Pregnancy outcome of “delayed start” GnRH antagonist protocol versus GnRH antagonist protocol in poor responders: A clinical trial study

Abstract

Background:Management of poor-responding patients is still major challenge in assisted reproductive techniques (ART). Delayed-start GnRH antagonist protocol is recommended to these patients, but little is known in this regards.Objective:The goal of this study was assessment of delayed-start GnRH antagonist protocol in poor responders, and in vitro fertilization (IVF) outcomes.Materials and Methods:This randomized clinical trial included sixty infertile women with Bologna criteria for ovarian poor responders who were candidate for IVF. In case group (n=30), delayed-start GnRH antagonist protocol administered estrogen priming followed by early follicular-phase GnRH antagonist treatment for 7 days before ovarian stimulation with gonadotropin. Control group (n=30) treated with estrogen priming antagonist protocol. Finally, endometrial thickness, the rates of oocytes maturation, , embryo formation, and pregnancy were compared between two groups. Results:Rates of implantation, chemical, clinical, and ongoing pregnancy in delayed-start cycles were higher although was not statistically significant. Endometrial thickness was significantly higher in case group. There were no statistically significant differences in the rates of oocyte maturation, embryo formation, and IVF outcomes between two groups.Conclusion:There is no significant difference between delayed-start GnRH antagonist protocol versus GnRH antagonist protocol.

Does the “delayed start” protocol with gonadotropin-releasing hormone antagonist improve the pregnancy outcome in Bologna poor responders? a randomized clinical trial

“…Similarly, Maged et al; in a first randomized clinical trial on 160 patients with POR diagnosis showed that the delayed start protocol improved cycle outcome by reducing the total dose of used gonadotropin, improving estradiol levels (E 2 ) and endometrial thickness on the day of hCG administration and increasing the total number of retrieved and mature oocytes [9]. However, Aflatoonian et al in a randomized pilot study on 60 POR failed to show any significant difference between this new strategy and routine antagonist protocol [10]; although the non-significant results may relate to small sample size. In our study, the clinical pregnancy rate in both study and control groups were low (8.7% vs. 7.1%, respectively).…”

“…Recently, Cakmak et al, in a retrospective study introduced a novel approach with delaying the start of COS along with GnRH antagonist pretreatment for 7 days after estrogen priming for further suppression of endogenous FSH during the early follicular phase, resulting in more FSH-responsive follicles and thus improving synchronous follicular development [8]. Also, two clinical trials have examined this strategy and reported controversial results [9, 10]. The present randomized clinical trial was designed to compare the efficacy of delayed-start GnRH antagonist protocol versus GnRH antagonist protocol in patients with poor ovarian response diagnosis on the basis of Bologna criteria.…”

Pregnancy outcome in delayed start antagonist versus microdose flare GnRH agonist protocol in poor responders undergoing IVF/ICSI: An RCT

“…Aflatoonian and colleagues in a clinical trial concluded that in poor responders delayed-start protocol slightly but not significantly improves pregnancy and implantation rate. They compared conventional antagonist protocol with delayed-start protocol ( 16 ). In our study delayed protocol was compared with microdose flare to find a suitable ART protocol in poor responders and the results indicated that the number of retrieved oocytes, mature oocytes, number of 2 PN and implantation rate were significantly higher in delayed antagonist group.…”

Comparison of an estradiol patch and GnRH-antagonist protocol with a letrozole/antagonist protocol for patients without oocyte development, fertilization and/or embryo development in previous IVF cycles

“…The presence of various developmental stages of antral follicles due to different FSH receptor levels can cause different susceptibility to FSH and thus lead to heterogeneous follicular development. The resulting size heterogeneity causes asynchronous growth and poor follicular response at the beginning of COH treatment [5][6][7]. Estradiol is the main hormone involved in the negative regulation of FSH.…”