Vargas-Uricoechea Hernando, Castellanos-Pinedo Alejandro, Meza-Cabrera Ivonne A, Pinzón-Fernández María V, Urrego-Noguera Karen, Vargas-Sierra Hernando
Metabolic Diseases Study Group, Department of Internal Medicine, Universidad del Cauca, Carrera 6 No 13N-50, Popayán 190001, Colombia.
Faculty of Medicine, Universidad del Sinú, Hospital San Jerónimo, Montería 230001, Colombia.
Diseases. 2025 May 23;13(6):166. doi: 10.3390/diseases13060166.
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.
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.
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.
INPLASY202540074.
桥本甲状腺炎（HT）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））失去耐受性，通常可检测到针对这些甲状腺自身抗原的循环抗体（Abs）（TPOAb和/或TgAb），同时伴有显著的淋巴细胞浸润，导致甲状腺功能减退风险增加。在描述的HT发病的多种机制中，包括碘在内的几种微量营养素的营养状况是其中之一。碘缺乏或过量与甲状腺功能紊乱以及可能的甲状腺自身免疫有关。因此，碘盐摄入[尤其是通过全民食盐加碘（USI）计划]可能会影响HT的患病率。本系统评价的目的是描述和分析实施USI计划后HT患病率随时间的变化。
查阅了以下数据库中1965年1月至2025年1月发表的文章：Pubmed/Medline；ProQuest；Scopus；Biosis；Web of Science；以及谷歌学术。检索词如下：“碘”、“盐”、“摄入”、“患病率”以及“桥本甲状腺炎”。仅纳入英文文章，并根据JBI批判性评价清单对每篇文章进行审查。仅纳入那些描述了设计、研究人群、参与者数量、国家、USI后评估时间（年）以及甲状腺抗体阳性患病率的研究。总共确定了74项研究，其中31项评估了USI后的甲状腺抗体值。
在没有充分随访和监测计划的情况下，由USI计划介导的碘摄入过量可能（至少部分地）解释了HT的患病率和分布情况；因此，在人群中实现健康盐摄入、USI计划策略以及可能的功能结果和甲状腺自身免疫之间的平衡是一项真正的挑战。
INPLASY202540074。
