endometrial hyperplasia, an abnormal condition characterized by overgrowth of the endometrium resulting from sustained stimulation by estrogen (of endogenous or exogenous origin) that is not opposed by progesterone. Estrogen acts as a growth hormone for the endometrium. Through a complex intercellular mechanism, endometrial cells bind estrogen preferentially and undergo changes characteristic of the proliferative phase of the menstrual cycle. If estrogen stimulation continues for 3 to 6 months without periodic cessation or counteractive progesterone stimulation, as occurs in anovulatory or perimenopausal women and in those receiving replacement estrogen without added progestogen, the endometrium becomes abnormally thickened and glandularized. The causative relationship between estrogen and endometrial hyperplasia is well established; there is some indication but no proof that estrogen also provokes the change from hyperplasia to neoplasia and malignancy. Endometrial hyperplasia often results in abnormal uterine bleeding. ▪ OBSERVATIONS: Unremitting estrogen stimulation eventually causes cystic or adenomatous endometrial hyperplasia. The latter is a premalignant lesion that undergoes malignant degeneration in approximately 25% of cases. ▪ INTERVENTIONS: Progestogen therapy is effective in reversing the abnormal histopathological changes of endometrial hyperplasia. If hyperplasia is adenomatous, hysterectomy is commonly performed. ▪ PATIENT CARE CONSIDERATIONS: Bleed, particularly in older women, constitutes an indication for biopsy or curettage of the endometrium to establish histopathological diagnosis and to rule out malignancy. A functioning estrogen-secreting tumor is suspected if the woman is not taking estrogen medication.
