Abstract

Direct effects of a gonadotropin-releasing hormone agonist (GnRHa), danazol, or estrogen/progestogen (E/P) on experimental endometriosis were evaluated in castrated female rats. Endometrial explants decreased in size following castration, but there was no further change in the treatment groups. Histologic examination indicated atrophy and regression of experimental endometriosis in all groups of castrated animals. As expected, following castration, serum estradiol (E2) became undetectable, serum progesterone (P4) decreased, and cytosolic E2 and P4 binding capacity in the endometrial explants was lower. However, in danazol-treated animals, serum P4 and E2 receptor concentrations were significantly higher than in all other castrated groups, and in both danazol and E/P treated animals, concentrations of P4 receptor were significantly higher than in castrated controls. In contrast, GnRHa treatment had no effect on serum E2 and P4 levels nor on E2 or P4 receptors. The authors conclude that danazol and E/P preparations may have a direct effect on the ectopic endometrium through interaction with steroid receptors.

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