Impact of Addition of Gonadotropin Releasing Hormone Agonist to Luteal Phase Support on Antagonist ICSI Cycles

Hormonal milieu during implantation is crucial to embryo-endometrium interaction and to the viability of the conceptus. There are many protocols of luteal phase support (LPS) in assisted reproductive technology (ART) cycles. GnRH-agonist (GnRH-a) is a new and promising modality for LPS. Regimens for using GnRH-a in LPS, including single mid-luteal bolus or the addition of a GnRH-a to progesterone supplementation, have been recently suggested. If the GnRH-a is administered in the mid-luteal phase, an initial flare-up with increased levels of LH takes 3-4 days before receptor down-regulation kicks in. The increased luteinizing hormone (LH) results in increased support for the corpus luteum (CL), leading to higher output of P4 and providing stronger LPS. In earlier studies, the inadvertent administration of GnRH-a in the mid-luteal phase, did not compromise pregnancy outcomes but rather enhanced implantation rates. Therefore, the use of GnRH-a in LPS was investigated and found to enhance clinical outcomes after GnRH-a and GnRH antagonist- treated ovarian stimulation cycles, as well as, in recipients of donated oocytes. Several studies since then investigated the role of GnRHa for LPS, found that luteal support with GnRH-a could be used as the first choice in patients at high risk for ovarian hyperstimulation syndrome (OHSS), or even as the sole source of LPS in a GnRH-a-triggered antagonist ovarian stimulation cycle. Although many trials have showed substantial efficacy of GnRH-a addition for luteal support on pregnancy outcomes in women undergoing IVF/ICSI, others, found no benefit of its addition to the standard LPS. A meta-analysis concluded that there is benefit, however, this evidence is of very low quality. The aim of this study is to evaluate the impact of addition of mid-luteal single-dose or multiple-dose GnRH agonist to the routine luteal phase support in patients undergoing ICSI cycles using GnRH antagonist protocol.