Objective: To compare clinical pregnancy, live birth, pregnancy loss, and ovarian hyperstimulation outcomes among infertile couples undergoing intracytoplasmic sperm injection (ICSI) using either a GnRH agonist long protocol or a GnRH antagonist protocol.
Methods: This retrospective comparative study evaluated 194 ICSI cycles with complete outcome data (98 agonist, 96 antagonist). Categorical outcomes were compared using chi-square or Fisher’s exact tests as appropriate. To strengthen interpretation of the primary endpoints, crude relative risks (RRs) with 95% confidence intervals (CIs) were calculated from the observed counts.
Results: The GnRH antagonist protocol was associated with a higher clinical pregnancy rate than the GnRH agonist long protocol (65.6% vs. 21.4%; RR 3.06, 95% CI 2.04–4.60; p < 0.001). Aggregate live birth was also higher in the antagonist group (42.7% vs. 8.2%; RR 5.23, 95% CI 2.59–10.57; p < 0.001). Pregnancy losses occurred in both groups; however, detailed category-specific comparisons were interpreted cautiously because of sparse cells. Ovarian hyperstimulation syndrome was infrequent in both groups and did not differ significantly between protocols.
Conclusion: In this retrospective cohort, GnRH antagonist stimulation was associated with improved clinical pregnancy and live birth outcomes without an observed increase in OHSS. Because the study was non-randomized and unadjusted, these findings should be interpreted as associative rather than causal, but they support further prospective evaluation of antagonist-based stimulation in routine ICSI practice.
Objective: To compare clinical pregnancy, live birth, pregnancy loss, and ovarian hyperstimulation outcomes among infertile couples undergoing intracytoplasmic sperm injection (ICSI) using either a GnRH agonist long protocol or a GnRH antagonist protocol.
Methods: This retrospective comparative study evaluated 194 ICSI cycles with complete outcome data (98 agonist, 96 antagonist). Categorical outcomes were compared using chi-square or Fisher’s exact tests as appropriate. To strengthen interpretation of the primary endpoints, crude relative risks (RRs) with 95% confidence intervals (CIs) were calculated from the observed counts.
Results: The GnRH antagonist protocol was associated with a higher clinical pregnancy rate than the GnRH agonist long protocol (65.6% vs. 21.4%; RR 3.06, 95% CI 2.04–4.60; p < 0.001). Aggregate live birth was also higher in the antagonist group (42.7% vs. 8.2%; RR 5.23, 95% CI 2.59–10.57; p < 0.001). Pregnancy losses occurred in both groups; however, detailed category-specific comparisons were interpreted cautiously because of sparse cells. Ovarian hyperstimulation syndrome was infrequent in both groups and did not differ significantly between protocols.
Conclusion: In this retrospective cohort, GnRH antagonist stimulation was associated with improved clinical pregnancy and live birth outcomes without an observed increase in OHSS. Because the study was non-randomized and unadjusted, these findings should be interpreted as associative rather than causal, but they support further prospective evaluation of antagonist-based stimulation in routine ICSI practice.
