Hernando Vargas-Uricoechea, Alejandro Castellanos-Pinedo, Ivonne A Meza-Cabrera, María V Pinzón-Fernández, Karen Urrego-Noguera, Hernando Vargas-Sierra
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Thus, iodized salt intake [especially through universal salt iodization (USI) programs] may be influencing the prevalence of HT. The objectives of this systematic review are to describe and analyze changes over time in the prevalence of HT following the implementation of USI programs.</p><p><strong>Methods and results: </strong>The following databases were consulted for articles published from January 1965 to January 2025: Pubmed/Medline; ProQuest; Scopus; Biosis; Web of Science; and Google Scholar. The search terms were as follows: \"iodine\", \"salt\", \"intake\", \"prevalence\", AND Hashimoto's thyroiditis. Only English language articles were taken into account, and each of them was scrutinized according to the JBI Critical Appraisal Checklist. Only those studies in which the design, study population, number of participants, country, evaluation post-USI (years)<i>,</i> and the prevalence of thyroid Abs positivity were described were included. 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引用次数: 0
摘要
背景：桥本甲状腺炎（桥本甲状腺炎）的特征是对甲状腺自身抗原[甲状腺过氧化物酶（TPO）和甲状腺球蛋白（Tg）]的耐受性丧失，通常识别针对这些甲状腺自身抗原（TPOAb和/或TgAb）的循环抗体（Abs），并伴有明显的淋巴细胞浸润，导致甲状腺功能减退的风险增加。在描述HT发展的多种机制中，几种微量营养素的营养状况，包括碘。碘缺乏或过量与甲状腺功能障碍有关，可能与甲状腺自身免疫有关。因此，碘盐摄入[特别是通过普遍食盐碘化（USI）计划]可能会影响HT的患病率。本系统综述的目的是描述和分析实施USI项目后HT患病率随时间的变化。方法与结果：查询1965年1月至2025年1月发表的文章：Pubmed/Medline；它;斯高帕斯;生命现象;Web of Science；b谷歌Scholar。搜索词为：“碘”、“盐”、“摄入量”、“患病率”和桥本甲状腺炎。只有英文文章被考虑在内，每一篇文章都是根据JBI关键评估清单进行审查的。仅包括那些描述了设计、研究人群、参与者数量、国家、usi后评估（年）和甲状腺抗体阳性患病率的研究。总共鉴定了74项研究，其中31项评估了usi后的甲状腺抗体值。结论：过量的碘摄入，由USI项目介导，没有适当的随访和监测计划，可能解释（至少部分）HT的流行和分布；因此，在人群中建立健康盐摄入量、USI计划策略、可能的功能结果和甲状腺自身免疫之间的平衡是一个真正的挑战。注册号：INPLASY202540074。
Iodine Intake from Universal Salt Iodization Programs and Hashimoto's Thyroiditis: A Systematic Review.
Background: Hashimoto's thyroiditis (HT) is characterized by the loss of tolerance to thyroid autoantigens [thyroid peroxidase (TPO) and thyroglobulin (Tg)], usually identifying circulating antibodies (Abs) against these thyroid autoantigens (TPOAb and/or TgAb), together with a significant lymphocytic infiltration, causing an increased risk of hypothyroidism. Among the multiple mechanisms described for the development of HT is the nutritional status of several micronutrients, including iodine. Iodine deficiency or excess is associated with thyroid function disorders and, likely, thyroid autoimmunity. Thus, iodized salt intake [especially through universal salt iodization (USI) programs] may be influencing the prevalence of HT. The objectives of this systematic review are to describe and analyze changes over time in the prevalence of HT following the implementation of USI programs.
Methods and results: The following databases were consulted for articles published from January 1965 to January 2025: Pubmed/Medline; ProQuest; Scopus; Biosis; Web of Science; and Google Scholar. The search terms were as follows: "iodine", "salt", "intake", "prevalence", AND Hashimoto's thyroiditis. Only English language articles were taken into account, and each of them was scrutinized according to the JBI Critical Appraisal Checklist. Only those studies in which the design, study population, number of participants, country, evaluation post-USI (years), and the prevalence of thyroid Abs positivity were described were included. In total, 74 studies were identified, of which 31 evaluated thyroid Abs values post-USI.
Conclusions: Excess iodine intake, mediated by USI programs without an adequate follow-up and monitoring plan, may explain (at least in part) the prevalence and distribution of HT; therefore, it is a real challenge to establish a balance between healthy salt intake, USI program strategies, and possible functional outcomes and thyroid autoimmunity in the population.
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