term population surveys show that a higher than adequate population iodine intake due to a poorly controlled program of iodine prophylaxis could induce thyroid dysfunction, including thyroid autoimmunity mostly represented by euthyroid or subclinical hypothyroid autoimmune thyroiditis. Close monitoring iodine prophylaxis is therefore advised to ensure that effects of both iodine deficiency and iodine excess are avoided.

充足的碘摄入量是正常甲状腺功能所必需的。碘缺乏症与严重的并发症有关，但碘过量会导致甲状腺功能障碍，旨在预防碘缺乏症的碘补充剂与甲状腺自身免疫的发展有关。自实施碘预防措施以来，甲状腺疾病的流行病学发生了深刻的变化，特别是通过富含碘的盐，特别是降低了甲状腺肿和新生儿甲状腺功能减退症的患病率，改善了婴儿期的认知功能发展，并降低了更具侵略性形式的发病率。甲状腺癌。我们在这篇综述中解决的主要问题是使用富碘盐纠正碘缺乏症可能对自身免疫产生影响的临床相关性。在动物模型中，外源性碘能够引发或加剧甲状腺自身免疫，但尚不清楚观察到的免疫学变化是由于碘对免疫反应的直接影响，还是它们是否代表对碘的毒性作用的继发性反应。碘对甲状腺组织。人群以前的碘状况似乎会影响甲状腺功能对碘摄入量增加的反应，并可能影响甲状腺自身免疫的发展。此外，被视为自身免疫性甲状腺疾病标志的甲状腺抗体的患病率在遗传和环境因素的影响下因人群而异，甲状腺抗体的存在并不总是与甲状腺疾病的存在或其未来发展相吻合。此外，近几十年来，自身免疫性疾病的发病率总体呈上升趋势。由于所有这些原因，可用数据非常多样化，难以分析和比较。总之，来自长期人口调查的现有数据表明，由于碘预防计划控制不佳而导致人群碘摄入量过高可能导致甲状腺功能障碍，包括主要以甲状腺功能正常或亚临床甲状腺功能减退性自身免疫性甲状腺炎为代表的甲状腺自身免疫。因此，建议密切监测碘预防，以确保避免碘缺乏和碘过量的影响。来自长期人口调查的现有数据表明，由于碘预防计划控制不佳而导致人群碘摄入量过高可能导致甲状腺功能障碍，包括主要以甲状腺功能正常或亚临床甲状腺功能减退性自身免疫性甲状腺炎为代表的甲状腺自身免疫。因此，建议密切监测碘预防，以确保避免碘缺乏和碘过量的影响。来自长期人口调查的现有数据表明，由于碘预防计划控制不佳而导致人群碘摄入量过高可能导致甲状腺功能障碍，包括主要以甲状腺功能正常或亚临床甲状腺功能减退性自身免疫性甲状腺炎为代表的甲状腺自身免疫。因此，建议密切监测碘预防，以确保避免碘缺乏和碘过量的影响。