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给严重碘缺乏儿童引入加碘盐不会引发甲状腺自身免疫:摩洛哥北部的一项为期一年的前瞻性试验。

Introduction of iodized salt to severely iodine-deficient children does not provoke thyroid autoimmunity: a one-year prospective trial in northern Morocco.

作者信息

Zimmermann Michael B, Moretti Diego, Chaouki Noureddine, Torresani Toni

机构信息

The Human Nutrition Laboratory, Swiss Federal Institute of Technology, Zürich, Switzerland.

出版信息

Thyroid. 2003 Feb;13(2):199-203. doi: 10.1089/105072503321319512.

DOI:10.1089/105072503321319512
PMID:12699595
Abstract

To determine if introduction of iodized salt induces thyroid autoimmunity in goitrous children, we conducted a prospective trial in iodine-deficient Moroccan schoolchildren (n = 323). Local salt was iodized at 25 microg iodine per gram of salt and distributed to households. Before introduction of iodized salt and at 10, 20, 40, and 52 weeks, we measured antithyroid peroxidase antibodies (TPO-Ab), antithyroglobulin antibodies (Tg-Ab), urinary iodine (UI), and thyroid hormones, and examined the thyroid using ultrasound. At baseline, median UI was 17 microg/L and the prevalence of goiter and hypothyroidism was 72% and 18%, respectively. Provision of iodized salt maintained median UI at 150-200 microg/L for the year (p < 0.0001). There was a significant increase in mean total thyroxine (T(4)) and a significant reduction in the prevalence of hypothyroidism (p < 0.001). There was a transient increase in the prevalence of detectable antibodies after introduction of iodized salt (p < 0.0001) with levels returning to baseline at 1 year. Only congruent with 1% of children had elevated TPO-Ab and none had elevated Tg-Ab over the course of the study, and no child with elevated TPO-Ab had abnormal thyrotropin (TSH) or T(4) concentrations. None developed clinical or ultrasonographic evidence of thyroid autoimmune disease and/or iodine-induced hypothyroidism or hyperthyroidism. Rapid introduction of iodized salt does not provoke significant thyroid autoimmunity in severely iodine-deficient children followed for 1 year.

摘要

为了确定加碘盐的引入是否会在甲状腺肿儿童中诱发甲状腺自身免疫,我们在缺碘的摩洛哥学童(n = 323)中进行了一项前瞻性试验。将当地的盐按每克盐含25微克碘进行碘化处理,然后分发给各个家庭。在引入加碘盐之前以及在第10、20、40和52周时,我们测量了抗甲状腺过氧化物酶抗体(TPO-Ab)、抗甲状腺球蛋白抗体(Tg-Ab)、尿碘(UI)和甲状腺激素,并使用超声检查甲状腺。基线时,尿碘中位数为17微克/升,甲状腺肿和甲状腺功能减退的患病率分别为72%和18%。提供加碘盐使尿碘中位数在这一年中维持在150 - 200微克/升(p < 0.0001)。总甲状腺素(T4)均值显著增加,甲状腺功能减退的患病率显著降低(p < 0.001)。引入加碘盐后,可检测到的抗体患病率出现短暂上升(p < 0.0001),1年后水平恢复到基线。在研究过程中,只有1%的儿童TPO-Ab升高,没有儿童Tg-Ab升高,且没有TPO-Ab升高的儿童促甲状腺激素(TSH)或T4浓度异常。没有儿童出现甲状腺自身免疫性疾病和/或碘诱发的甲状腺功能减退或甲状腺功能亢进的临床或超声证据。对严重缺碘儿童快速引入加碘盐并随访1年,不会引发明显的甲状腺自身免疫。

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