[Factors influencing redox homeostasis in Hashimoto's thyroiditis]

Hashimoto's thyroiditis is the most common form of autoimmune thyroid disease, in which the immune system induces chronic lymphocytic inflammation, destruction of thyroid follicles, and ultimately hypothyroidism through multiple pathogenic mechanisms. In addition to genetic predisposition, epigenetic modifications, environmental influences, and medications contribute to disease development. Key pathogenetic factors include increased hydrogen peroxide production in the thyroid gland, insufficient antioxidant enzymatic defense, imbalances in iodine and metal ion homeostasis, and dysregulation of iodothyronine deiodinase activity. From an immunological perspective, a predominance of cellular immune responses is observed, accompanied by excessive production of proinflammatory cytokines. Autoantibodies directed against thyreoperoxidase and thyroglobulin, and less frequently against the thyroid-stimulating hormone receptor, are commonly detected. Collectively, these complex alterations characterize Hashimoto's thyroiditis as a sensitive, multilevel immuno-endocrine disorder. Despite the heterogeneous clinical manifestations of autoimmune thyroid diseases, accumulating evidence suggests a shared immunological background. Orv Hetil. 2026; 167(17): 673-681.