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ER, PR and Ki‐67 expression status in granulomatous and chronic non‐specific endometritis
Author(s) -
Mishra Kiran,
Wadhwa Neelam,
Guleria Kiran,
Agarwal Sarla
Publication year - 2008
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/j.1447-0756.2007.00700.x
Subject(s) - endometritis , medicine , stromal cell , endometrium , endometrial biopsy , immunohistochemistry , estrogen receptor , estrogen , biopsy , progesterone receptor , ki 67 , pathology , endocrinology , biology , pregnancy , genetics , cancer , breast cancer
Aim:  To study the changes in the histological pattern, distribution and intensity of sex steroid receptors (estrogen and progesterone) and cell proliferation by Ki‐67 expression by semi‐quantitative scores in granulomatous and chronic non‐specific endometritis in the premenstrual phase. Methods:  A retrospective study was conducted on 20 cases of granulomatous endometritis, 10 of chronic non‐specific endometritis and 30 age matched (±2 years) controls with no endometrial lesions. Morphological changes were noted on histological examination and semi‐quantitative scoring of Estrogen Receptor (ER), Progesterone Receptor (PR) and Ki‐67 expression was done by immunohistochemistry. Results:  There was significantly higher ER, PR and Ki‐67 expression in endometrial glandular and stromal cells in inflamed endometria as compared with the controls (all P ‐values < 0.02) regardless of the character of the inflammation. The cases with morphology not conforming to the secretory phase at which biopsy was taken had significantly higher ER, PR and Ki‐67 expression in both endometrial and stromal cells indicating a lag in the endometrial maturation (all P ‐values < 0.02). Interestingly, all parameters except PR expression in glandular cells had a significantly higher expression even in cases with secretory morphology indicating disturbances in local milieu. Conclusion:  Endometrial inflammation interferes with local expression of ER, PR and Ki‐67. This may contribute to infertility regardless of other factors and other endometrial dysfunctional states.

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