• Raquel Papandreus Dibi, Claudio Galleano Zettler, Carla Maria de Martini Vanin, Rafaela Vanin Pinto Ribeiro, Júlia Monteiro de Oliveira, Thaysa Guglieri Kremer, Josiane Borges, and Sérgio Kakuta Kato.
• MD, PhD. Professor, Department of Gynecology and Obstetrics, Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA); and Professor, Gynecology and Obstetrics Service, Irmandade Santa Casa de Misericórdia de Porto Alegre (ISCMPA), Porto Alegre (RS), Brazil.
• Sao Paulo Med J. 2020 Jan 1; 138 (1): 646864-68.

BackgroundEndometrial polyps are common in postmenopausal women, and the effect of tamoxifen use (a risk factor for endometrial polyps) on their pathogenesis is unclear.ObjectivesTo evaluate the expression of hormone receptors and markers for proliferation/apoptosis (Ki-67 and Bcl-2) in endometrial polyps in postmenopausal users and nonusers of tamoxifen.Design And SettingCross-sectional analytical study in a tertiary-level academic hospital.Methods46 women (14 tamoxifen users and 32 nonusers) with postmenopausal bleeding underwent hysteroscopic resection of endometrial polyps. Polyp samples were immunohistochemically assessed for detection of Ki-67, Bcl-2 and estrogen and progesterone receptors.ResultsAnalysis on the glandular component of the polyps revealed progesterone receptor expression in the polyps of 96.9% of the nonusers of tamoxifen, and 92.3% of the tamoxifen users (P = 0.499). All polyps in nonusers and 92.3% of those in users were also positive for estrogen receptors (P = 0.295). Ki-67 was expressed in 75% of the polyps in the tamoxifen users and 82.8% of those in the nonusers. All endometrial polyps expressed Bcl-2.ConclusionsThe immunohistochemical analysis on endometrial polyps demonstrated that, although tamoxifen is considered to be a risk factor for endometrial polyps, there were no significant differences in the expression of hormone receptors between users and nonusers of tamoxifen. There were no between-group differences in Ki-67 and Bcl-2 expression, and all patients displayed inhibition of apoptosis by Bcl-2, thus supporting the theory that polyps develop due to inhibition of apoptosis, and not through cell proliferation.

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