STEROIDAL REGULATION OF ENDOMETRIOSIS TISSUE - LACK OF INDUCTION OF 17-BETA-HYDROXYSTEROID DEHYDROGENASE-ACTIVITY BY PROGESTERONE, MEDROXYPROGESTERONE ACETATE, OR DANAZOL

  • 1 January 1985
    • journal article
    • research article
    • Vol. 43  (2) , 218-224
Abstract
Cytosol and nuclear estrogen receptors were detected in 73 and 89% of untreated endometriosis specimens, respectively. The corresponding figures for cytosol and nuclear progestin receptors were 94 and 100%, respectively. Compared with the endometrium, the concentrations in endometriosis tissue were low. The anatomic site, the severity of the disease, and the phase of the menstrual cycle had no significant influence on receptor concentrations in endometriosis tissue. The activities of 17.beta.-hydroxysteroid dehydrogenase (17.beta.-HSD) did not increase the luteal phase. Danazol for 1, 3, 7 to 11, and 18 to 30 days, or medroxyprogesterone acetate for 5 days, had no effect on receptor concentrations or 17.beta.-HSD activity in endometriosis tissue. The frequent presence of the receptors suggests that endometriosis lesions are under the control of steroid hormones. The lack of effect by progesterone and progestins on 17.beta.-HSD shows that this regulation is different in endometriosis tissue and in the endometrium.