ENDOMETRIOSIS AND THYROID DYSFUNCTION: EPIDEMIOLOGICAL EVIDENCE, THYROID AUTOIMMUNITY, AND TSH-T3/T4 AXIS MECHANISMS IN ENDOMETRIOSIS PATHOPHYSIOLOGY

Background: Endometriosis is a chronic inflammatory gynecological condition characterized by immune dysregulation and a wide range of systemic complications. Thyroid disorders are also common in women of reproductive age and may overlap with endometriosis through shared autoimmune pathways and endocrine signaling. Objective: This review aims to summarize epidemiological and clinical evidence linking endometriosis with thyroid dysfunction and thyroid autoimmunity and to place these findings in the context of mechanistic research on the TSH–T3/T4 axis. Methods: Researchers searched for original studies reporting both diagnosed endometriosis and thyroid-related outcomes, including thyroid disorders, autoimmune thyroiditis, thyroid autoantibodies, TSH receptor antibodies, and thyroid neoplasms. The evidence was synthesized narratively. Results: Large EHR- and claims-based studies generally reported increased risks of hypothyroidism, hyperthyroidism, Graves’ disease, thyroiditis, goiter, and thyroid neoplasms after an endometriosis diagnosis. Clinical and biomarker studies were more variable: one case–control cohort found comparable rates of thyroid dysfunction and anti-thyroid antibodies in cases and controls, whereas other cohorts reported a higher prevalence of autoimmune thyroiditis, lower free T4 levels, associations between anti-thyroid peroxidase antibody levels and endometrioma size, and a higher prevalence of Hashimoto thyroiditis in an IVF/ICSI population. In one diagnostic biomarker study, adding anti-thyroid peroxidase and thyroglobulin antibodies to CA125 improved discrimination between ovarian endometriomas and other benign ovarian tumors (AUC 0.924). Studies of TRAb suggested elevated titers in some cohorts, but this finding was not reproduced with routine clinical TRAb assays, underscoring assay dependence. Mechanistic studies support biological plausibility by showing altered thyroid hormone metabolism in endometriotic tissue and proliferative, pro-oxidative effects of TSH, T3, and T4. Conclusions: Overall, the literature points to an association between endometriosis and thyroid-related outcomes; however, substantial heterogeneity and potential bias make it difficult to translate these findings into clear screening recommendations. Future research should prioritize standardized phenotyping, harmonized antibody testing, and prospective studies linking clinical thyroid status with the biology of endometriosis.