Management of Endometrial Hyperplasia in Reproductve Age Women

Backgrounds: The endometrium may develop endometrial hyperplasia (EH), which includes non-neoplastic entities (disordered proliferative endometrium, benign hyperplasia, simple and complex hyperplasias without atypia) characterized by a proliferation of endometrial glands of irregular size and shape, and precancerous neoplasms (endometrial intraepithelial neoplasms [EIN], and all atypical complex hyperplasia) characterized by neoplastic features but without invasion. EH frequently results from chronic estrogen stimulation unopposed by the counterbalancing effects of progesterone.The management of EH is determined by clinical factors and by the diagnostic classification. Classification is based upon histologic features and risk of progression to endometrial carcinoma. Clinical factors to consider in all types of EH are: Risk factors for recurrence or progression (eg, obesity, ovulatory dysfunction, increased genetic risk),Desire for fertility and Contraceptive needs .Material and Method: Management decisions depend on the EH pathologic classification. We encourage standardization using the 2015 World Health Organization classification criteria Diagnostic categories are based primarily upon two factors: Nuclear atypia and Degree of glandular crowding and complexity .The presence or absence of nuclear atypia is the primary factor in determining risk for concomitant endometrial carcinoma or progression to endometrial carcinoma that further informs initial treatment, maintenance therapy, and long-term surveillance. Options for the management of EH include surveillance, progestin therapy, or hysterectomy. Other treatment approaches include pharmacologic treatments other than progestins or conservative surgical treatment All management strategies should also be accompanied by removal of the extrinsic or intrinsic source of unopposed estrogen, since excess exposure to estrogen is the main etiology of endometrial neoplasia. Weight loss in obese women has multiple health benefits in addition to reducing high levels of endogenous estrogens due to estradiol and estrone production by adipocytes. Bariatric surgery may be of benefit in reducing this risk. For women with ovulatory dysfunction, the etiology should be treated (eg, prolactinoma), or if the ovulatory dysfunction is likely to be chronic (eg, polycystic ovarian syndrome), women may need maintenance progestin therapy after EH regression .Result: Common progestin treatments for EH include: the levonorgestrel-releasing intrauterine device, 52 mg with a release rate of 20 mcg/day over five years (Mirena; LNg52/5), oral medroxyprogesterone acetate, or oral megestrol acetate. Oral estrogen/progestin contraceptives have not been well studied for EH treatment, but are an option for women with EH without atypiaCommon progestin treatments for EH include: the levonorgestrel-releasing intrauterine device, 52 mg with a release rate of 20 mcg/day over five years (Mirena; LNg52/5), oral medroxyprogesterone acetate, or oral megestrol acetate. Oral estrogen/progestin contraceptives have not been well studied for EH treatment, but are an option for women with EH without atypia.For women with EH without atypia, we recommend the LNg52/5 intrauterine device rather than systemic progestins. For women with atypical EH who are postmenopausal or who are premenopausal and have completed childbearing, we recommend hysterectomy rather than progestin therapy. Progestin therapy is an option for premenopausal women with atypical EH who wish to preserve fertility or those of any menopausal status who cannot tolerate surgery.metformin has propunded as a new drug for treatment of EH especially as an adjuvant treatment in conservative management of atyphcal endometrial hyperplasia.Conclusion: For women with atypical EH who are premenopausal and wish to preserve fertility it is reasonable to treat with a progestin rather than hysterectomy These women must be able to comply with medical therapy and follow-up endometrial sampling.