Gonadotropin-releasing hormone agonist versus HCG for oocyte triggering in antagonist assisted reproductive technology cycles

Ovarian hyperstimulation syndrome prevention by gonadotropin-releasing hormone agonist triggering of final oocyte maturation in a gonadotropin-releasing hormone antagonist protocol in combination with a “freeze-all” strategy: a prospective multicentric study

“…It has been shown that the administration of a GnRH agonist to induce final oocyte maturation after ovarian stimulation, which is feasible in a GnRH antagonist protocol (1), results in a reduced risk of moderate-to-severe ovarian hyperstimulation syndrome (OHSS) (2)(3)(4) by rapid demise of the corpora lutea (CL).…”

Different ART outcomes at increasing peak estradiol levels with long and antagonist protocols: retrospective insights from ten years experience

“…Accordingly, GnRH agonist ovulation triggering coupled with aggressive luteal support seem able to save the fresh embryo transfer with extremely interesting pregnancy rates and extremely low or no risk at all of both early and late OHSS [25]. If a residual detrimental effect of GnRH agonist triggering on pregnancy rates in fresh cycles with high response [26] could be completely avoided by embryo freezing/vitrification and delayed thawed/warmed embryo transfer on unstimulated cycles, it should be addressed by future studies. So far, preliminary data show high pregnancy rates with a clinical approach that combines GnRH agonist triggering, pronuclear zygotes vitrification, and delayed warmed embryo transfer [27,28].…”

Retrieving oocytes from small non-stimulated follicles in polycystic ovary syndrome (PCOS): in vitro maturation (IVM) is not indicated in the new GnRH antagonist era

“…In a meta-analysis retaining 8 RCTs, OHSS risks were profoundly reduced following GnRH-a triggering, but so were pregnancy chances (37). In an RCT, Humaidan et al (38) found more matured (MII) oocytes in women (n ¼ 55) undergoing GnRHa trigger as opposed to receiving hCG for ovulation induction (n ¼ 67), possibly an effect of the FSH elevation induced by GnRH-a.…”