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

Triggering final oocyte maturation with gonadotropin-releasing hormone agonist (GnRHa) versus human chorionic gonadotropin (hCG) in breast cancer patients undergoing fertility preservation: an extended experience

“…In a recent meta-analysis of GnRH antagonist freshautologous IVF cycles, women triggered with GnRHa had significantly lower pregnancy and live birth rates compared to women triggered with hCG, although the rate OHSS was significantly lower in the GnRHa group [30]. This finding suggests that GnRHa trigger may contribute to a luteal phase defect resulting in lower implantation and pregnancy rates [31].…”

The state of “freeze-for-all” in human ARTs

“…Unlike indirect pituitary suppression induced by GnRH agonists, administration of GnRH antagonists causes immediate and dose-related suppression of gonadotropin release by competitive occupancy of GnRH receptors in the pituitary [24], which results in a much shorter duration of stimulation and absence of side effects caused by profound hypoestrogenemia [25,26]. A meta-analysis by AlInany et al demonstrated that the live birth rates between the use of GnRH antagonists and agonist protocols were comparable [27], but the majority of trials clearly support GnRH antagonists resulting in a significantly lower incidence (50 %) of OHSS compared with GnRH agonists [27][28][29]. Following the introduction of the antagonist protocols, complementary measures came along to avoid the risk of OHSS even more, like triggering ovulation induction with GnRH agonists instead of human chorionic gonadotropin (HCG) [30][31][32][33].…”

“…A meta-analysis by AlInany et al demonstrated that the live birth rates between the use of GnRH antagonists and agonist protocols were comparable [27], but the majority of trials clearly support GnRH antagonists resulting in a significantly lower incidence (50 %) of OHSS compared with GnRH agonists [27][28][29]. Following the introduction of the antagonist protocols, complementary measures came along to avoid the risk of OHSS even more, like triggering ovulation induction with GnRH agonists instead of human chorionic gonadotropin (HCG) [30][31][32][33]. Still, this approach is not 100 % safe as a few anecdotal cases of severe OHSS following GnRH agonist triggering with no luteal supplementation have been reported [34][35][36].…”

“…GnRH agonist triggering has been associated with luteal phase defects, presumably due to excessive negative steroid feedback [37][38][39]. Two consecutive Cochrane reviews by the same author state that: BGnRH agonist triggering is associated with a lower ongoing pregnancy rate compared with conventional hCG^ [29,40]. This conclusion was qualified as premature and mistaken based on the following: (1) Cochrane reviews should not be conducted in the research phase when new concepts are being developed, and (2) the authors missed the fact that the variable that affects results is luteal phase support itself and not the use of GnRH agonist trigger for final oocyte maturation [39].…”

Role of Kisspeptine in Regulation of Reproductive Function

“…Некоторые стратегии, такие как использование прогестерона вместо ХГЧ для поддержки лютеиновой фазы цикла или уменьшение дозы гонадотропинов у пациентов с высоким риском СГя, широко применяются, так как не оказывают отрицательного влияния на частоту наступления беременности [131]. Другие стратегии, включая использование аГнРГ в качестве триггера выброса эндогенного ЛГ, связаны с меньшей частотой наступления беременности и, таким образом, применяются более редко [132]. Хотя созревание ооцитов in vitro предполагает отсутствие или ограничение необходимости стимуляции яичников в целом, технические препятствия и относительно низ-кая эффективность существующих технологий стимуляции созревания ооцитов в значитель-ной мере ограничивают использование данного метода [127].…”