Endometriosis: The Ultimate Hormonal Disease
Endometriosis exhibits progesterone resistance and altered expression of aromatase, 17beta-HSD type 2, and PR-B/PR-A ratio, contributing to its hormonal pathology.
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This review discusses estrogen and progesterone regulation in endometrium versus endometriosis, focusing on steroidogenic and metabolic pathways involving aromatase, 17β-hydroxysteroid dehydrogenase type 2, and progesterone receptor isoforms. It reports that progesterone normally inhibits estrogen-driven proliferation and induces 17β-HSD type 2 to inactivate estradiol in endometrium, whereas these progesterone-dependent inhibitory/differentiative effects are less pronounced in endometriosis tissue. The review highlights observed abnormalities in endometriosis tissue expression of aromatase, 17β-HSD type 2, and the PR-B/PR-A ratio, and considers their functional consequences, while noting the paper is a narrative review synthesizing prior findings rather than presenting new experimental data. This paper is centrally about endometriosis — it frames endometriosis as a progesterone-resistant hormonal disorder driven by altered estrogen synthesis and metabolism.
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