Abstract
BackgroundThe resistance of endometriotic tissue to progesterone can be explained by alterations in the distribution of progesterone receptor (PR) and estrogen receptor (ER) isoforms. The aims of this study were to examine the expressions of PR-A, PR-B, ERα and ERβ in endometrioma and assess whether these expressions are affected by dienogest or leuprolide acetate (LA) treatment.MethodsWe enrolled 60 females, including 43 patients with endometriosis (14 who received no medical treatment, 13 who received dienogest and 16 who received LA before undergoing laparoscopic surgery) and 17 patients with leiomyoma. The expression levels of PR and ER isoforms in eutopic and ectopic endometrium were assayed with quantitative real-time PCR, and confirmed with immunohistochemistry.ResultsA decreased PR-B/PR-A ratio and an increased ERβ/ERα ratio were demonstrated in ectopic endometrium derived from females with endometriosis compared with the ratios observed in eutopic endometrium obtained from females without endometriosis. Although LA treatment did not affect the PR-B/PR-A and ERβ/ERα ratios, dienogest treatment increased the PR-B/PR-A ratio and decreased the ERβ/ERα ratio in patients with endometriomas.ConclusionsDienogest may improve progesterone resistance in endometriotic tissue by increasing the relative expressions of PR-B and PR-A, and decreasing the relative expressions of ERβ and ERα.
Highlights
The resistance of endometriotic tissue to progesterone can be explained by alterations in the distribution of progesterone receptor (PR) and estrogen receptor (ER) isoforms
This study investigated whether treatment with dienogest or leuprolide acetate attenuates the expression of PR isoforms in ectopic endometrium
ER isoform expression and ERβ/ERα ratios in eutopic and ectopic endometrium This study investigated whether treatment with dienogest or leuprolide acetate attenuates the expression of ER isoforms in ectopic endometrium
Summary
The resistance of endometriotic tissue to progesterone can be explained by alterations in the distribution of progesterone receptor (PR) and estrogen receptor (ER) isoforms. Endometriosis is an estrogen-dependent inflammatory disease that affects 6-10% of females of reproductive age [1]. It is characterized by the presence of endometrium-like tissue outside the uterine cavity, primarily on the ovaries, and represents one of the most common causes of chronic pelvic pain, dysmenorrhea and infertility [2]. The main aims of treatment are to alleviate pain and other symptoms, reduce the size of the endometriotic lesions and improve the quality of life of affected individuals. A general tendency for relative progesterone resistance within the eutopic and ectopic endometrium of females with endometriosis is welldocumented [1,10]
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