Fangping Li, Jiahao Tang, Shuanghong Shan, Peng Yun
Journal: Medicine 2024;102(52):e36759
PMID: 38206745
Hashimoto’s thyroiditis (HT) is an autoimmune disorder characterised by chronic inflammation of the thyroid gland, often leading to hypothyroidism. Vitamin D has immunomodulatory effects, and its deficiency has been linked to various autoimmune diseases. The primary aim of this study was to systematically review and analyse the effects of vitamin D supplementation on thyroid autoantibodies (anti-thyroid peroxidase [TPOAb] and anti-thyroglobulin [TgAb]) and thyroid function (TSH, FT4, and FT3 levels) in patients with Hashimoto’s thyroiditis. This research is a systematic review and meta-analysis, incorporating data from multiple randomised controlled trials and observational studies. Results showed that vitamin D supplementation significantly reduced TPO-Ab and TG-Ab titers among HT patients, leading to improvements in thyroid function characterised by decreased TSH levels and increased FT3 and FT4 levels. Authors concluded that the findings of this study support the potential benefit of vitamin D supplementation in managing autoimmune aspects of Hashimoto’s thyroiditis, though further research is needed to confirm these effects and determine optimal dosing.
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Regular monitoring of vitamin D levels in patients with Hashimoto’s Thyroiditis is recommended to prevent exacerbation of their symptoms and condition. Ideally, this should be carried out by a qualified healthcare professional.
A higher prevalence of vitamin D insufficiency or deficiency has been found in people with Hashimoto’s Thyroiditis (HT). This may be a contributing factor to the aetiology of HT due to vitamin D’s regulatory role on the immune system. Supplementation with 25-hydroxyvitamin D (25(OH)D) may improve thyroid function and reduce thyroid antibodies, however, there is conflicting evidence. The aim of this study was to evaluate the efficacy of 25(OH)D supplementation for improving HT based on a meta-analysis of randomised controlled trials (RCTs).
25(OH)D Supplementation may be beneficial for improving thyroid function and modulating immune responses in people with HT. Further prospective studies with large and diverse populations are needed to confirm these results.

BACKGROUND
Hashimoto's thyroiditis (HT) is the prevailing form of autoimmune thyroiditis and the leading cause of hypothyroidism in iodine-sufficient regions worldwide. This study aims to evaluate the efficacy of vitamin D supplementation on HT through a meta-analysis of randomized controlled trials (RCTs).
METHODS
The databases searched included PubMed, and others. We included RCTs that the treatment group received vitamin D, while the control group received either a placebo or no treatment. The studies measured the baseline and endpoint levels of 25-hydroxyvitamin D [25(OH)D], thyroid-stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), anti-thyroid peroxidase antibody (TPO-Ab), and thyroglobulin antibody (TG-Ab). We performed a meta-analysis to calculate the standardized mean difference (SMD) and 95% confidence interval (CI).
RESULTS
A total of 12 studies involving 862 individuals were included. Vitamin D supplementation has a significant impact on reducing the titers of TPO-Ab (SMD = -1.084, 95% CI = -1.624 to -0.545) and TG-Ab (SMD = -0.996, 95% CI = -1.579 to -0.413) in patients with HT, and it also improves thyroid function by decreasing TSH level (SMD = -0.167, 95% CI = -0.302 to 0.031) and increasing FT3 (SMD = 0.549, 95% CI = 0.077-1.020) and FT4 (SMD = 0.734, 95% CI = 0.184-1.285) levels. Active vitamin D (calcitriol) significantly reduces the titer of TPO-Ab compared to naive forms of vitamin D (vitamin D2 or D3); treatment durations > 12 weeks result in a more effective reduction of TPO-Ab levels and a more significant increase in FT4 and FT3 levels in patients with HT (meta-regression P < .05).
CONCLUSION
Vitamin D supplementation may have beneficial effects on HT patients by modulating immune responses and improving thyroid function.
Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.
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