engleski

TRIGGERING OF FINAL OOCYTE MATURATION WITH GONADOTROPIN-RELEASING HORMONE AGONIST AND PROBABILITY OF CLINICAL PREGNANCY IN IVF CYCLES USING A GONADOTROPIN-RELEASING HORMONE ANTAGONIST PROTOCOL

It has been shown that replacement of human chorionic gonadotropin (hCG) by gonadotropin- releasing hormone agonist (GnRHa) to trigger final oocyte maturation in IVF cycles using a gonadotropin-releasing hormone (GnRH) antagonist protocol reduce the risk of ovarian hyperstimulation syndrome (OHSS) in high responders. However, the triggering of final oocyte maturation using GnRHa is frequently associated with lower chances for pregnancy. The objective of this study was to investigate the impact of baseline patient characteristics, initial gonadotropin dose and intermediate IVF outcome measures on clinical pregnancy rates (CPR) after GnRH antagonist cycles in patients triggered with hCG and GnRHa. This retrospective analysis included medical record data on 735 patients <40 years of age on the day of oocyte retrieval who underwent GnRH antagonist-IVF cycle and for whom all assessed parameters were collected. The following parameters were assessed: baseline patients characteristics (antral follicle count (AFC), anti-Müllerian hormone (AMH), FSH, LH, E2, BMI, HOMA-IR), initial gonadotropin dose and the intermediate IVF outcome measures (peak E2 and peak P concentrations, the number of oocytes retrieved). The patients were split into groups according to trigger administrated for the final oocyte maturation: GnRHa-group (N=253) and hCG- group (n=485). Ovarian stimulation was commenced on the cycle day 3, administration of the GnRH antagonist (cetrorelix acetate, 0.25 mg, SC) was started on the cycle day 8, both continued until the day of triggering final oocyte maturation. GnRHa (triptorelin acetate, 0.2 mg, SC) was administered if >11 follicles >11 mm in diameter were visualized ultrasonographically. Otherwise, hCG (10 000 IU, IM) was administered. GnRHa triggered patients received 1500 IU hCG within 1 hour after oocyte retrieval (OOR). All patients were given luteal phase support with micronized progesterone, 3x200 mg daily, from the day of OOR. Clinical pregnancy was confirmed by the presence of fetal cardiac activity ≥28 days after OOR. The assessed parameters in the hCG-group and the GnRHa-group are presented in Table 1. CPR was higher in the GnRHa-group than in the hCG-group (42.3% vs 34.4%, P=0.043). The effect of parameters that could explain the observed difference in CPR was assessed using logistic multivariate regression analysis, which identified only age as being independently associated with clinical pregnancy. However, after age-matching, comparison of CPR between the GnRHa-group and the hCG-group showed that CPR were similar in all age- categories except in 34-36 years age-category where CPR was higher in the GnRHa group. These data indicate that by opting for GnRHa trigger clinicians do not trade between efficacy and safety. Lower pregnancy chances in IVF cycles using GnRHa trigger could be associated with the overall clinical approach rather than with the exclusive effect of the trigger used.

hCG; GnRH antagonist-IVF cycle; GnRH agonist; clinical pregnancy rate; oocyte maturation

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