P-738: 367 intrauterine insemination cycles with or without a GnRH antagonist: A prospective randomized study

Abstract

Multifollicular recruitment during controlled ovarian hyperstimulation in intrauterine insemination (COH-IUI) can bring about a sudden increase in E2 serum levels that is enough to induce an LH surge while follicular growth is still in progress. Thus, to avoid the risk of an unexpected follicular luteinization, ovulation is generally induced as soon as the leading follicle has reached the 18 mm boundary. However, this decreases the possibilities for gestation since it changes the IUI cycle from multi- to monofollicular. Suppressing gonadotropin-LH release with a GnRH antagonist will prevent premature LH surges and follicle luteinization, and allow us to postpone ovulation. With this in mind, we thought that if pregnancy rates in IUI were related to the number of mature follicles present on the day HCG was indicated and, if the limiting factor for follicular development was premature luteinization, why couldn’t any unexpected LH surge be controlled with a GnRH antagonist during the COH-UIU cycle? Thus, the objective of this study was to determine whether including a GnRH antagonist in COH-IUI cycles would increase pregnancy rates. Prospective randomized study. 367 women (19-38 years old) with primary or secondary infertility were included in this prospective randomized study. PCO and endometriosis were excluded. The patients were randomly (by a computer) assigned to controlled ovarian stimulation with rFSH + the GnRH antagonist (Ganirelix Acetate) initiated when the recruited follicles were ≥16mm (n=184) or with rFSH alone (n=183). Ovulation was induced with HCG 5,000 IU/ i.m. A single insemination was performed, 36-38 hours post-HCG, in both groups. Continuous variables were compared with Student’s t test. The Chi-Squared test and Fisher test were used to compare clinical outcome between the two groups. P 4 follicles ≥16 mm), eight in the antagonist group and six in the control group. A non significant increase in the total amount of rFSH (629.5±358 vs 698.1±310 units) and cycle length (6.9 ±3.3 vs 7.8±2.3) was seen in the GnRH antagonist group with respect to the control group. The mean number of antagonist ampoules used was 2±1.2. The number of mature follicles (2.1±1.3 vs. 1.7±1.09, p<0.05) and pregnancy rates (25% vs. 11%, p<0.05) were significantly higher in patients treated with GnRH antagonist than in the control group, respectively. A similar number of twin pregnancies occurred in both groups (two and three, respectively), but the antagonist group also had one triplet gestation. Adding GnRH antagonist to COH-IUI cycles significantly increases pregnancy rates. This increase seems to be related with the number of follicles recruited, and thus, first, the use of GnRH antagonist is not recommended in monofollicular IUI cycles and, second, the risk of multiple gestations needs to be carefully evaluated.