Abstract
Background: Endometriosis (EMT) and adenomyosis (AM) are common estrogen-dependent gynecologic disorders with overlapping clinical manifestations yet distinct pathological features. This study was designed to characterize serum HOXA10 and EMX2 expression and to examine their association with estrogen-related biochemical alterations in EMT and AM. Methods: A total of 168 women of reproductive age treated in our hospital between May 2024 and October 2025 were included, comprising 64 controls, 49 patients with EMT, and 55 patients with AM. Serum estradiol (E2) and estrone (E1) were measured by electrochemiluminescence immunoassay and enzyme-linked immunosorbent assay, respectively. Serum RNA was isolated and reverse-transcribed after quality assessment. The expression levels of HOXA10, EMX2, and six estrogen metabolism-related genes were then measured by real-time quantitative PCR. Correlations between the core genes and estrogen-related indicators were analyzed, and receiver operating characteristic (ROC) analysis was performed to evaluate the discriminatory efficacy of HOXA10 and EMX2 for identifying endometriosis (EMT) and adenomyosis (AM). Results: Serum HOXA10 expression was decreased, whereas EMX2 expression was increased, in both the EMT and AM groups compared with controls. The HOXA10/EMX2 ratio was also reduced in both disease groups, with a significantly greater decline observed in the AM group compared with the EMT group (P<0.05). Serum E2 and E1 levels were elevated in both disease groups. Genes involved in estrogen synthesis and activation were generally upregulated, while those related to estrogen inactivation were downregulated, indicating enhanced estrogenic activity, especially in AM. HOXA10 and EMX2 were correlated with several estrogen-related indicators, although the correlation patterns differed between EMT and AM. Conclusion: EMT and AM are accompanied by coordinated changes in serum HOXA10, EMX2, and estrogen metabolism-related indices.
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Naknadno pridodat članak: provera, normiranje i linkovanje referenci u toku. |
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