Association between G protein-coupled estrogen receptor 1 (GPER 1) and Hashimoto thyroiditis GPER1 and Hashimoto's...

Hashimoto's thyroiditis is a common autoimmune endocrine disorder with a significant female predominance, suggesting that the estrogen/estrogen receptor axis may play a critical role in its pathogenesis. While classical nuclear receptors are well-studied, the role of G protein-coupled estrogen receptor 1 (GPER1) in Hashimoto's thyroiditis remains largely unexplored. This study aimed to evaluate serum GPER1 levels in patients with Hashimoto's thyroiditis and investigate its potential as a diagnostic biomarker.

This clinical study included 22 newly diagnosed, treatment-naive female patients with Hashimoto's thyroiditis and 40 healthy female controls. Serum GPER1 levels were measured using the ELISA method. Demographic data, thyroid function tests (TSH, FT4, FT3), and anti-thyroid peroxidase (anti-TPO) antibody levels were recorded for all participants. Statistical analyses, including ROC curve and Spearman's correlation, were performed to assess diagnostic efficiency and clinical relationships.

Serum GPER1 levels were significantly higher in the Hashimoto's thyroiditis group compared to the control group. ROC curve analysis demonstrated that GPER1 had high diagnostic power, with an area under the curve (AUC) of 0.997 (95% CI: 0.990-1.000). Using a cut-off value of 0.400, GPER1 exhibited 95.5% sensitivity and 100% specificity for distinguishing Hashimoto's thyroiditis patients from healthy individuals. Furthermore, a strong positive correlation was identified between serum GPER1 and anti-TPO antibody levels.

Our findings indicate that GPER1 levels are markedly elevated in patients with Hashimoto's thyroiditis and correlate strongly with thyroid autoimmunity. These results raise the possibility that GPER1 is related to inflammatory activity in Hashimoto's thyroiditis and could serve as a promising novel biomarker for its diagnosis. Further prospective studies are warranted to elucidate the exact mechanism of GPER1 in autoimmune thyroid disease.