Gonadotropin-releasing hormone analog repairs reduced endometrial cell apoptosis in endometriosis in vitro

OBJECTIVE: Impaired sensitivity of endometrial tissue to spontaneous apopto sis in women with endometriosis contributes to the abnormal implantation an d growth of endometrium at ectopic sites. Our purpose was to examine the ef fect of gonadotropin-releasing hormone analog, widely used in the treatment of endometriosis, on the reduced rate of endometrial apoptosis in endometr iosis. STUDY DESIGN: Paired ectopic and eutopic endometrial tissue specimens were obtained from 13 patients with endometriosis, and control samples were take n from 8 patients with uterine myoma. Apoptotic cell death was assessed bio chemically and morphologically with an enzyme-linked immunoassay and Hoechs t No. 33342 staining of deoxyribonucleic acid fragment, respectively. RESULTS: Spontaneous apoptosis was significantly lower in ectopic and eutop ic endometrial tissue from patients with endometriosis (0.22 +/- 0.082 in a bsorbance) than in endometrial tissue from control subjects (0.52 +/- 0.483 )(P < 0.001). Incubation with a gonadotropin-releasing hormone analog (1 mu mol/L) increased the apoptotic rate of endometrial cells from patients wit h endometriosis to 0.56 +/- 0.501 (P < .001). The effect of this gonadotrop in-releasing hormone revealed a dose dependency; a half-maximal effect occu rred with 10 nmol/L; however, the control endometrium was not affected. CONCLUSION: Exposure to gonadotropin-releasing hormone results in changes o f the sensitivity of endometriotic endometrium to spontaneous apoptosis; th ese changes in sensitivity may, in turn, release endometrial cells from res istance to apoptosis and result in reduced survival and growth. This phenom enon could, at least in part, account for the therapeutic action of gonadot ropin-releasing hormone analog on endometriosis.