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  • Title: Effects of hormone therapy on the endometrium.
    Author: Deligdisch L.
    Journal: Mod Pathol; 1993 Jan; 6(1):94-106. PubMed ID: 8426860.
    Abstract:
    Hormone therapy induces a variety of histologic changes in the endometrium. Histologic patterns encountered in the most commonly used hormonal regimens are described. Oral contraceptives are associated with inactive, atrophic, or pseudosecretory glands and edematous stroma, decidual reaction without spiral arterioles, and stromal granulocytes. A high-potency progesterone may induce marked stromal and vascular hyperplasia and stromal myomatous nodules. Ovulation induction therapy accelerates the maturation of the stroma and is often associated with a discrepancy between the glands showing early secretory changes and an edematous, decidualized stroma. Hormone replacement therapy may stimulate endometrial proliferation if estrogens are used alone and produce endometrial hyperplasia and neoplasia. When estrogen and progesterone regimens are used, a wide range of histologic pattern may be found in various combinations: proliferative and secretory endometrium, glandular and adenomatous hyperplasia, stromal hyperplasia and decidual transformation, glandular metaplasia, atrophic endometrium, and any of the above with endometrial atrophy. Progesterone therapy for endometrial hyperplasia and neoplasia is followed by secretory changes of the endometrium, mostly subnuclear vacuoles, decidual reaction, and sometime squamoid "morules." Secretory changes seen after progesterone therapy in the endometrium do not rule out residual carcinoma. For hormone therapy for breast carcinoma, tamoxifen acts as an antiestrogen on the breast but often acts as an estrogen agonist on the endometrium; tamoxifen therapy may be associated with endometrial hyperplasia, polyps, adenomyosis, adenomatous hyperplasia, and adenocarcinoma. Steroid sex hormones cause immediate changes in the endometrium. The histologic effect depends on the hormone, the potency, dosage, and the host receptor status. Oral contraceptives (OCs) containing a low-dose, low-potency progesterone and low-dose estrogen stop proliferation of the glands during the 1st few cycles and the glands are straight and unevenly distributed, with considerable stroma between them. The minimal secretory features of the glands disappear with longterm use of these OCs, resulting in complete atrophy of the glands and of the stroma. These OCs also cause decidual reaction without spiral arterioles and stromal granulocytes. OCs with high potency progesterone cause distinct hyperplasia of the endometrial stroma and vessels, atrophy of the glands, and stromal myomatous nodules. Ovulation induction therapy consists of various combinations of some drugs (clomid, human menopausal gonadotropins, gonadotropin-releasing hormone, and human chorionic gonadotropin). This therapy accelerates secretory changes in the stroma, resulting in enhancement of the endometrial maturation process. It makes it difficult to differentiate between glands displaying early secretory changes and an edematous, decidualized stroma. Hormone replacement therapy using estrogens and progesterone cause different histologic patterns, including stromal hyperplasia and decidual transformation, glandular and adenomatous hyperplasia, glandular metaplasia, proliferative and secretory endometrium, atrophic endometrium, and any of these with endometrial atrophy. Progesterone therapy for endometrial hyperplasia and neoplasia produces secretory changes of the endometrium, such as subnuclear vacuole, decidual reaction, and squamoid "morules." These changes can result in residual carcinoma. Tamoxifen therapy for breast cancer is linked with endometrial hyperplasia, polyps, adenomyosis, adenomatous hyperplasia, and adenocarcinoma.
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