P-779: Differentially decreased ovarian response to controlled ovarian hyperstimulation in patients with unilateral endometriomas

Abstract

A growing body of data clearly associates ovarian endometriosis with decreased ovarian response to controlled ovarian hyperstimulation (COH). Surgical removal of ovarian endometriomas (OE) have failed to improve ovarian responsiveness to subsequent COH, suggesting that directly proceeding to COH in asymptomatic women decreases time to pregnancy and potential complications of surgery. However, it is unclear whether this decreased ovarian reserve is a systemic effect of endometriosis or a localized reaction caused by the genesis of OE. This study aims to address this issue by comparing COH responses between ovaries in women with one normal and one endometrioma-affected ovary. Paired-comparison study. Patients with unilateral endometriomas on transvaginal ultrasound ranging from 1 to 4cm in diameter and undergoing COH were identified from January 2005 to March 2006. The diagnosis by transvaginal ultrasonography was made with evidence of well-accepted criteria for OE. The inclusion criteria were women <37 years of age with regular 27-35 day menstrual cycles. Excluded were patients with PCOS, poor response to previous COH cycles, history of ovarian surgeries, autoimmune diseases, systemic therapies for cancer, and smokers. A total of 41 patients fulfilled the inclusion and exclusion criteria. All patients received oral contraception suppression to LH<4 mIU/ml, E2<50 pg/ml, and follicular diameters <4mm prior to therapy. Ovarian hyperstimulation was achived with either 150 or 225 IU of recombinant FSH daily to reach stimulation values of FSH>12 mIU/ml. The mean number of dominant follicles ≥16mm produced by the OE ovaries on the day of HCG administration was calculated; this was compared to the mean number of follicles produced by the normal, contralateral ovaries using a Wilcoxon Signed-Ranks test for matched pairs. The subjects’ age ranged from 25 to 37 years old (mean 32.6 ± 3.3 years) and had unilateral endometriomas with mean size of 2.8 ± 0.5 cm. Their mean starting FSH and E2 values were 5.5 ± 2.1 mIU/ml and 33.4 ± 14.1 pg/ml, respectively. The mean FSH after stimulation and peak E2 levels were 14.3 ± 4.4 mIU/ml and 1240.9 ± 772.2 pg/ml. The mean number of follicles produced by a normal ovary undergoing COH was 4.0 ± 2.3, and the mean number of follicles produced by the contralateral, endometrioma-affected ovary was found to be significantly lower at 2.5 ± 1.4 (p<0.0002; 95% CI -2.18 to -0.89). Of the diseased ovaries, 7.3% (3/41) had no dominant follicles at all, where as none of the normal ovaries failed to produce any follicles. In 73% (30/41) of the subjects, there was significant incongruity in follicular development, where the normal ovary produced ≥50% more follicles than the OE ovary. The size of an endometrioma had no linear relationship to either the number of follicles produced or the incongruity ratio of follicular development between the two ovaries. The results suggest that ovaries affected by even a small endometrioma have significantly decreased production of dominant follicles when compared to their normal counterparts under superovulation with gonadotropins. Furthermore, it appears this impaired ovarian response is differentially related to the localized effects present in the endometrioma-affected ovary and may be related to the multiple factors included in the genesis of the endometrioma.