4.7 Article

Estrogen and progesterone receptor isoform distribution through the menstrual cycle in uteri with and without adenomyosis

Journal

FERTILITY AND STERILITY
Volume 95, Issue 7, Pages 2228-U135

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.fertnstert.2011.02.051

Keywords

Adenomyosis; estrogen receptors; progesterone receptors; uterus; menstrual cycle

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Objective: To test the hypothesis that the expression of the different isoforms of the estrogen receptor alpha (ER-alpha) and beta (ER-beta) and the progesterone receptor A (PR-A) and B (PR-B) would be differentially modulated in uteri with adenomyosis compared with controls and that modulation would be related to the menstrual cycle. Design: Case control, blinded comparison. Setting: University department. Patient(s): 54 premenopausal women with and 35 without uterine adenomyosis as the sole pathology. Intervention(s): Multiple samples studied using immunohistochemistry for estrogen and progesterone receptors. Main Outcome Measure(s): Histomorphometric analysis of receptor expression. Result(s): The ER-alpha expression in the adenomyotic endometrium was different from that of the normal endometrium and the foci in the midsecretory phase of the cycle, but expression of ER-alpha in the inner and outer myometrium was not statistically significantly different. The ER-beta expression was statistically significantly elevated in the adenomyotic functionalis gland during the proliferative phase and throughout the myometrium across the entire menstrual cycle. Expression of PR-A was similar to that of PR-B, with reduced expression in the basalis stroma, and inner and outer myometrium in the adenomyotic samples. The pattern of ER-beta, PR-A, and PR-B expression was similar in the endometrial basalis and adenomyotic foci. Conclusion(s): These data suggest ER-beta expression and the lack of PR expression are related to the development and/or progression of adenomyosis and might explain the poor response of adenomyosis-associated menstrual symptoms to progestational agents. (Fertil Steril (R) 2011;95:2228-35. (C)2011 by American Society for Reproductive Medicine.)

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