ABSTRACT
Endometriosis is one of the most prominent public health problems in the US.1,2 It is characterized by the presence of endometrial glands and stroma within the pelvic peritoneum and other extrauterine sites, and is linked to pelvic pain and infertility. It is estimated to affect 5% of women of reproductive age.1,2 Endometriosis is a polygenically inherited disease of complex multifactorial etiology.3 Sampson’s theory of transplantation of endometrial tissue on the pelvic peritoneum via retrograde menstruation is the most widely accepted explanation for the development of pelvic endometriosis because of convincing circumstantial and experimental evidence.4 Because retrograde menstruation is observed in almost all cycling women, endometriosis is postulated to develop as a result of the coexistence of a defect in clearance of the menstrual efflux from pelvic peritoneal surfaces, possibly involving the immune system.5 Alternatively, intrinsic molecular aberrations in pelvic endometriotic implants have been proposed to significantly contribute to the development of endometriosis. Aberrant expression of aromatase, certain cytokines and tissue metalloproteinases, deficiency of 17βhydroxysteroid dehydrogenase (17β-HSD) type 2, and resistance to the protective action of progesterone are some of these molecular abnormalities.6-12 Because endometriosis is an estrogendependent disorder, aromatase expression and 17β-HSD type 2 deficiency are of paramount importance in its pathophysiology. Aromatase causes the accumulation of the biologically active estrogen estradiol (E2) in this tissue. 17β-HSD type 2, which metabolizes E2 to estrone (E1), is deficient in endometriosis. The combination of these two abnormalities serves to maintain high levels of E2 in endometriotic tissue.
