Sex steroids and endometriosis

Abstract

Endometriosis develops mostly in women of reproductive age and regresses after menopause, suggesting that the growth of lesions is estrogen dependent. Estrogen metabolism differs considerably in women with a normal endometrium compared to those with estrogen-dependent uterine diseases, including endometriosis, adenomyosis, or fibromas. Altered expression patterns of estrogen receptor (ER)-α/ER-β, progesterone receptor (PR)-A/PR-B, and 17β-hydroxysteroid dehydrogenase type 1 (HSD17B1)/type 2 (HSD17B2) in endometriotic tissue may upregulate aromatase and increase local estrogenic activity. Polymorphisms in ESR1, ESR2, PR, HSD17B1, 17α-hydroxylase (CYP17A1), and aromatase (CYP19) genes have been investigated putative associations with endometriosis susceptibility.