Population Health Program, QIMR Berghofer Medical Research Institute, Brisbane, Australia.
School of Public Health, The University of Queensland, Brisbane, Australia.
Thyroid. 2023 Nov;33(11):1302-1310. doi: 10.1089/thy.2023.0317. Epub 2023 Oct 5.
Hypothyroidism is common, and in iodine-sufficient areas, it is primarily caused by autoimmune destruction of the thyroid gland. Observational studies have consistently shown an inverse association between serum 25-hydroxyvitamin D concentration and autoimmune diseases; however, there is a lack of evidence from randomized controlled trials to support a benefit of vitamin D supplementation, particularly for autoimmune thyroid diseases. We, therefore, aimed to assess the effect of vitamin D supplementation on the incidence of hypothyroidism. We analyzed data from the D-Health Trial ( = 21,315), a randomized double-blind placebo-controlled trial of 60,000 international units per month of supplemental vitamin D among Australians aged 60 years and over. Hypothyroidism, a tertiary outcome of the D-Health Trial, was defined by treatment with levothyroxine, ascertained through linkage with the Australian Pharmaceutical Benefits Scheme. The outcome was time to first prescription of levothyroxine. We began follow-up at 12 months after randomization; people who had died or who had been dispensed levothyroxine during the first year were excluded. Flexible parametric survival models were used to assess the effect of vitamin D supplementation on hypothyroidism, overall and within strata defined by age, sex, body mass index, and predicted baseline vitamin D status. We included 17,851 participants in the main analysis (vitamin = 8939; placebo = 8912). During a median follow-up of 4.1 years (interquartile range 4.1-4.1), 293 participants developed hypothyroidism (vitamin = 138 [1.5%]; placebo = 155 [1.7%]). Vitamin D supplementation did not significantly reduce the incidence of hypothyroidism (overall hazard ratio [HR] 0.89; 95% confidence interval [CI] 0.71-1.12). There was some suggestion of an effect in females (overall HR 0.78; CI 0.58-1.06) but not in males (overall HR 1.06; CI 0.74-1.50; interaction 0.20). Vitamin D supplementation did not reduce the incidence of hypothyroidism overall; however, the possible beneficial effect observed in females warrants further investigation. Australian New Zealand Clinical Trials Registry: ACTRN12613000743763.
甲状腺功能减退症很常见，在碘充足的地区，主要由自身免疫性甲状腺破坏引起。观察性研究一致表明血清 25-羟维生素 D 浓度与自身免疫性疾病之间存在负相关；然而，随机对照试验缺乏支持维生素 D 补充有益的证据，特别是对于自身免疫性甲状腺疾病。因此，我们旨在评估维生素 D 补充对甲状腺功能减退症发病率的影响。
我们分析了来自 D-Health 试验（ = 21,315）的数据，这是一项针对澳大利亚 60 岁及以上人群每月补充 60,000 国际单位维生素 D 的随机双盲安慰剂对照试验。甲状腺功能减退症是 D-Health 试验的三级结局，通过与澳大利亚药品福利计划的联系确定，用左旋甲状腺素治疗。结局是首次开处方左旋甲状腺素的时间。我们从随机分组后 12 个月开始随访；在第一年死亡或已开处方左旋甲状腺素的人被排除在外。使用灵活的参数生存模型评估维生素 D 补充对甲状腺功能减退症的总体影响，以及根据年龄、性别、体重指数和预测基线维生素 D 状态定义的分层。
我们纳入了主要分析中的 17,851 名参与者（维生素组 = 8939；安慰剂组 = 8912）。在中位随访 4.1 年（四分位间距 4.1-4.1）期间，293 名参与者发生甲状腺功能减退症（维生素组 138 例[1.5%]；安慰剂组 155 例[1.7%]）。维生素 D 补充并未显著降低甲状腺功能减退症的发病率（总体危险比[HR]0.89；95%置信区间[CI]0.71-1.12）。在女性中似乎有一定的效果（总体 HR 0.78；CI 0.58-1.06），但在男性中没有（总体 HR 1.06；CI 0.74-1.50；交互作用 0.20）。
维生素 D 补充并未总体降低甲状腺功能减退症的发病率；然而，在女性中观察到的可能有益效果需要进一步研究。
ACTRN12613000743763。
