LH level on ovulation trigger day has a different impact on the outcomes of agonist and antagonist regimens during in vitro fertilization

Abstract

Abstract Background To assess the impact of the luteinizing hormone level on ovulation trigger day (LHOTD) on in vitro fertilization (IVF) outcomes in gonadotropin-releasing hormone (GnRH) agonist and antagonist regimens during fresh embryo transfer cycles. Methods A stepwise, progressive multivariate regression model was introduced to assess the effect of the LHOTD on clinical pregnancy and live birth rates. Mantel‒Haenszel stratification analysis was used to examine the association between the LHOTD and clinical outcomes with the antagonist regimen. Results The LHOTD had different distributions in the agonist and antagonist regimens. The cycles were assigned into three LHOTD tertile groups. In the agonist regimen, compared with the 1st tertile (T1), in the 2nd (T2) and 3rd (T3) tertiles, the adjusted odds ratios (ORs) (95% confidence intervals [CIs], P value) were 1.187 (1.047–1.345, 0.007) and 1.420 (1.252–1.610, < 0.001) for clinical pregnancy, respectively, and 1.149 (1.009–1.309, 0.036) and 1.476 (1.296–1.681, < 0.001) for live birth. In the antagonist regimen, there was no significant difference in clinical pregnancy and live birth rates among the tertiles. However, in the stratified group of patients aged less than 35 years, the ORs (95% CIs, P value) of T2 and T3 were 1.316 (1.051–1.648, 0.017) and 1.354 (1.077–1.703, 0.009) for clinical pregnancy, respectively, and 1.275 (1.008–1.611, 0.043) and1.269 (0.999–1.611, 0.051) for live birth. Moreover, there was a discrepancy in the results among the subdivided LHOTD T1 groups adopting the antagonist regimen. Compared with that of the < 1.06 mIU/mL subgroup, the ORs (95% CIs, P value) of the > 1.5 mIU/mL subgroup were 1.693 (1.194–2.400, 0.003) for clinical pregnancy and 1.532 (1.057–2.220, 0.024) for live birth after eliminating potential confounders. Conclusions The LHOTD was profoundly suppressed in the agonist regimen, and its level was positively correlated with clinical pregnancy and live birth rates. In contrast, in the flexible antagonist regimen, the LHOTD was significantly higher than that in the agonist regimen and did not correlate with the outcome, except for women in the nonadvanced age group and those with an excessively suppressed LHOTD. Further investigation is required to determine the rationale for these findings.