Estrogen and progesterone receptor isoform distribution through the menstrual cycle in uteri with and without adenomyosis
- PMID: 21444077
- DOI: 10.1016/j.fertnstert.2011.02.051
Estrogen and progesterone receptor isoform distribution through the menstrual cycle in uteri with and without adenomyosis
Abstract
Objective: To test the hypothesis that the expression of the different isoforms of the estrogen receptor alpha (ER-α) and beta (ER-β) 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-α 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-α in the inner and outer myometrium was not statistically significantly different. The ER-β 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-β, PR-A, and PR-B expression was similar in the endometrial basalis and adenomyotic foci.
Conclusion(s): These data suggest ER-β 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.
Copyright © 2011 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
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