Although the endometrial response may vary from patient to patient, certain general histologic patterns for specific hormone therapies can be recognized. The same endometrium may display a number of changes under different conditions, resulting in a diversity of histologic patterns that may render some endometrial biopsies difficult to interpret. The histologic patterns of the endometrium associated with hormone therapy vary with the dosage, duration of therapy, and individual hormone receptor activity. As hormone therapy changes over time, with new regimens continuously being implemented, the effect on the endometrium can result in unpredictable structural changes. Various combinations of hyperplastic, proliferative, secretory, and atrophic changes of endometrial glands, stroma, and blood vessels may result in confusing histologic patterns. Hormone manipulation in fertility problems and hormonal substitution therapy result in histologic patterns that do not fit the classical descriptions of the cyclic and involutional changes of the endometrium. The physiologic changes of the endometrium during reproductive life and after menopause reflect the influence of ovarian-secreted steroid sex hormones and of their withdrawal. The endometrium is a sensitive target tissue for steroid sex hormones and is able to modify its structural characteristics with promptness and versatility. The histopathologic changes of the uterus, and particularly of the endometrium, associated with these therapies encompass a variety of morphologic features that are often difficult to interpret. Hormone therapy is widely used throughout the world by women of all ages for a variety of reasons, ranging from oral contraception and ovulation stimulation for family planning to hormone replacement therapy in menopause, to adjuvant therapy of tumors of the breast and uterus. Their causal relationship to tamoxifen therapy is debatable.ĭepartments of Pathology and Obstetrics-Gynecology and Reproductive Science, The Mount Sinai-NYU Medical Center, New York, New York Both endometrioid and nonendometrioid carcinomas are seen, often in polyps. Tamoxifen for breast carcinoma has an estrogen-agonist effect on the uterus in approximately 20% of patients, who develop endometrial polyps, glandular hyperplasia, adenomyosis, and/or leiomyomata. It generally produces endometrial atrophy. Lupron therapy produces a shrinking of uterine leiomyomas by accelerating their hyaline degeneration, similar to that in postmenopausal involution. Glandular proliferation is usually arrested, but neoplastic changes may persist and coexist with secretory changes. Progesterone therapy for endometrial hyperplasia and neoplasia induces glandular secretory changes, decidual reaction, and spiral arterioles. The use of both estrogen and progesterone elicits a wide range of histologic patterns, seen in various combinations: proliferative and secretory changes, often mixed in the same tissue sample glandular hyperplasia (in polyps or diffuse) ranging from simple to complex atypical stromal hyperplasia and/or decidual transformation epithelial metaplasia (eosinophilic, ciliated, mucinous) and inactive and atrophic endometrium. Hormone replacement therapy with estrogen alone may result in continuous endometrial proliferation, hyperplasia, and neoplasia. Ovulation induction therapy accelerates the maturation of the stroma and is often associated with a discrepancy between early secretory glands and an edematous or decidualized stroma with spiral arterioles. Prolonged use results in progressive endometrial atrophy. Oral contraceptives exert a predominant progestational effect on the endometriun, inducing an arrest of glandular proliferation, pseudosecretion, and stromal edema followed by decidualized stroma with granulocytes and thin sinusoidal blood vessels. This article discusses briefly endogenous hormonal effects (cyclic changes, luteal phase defect, unopposed estrogen effect) and describes the histologic patterns encountered in the most commonly used hormone therapies: oral contraceptives, ovulation stimulation, hormone replacement therapy, and antitumoral hormone therapy. The endometrial tissue is a sensitive target for steroid sex hormones and is able to modify its structural characteristics with promptness and versatility.
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