Selenium Supplementation in Patients with Hashimoto Thyroiditis: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.
Level 1 - systematic review of randomized trials
Systematic review and meta-analysis of randomized controlled trials
PubMed 38243784 · doi:10.1089/thy.2023.0556
What was done
Authors conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) across major databases through January 2023 (PROSPERO CRD42022308377). They evaluated selenium supplementation in Hashimoto thyroiditis on thyroid hormones, autoantibodies, ultrasound parameters, immune markers, and adverse events. Risk of bias was evaluated with Cochrane RoB 2, and evidence certainty was graded using GRADE. The primary outcome was serum TSH in patients not receiving thyroid hormone replacement therapy (THRT).
What was found
Across 35 unique studies, selenium supplementation reduced TSH in patients not on THRT (SMD -0.21 [95% CI -0.43 to -0.02]; 7 cohorts, 869 participants; I² = 0%). Across patients with and without THRT, selenium reduced TPOAb (SMD -0.96 [95% CI -1.36 to -0.56]; 29 cohorts, 2358 participants; I² = 90%) and malondialdehyde (SMD -1.16 [95% CI -2.29 to -0.02]; 3 cohorts, 248 participants; I² = 85%). Adverse events did not differ significantly from controls (OR 0.89 [95% CI 0.46 to 1.75]; 16 cohorts, 1339 participants; I² = 0%). No significant differences were observed for fT4, T4, fT3, T3, TGAb, thyroid volume, IL-2, or IL-10. Overall evidence certainty was moderate.
Why it matters
This review provides quantitative evidence that selenium supplementation is safe and modestly lowers TSH in untreated Hashimoto thyroiditis while reducing antibody and oxidative stress markers, though it does not alter circulating thyroid hormone concentrations.
Limits
Substantial statistical heterogeneity was observed for key secondary outcomes including TPOAb (I² = 90%) and malondialdehyde (I² = 85%). The primary outcome analysis of TSH in patients without THRT was limited to 7 cohorts (869 participants). The abstract does not report baseline selenium deficiency status, specific dosing regimens, or long-term clinical symptom outcomes.
Cited by
- supports Selenium is required for glutathione synthesis, the conversion of T4 to T3 thyroid hormone, and reducing thyroid autoantibodies.