Lower serum levels of inhibin A and pro-αC during the luteal phase after triggering oocyte maturation with gonadotropin releasing hormone (GnRH) agonist in comparison to human chorionic gonadotropin (hCG): possible relevance for the prevention of ovarian hyperstimulation (OHSS)

Abstract

Objective: Ovarian hyperstimulation syndrome (OHSS) is a major complication of ovarian stimulation. Ovulation triggering with GnRH agonist instead of hCG may prevent the development of OHSS. In the current study we investigated the effect of triggering oocyte maturation by GnRH agonist in comparison to hCG on corpus luteum function by measuring luteal phase levels of inhibin A and pro-αC, as non-steroidal markers of luteal function. Design: Prospective collection of serum samples from three study groups. Comparison of the first patients that completed the requirements of the study protocol. Materials/Methods: Serum samples were collected during the luteal phase of IVF-ET cycles in three different protocols: 1) GnRH antagonist for prevention of an LH surge and hCG for triggering of final oocyte maturation (antagonist-hCG group, n=8, 4/8 pregnant). 2) GnRH antagonist for prevention of an LH surge and GnRH agonist for triggering final oocyte maturation (antagonist-agonist group, n=8, 4/8 pregnant). 3) GnRH agonist in a long protocol and hCG for final oocyte maturation (agonist-hCG group, n=5, 2/5 pregnant). Samples were assayed for inhibin A, pro-αC, progesterone and estradiol. Transvaginal ultrasound was performed in mid-luteal phase for estimation of corpora lutea number and volume. Results: Serum levels of inhibin A, pro-αC, estrogen and progesterone were significantly lower from day 4 to day 14 after triggering final oocyte maturation by GnRH agonist, in comparison to hCG triggering. Corpora lutea volume in the mid-luteal phase was significantly higher in hCG groups. Pregnancy caused a late luteal elevation of inhibin A and pro-αC in 3 out of 4 patients in the hCG groups but not in the antagonist-agonist group. Non-pregnant patients showed no late luteal elevation of inhibin forms in all groups. Conclusions: Final oocyte maturation triggering with GnRH agonist instead of hCG in IVF cycles causes significantly lower luteal levels of inhibins and steroids hormones, suggesting that corpora lutea may secrete lower levels of other non-steroidal substances with vasoactive properties that may be involved in OHSS. This may explain the mechanism of OHSS prevention by the use of GnRH agonist. Supported by: The study was supported by a research fund of the department of Obstetrics and Gynecology in Rambam Medical Center.