title: Therapeutic options for management of endometrial hyperplasia.
abstract: 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 proliferative phase of the menstrual cycle to irregular, hyperchromatic lesions that are similar to endometrioid adenocarcinoma. Generally, EH is caused by continuous exposure of estrogen unopposed by progesterone, polycystic ovary syndrome, tamoxifen, or hormone replacement 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 key conservative treatment for prevention of the development of adenocarcinoma. Presently, cyclic progestin or hysterectomy constitutes the major treatment option for EH without or with atypia, respectively. However, clinical trials of hormonal therapies and definitive standard treatments remain to be established for the management of EH. Moreover, therapeutic options for EH patients who wish to preserve fertility are challenging and require nonsurgical management. Therefore, future studies should focus on evaluation of new treatment strategies and novel compounds that could simultaneously target pathways involved in the pathogenesis of estradiol-induced EH. Novel therapeutic agents precisely targeting the inhibition of estrogen receptor, growth factor receptors, and signal transduction pathways are likely to constitute an optimal approach for treatment of EH.
authors.affiliation: Department of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.|Division of Endocrinology, CSIR-Central Drug Research Institute, Lucknow, India.
authors.forename: Vishal
authors.identifier: http://orcid.org/0000-0002-5206-2313
authors.initials: V
authors.lastname: Chandra
authors.affiliation: School of Biotechnology, Yeungnam University, Gyeongsan, Korea.
authors.forename: Jong Joo
authors.identifier: http://orcid.org/0000-0001-9687-0075
authors.initials: JJ
authors.lastname: Kim
authors.affiliation: Department of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
authors.forename: Doris Mangiaracina
authors.identifier: http://orcid.org/0000-0001-7606-8245
authors.initials: DM
authors.lastname: Benbrook
authors.affiliation: Division of Endocrinology, CSIR-Central Drug Research Institute, Lucknow, India.
authors.forename: Anila
authors.identifier: http://orcid.org/0000-0001-8515-5551
authors.initials: A
authors.lastname: Dwivedi
authors.affiliation: School of Biotechnology, Yeungnam University, Gyeongsan, Korea. rajaniraiims@gmail.com.
authors.forename: Rajani
authors.identifier: http://orcid.org/0000-0003-3503-5265
authors.initials: R
authors.lastname: Rai
mesh_terms: D018931:Antineoplastic Agents, Hormonal / Q000009:adverse effects; D019468:Disease Management; D018450:Disease Progression; D004714:Endometrial Hyperplasia / Q000145:classification / Q000209:etiology / Q000628:therapy*; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000627:therapeutic use; D006801:Humans; D007044:Hysterectomy; D058990:Molecular Targeted Therapy / Q000379:methods; D045167:Progesterone Congeners / Q000627:therapeutic use; D012307:Risk Factors; D013629:Tamoxifen / Q000009:adverse effects
chemical_list: D018931:Antineoplastic Agents, Hormonal; D045167:Progesterone Congeners; D013629:Tamoxifen; D007987:Gonadotropin-Releasing Hormone
keywords: Endometrial Hyperplasia; Progestins; Receptors, Estrogen; Therapy