Aromatase as a therapeutic target in endometriosis

In contrast to normal endometrium, the expression of aromatase is aberant in endometriosis and is stimulated by prostaglandin E-2 (PGE(2)). This results in local production of estrogen, which induces PGE(2) formation and establishes a positive feedback cycle. Another abnormality in endometriosis - deficient 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) type 2 expression - impairs the inactivation, of estradiol (E-2) to estrone (E-1). These molecular aberrations collectively favor accumulation of increasing quantities of E-2, and PGE(2) in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis with art aromatase inhibitor.