Impact of Metformin on Thyroid Function and Autoimmune Antibody in Type 2 Diabetic Patients With Hashimoto’s Thyroiditis

Background Hashimoto’s thyroiditis is the most common autoimmune disease, characterized by elevated thyroid peroxidase antibodies (TPOAb) and thyroid globulin antibodies (TgAb). Recent studies have shown that metformin has therapeutic effects in various autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis, and inflammatory bowel disease. Methods This open‐label, single‐center, randomized controlled trial aims to evaluate the efficacy of metformin in modulating the autoimmune response in patients with Hashimoto’s thyroiditis and delaying disease progression in Type 2 diabetes patients. The trial recruited 60 Type 2 diabetic patients with Hashimoto’s thyroiditis. These patients were randomly assigned to two groups: the metformin group ( n = 30) received metformin treatment (initial dosage: 0.5 g/day, gradually increased to 1.5 g/day within 1 month), while the control group ( n = 30) was treated with other oral hypoglycemic drugs. After 6 months, the volume of the thyroid, TPOAb, thyroglobulin antibodies (TgAb), tumor necrosis factor‐α (TNF‐α), interferon‐γ (INF‐γ), interleukin‐2 (IL‐2), soluble Fas (sFas), and sFas ligand (sFas‐L) were evaluated in both groups. Results Six months post‐therapy, the levels of TPOAb, TgAb, and thyroiditis score in the metformin group decreased significantly, with normal thyroid volume (all p < 0.01), and all the indices were lower than those in the control group (all p < 0.05). In contrast, the control group showed no significant changes in the levels of TPOAb, TgAb, thyroiditis score, or thyroid volume. Compared to the control group, the metformin group exhibited significantly lower levels of TNF‐α, INF‐γ, and IL‐2, as well as reduced expression of Fas and sFas‐L in the blood (all p < 0.05). Conclusion Metformin hinders the advancement of Hashimoto’s thyroiditis in individuals with Type 2 diabetes, and its mode of action may be linked to the suppression of the Fas/Fas‐L‐mediated apoptotic pathway.