J Gynecol Oncol. 2016 Jan;27(1):e8 http://doi.org/10.3802/jgo.2016.27.e8 pISSN 2005-0380 · eISSN 2005-0399
Review Article Therapeutic options for management of endometrial hyperplasia
Vishal Chandra,1,2,* Jong Joo Kim,3,* Doris Mangiaracina Benbrook,1 Anila Dwivedi,2 Rajani Rai3
1Department of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA 2Division of Endocrinology, CSIR-Central Drug Research Institute, Lucknow, India 3School of Biotechnology, Yeungnam University, Gyeongsan, Korea
Received: Jun 25, 2015 ABSTRACT Revised: Jul 24, 2015 Accepted: Jul 31, 2015 Endometrial hyperplasia (EH) comprises a spectrum of changes in the endometrium ranging from a slightly disordered pattern that exaggerates the alterations seen in the late Correspondence to Rajani Rai proliferative phase of the menstrual cycle to irregular, hyperchromatic lesions that are similar School of Biotechnology, Yeungnam University, to endometrioid adenocarcinoma. Generally, EH is caused by continuous exposure of estrogen 280 Daehak-ro, Gyeongsan 38541, Korea. unopposed by progesterone, polycystic ovary syndrome, tamoxifen, or hormone replacement E-mail: [email protected] therapy. Since it can progress, or often occur coincidentally with endometrial carcinoma, EH is of clinical importance, and the reversion of hyperplasia to normal endometrium represents *The first two authors contributed equally to the key conservative treatment for prevention of the development of adenocarcinoma. this study. Presently, cyclic progestin or hysterectomy constitutes the major treatment option for EH Copyright © 2016. Asian Society of without or with atypia, respectively. However, clinical trials of hormonal therapies and Gynecologic Oncology, Korean Society of definitive standard treatments remain to be established for the management of EH. Moreover, Gynecologic Oncology therapeutic options for EH patients who wish to preserve fertility are challenging and require This is an Open Access article distributed nonsurgical management. Therefore, future studies should focus on evaluation of new under the terms of the Creative Commons Attribution Non-Commercial License (http:// treatment strategies and novel compounds that could simultaneously target pathways involved creativecommons.org/licenses/by-nc/4.0/) in the pathogenesis of estradiol-induced EH. Novel therapeutic agents precisely targeting the which permits unrestricted non-commercial inhibition of estrogen receptor, growth factor receptors, and signal transduction pathways are use, distribution, and reproduction in any likely to constitute an optimal approach for treatment of EH. medium, provided the original work is properly cited. Keywords: Endometrial Hyperplasia; Progestins; Receptors, Estrogen; Therapy ORCID Vishal Chandra http://orcid.org/0000-0002-5206-2313 Jong Joo Kim INTRODUCTION http://orcid.org/0000-0001-9687-0075 Doris Mangiaracina Benbrook The endometrium, the innermost glandular layer of the uterus, is a dynamic tissue that http://orcid.org/0000-0001-7606-8245 goes through a series of alterations (proliferation, secretion and menstruation/shedding) Anila Dwivedi during the menstrual cycle in a woman’s reproductive years [1]. This cyclic phase involves http://orcid.org/0000-0001-8515-5551 a complex interaction between the two female sex hormones, estradiol, and progesterone Rajani Rai (Fig. 1). Estrogen promotes epithelial cell proliferation resulting in thickening of the uterus, http://orcid.org/0000-0003-3503-5265 while progesterone encourages epithelial cell differentiation and the secretory phase of the endometrial cycle [2,3]. The fine equilibrium between endometrial proliferation and
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Conflict of Interest No potential conflict of interest relevant to this article was reported.
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