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Background: This study compared outcomes of the standard 6000 IU human chorionic gonadotropin (hCG) triggerwith a dual trigger comprised of 6000 IU hCG and 1 mg leuprolide acetate for final oocyte maturation in an intracytoplasmic sperm injection (ICSI) cycle. By convention, ICSI was performed in most cases at the clinic.Materials and Methods: In this retrospective study, a total of 50 women were included in each arm. Participantswere matched for age, indication and number of prior assisted reproduction technology (ART) cycles. Women at riskfor ovarian hyperstimulation syndrome (OHSS) were excluded. A flexible gonadotropin releasing hormone (GnRH)antagonist protocol was used and final oocyte maturation was triggered when two leading follicles were >17 mm.Distribution of variables was evaluated visually with histograms. Continuous variables were defined by mean (standarddeviation) or median (25th-75th percentile) depending on distribution characteristics. Categorical variables weredefined by numbers and percentages. Continuous variables were compared between the groups with the t test orMann-Whitney U test as appropriate. Categorical variables were compared by the chi-square test and its derivativesas appropriate. A two-sided P

A suggested explanation for the pituitary-suppressive effects of progestin-primed ovarian stimulation cycles (PPOS) is pituitary luteinizing hormone (LH) depletion with progestin exposure during the follicular phase. The GnRH agonist (GnRHa) trigger releases endogenous LH from the pituitary, and if the LH depletion theory is correct, the response to the agonist trigger would be dampened in PPOS cycles. In this study, we compared the performance of the GnRHa trigger after PPOS and GnRH antagonist ovarian stimulation cycles. All women who underwent ovarian stimulation with the GnRH antagonist or flexible PPOS (fPPOS) and received a GnRH agonist trigger were eligible for inclusion. Outcomes included number of metaphase-II (MII) oocytes retrieved per cycle, rates of empty follicle syndrome, maturation, fertilization, blastulation, and cumulative clinical pregnancy per stimulation cycle. During the screening period, there were 166 antagonists and 58 fPPOS cycles triggered with a GnRH agonist. Groups were matched for potential confounders using propensity score matching. Progestin-downregulated cycles had 19% high mature oocyte yield (median: 14 vs. 19 MII oocytes, P = 0.03). Cumulative ongoing pregnancy or live birth rates were estimated after matching for transferred embryo count, and rates were similar between GnRH antagonist and fPPOS group (57.0% vs. 62.1%, P = 0.68). However, the number of remaining blastocysts was higher in the fPPOS group (median: 5.0 vs. 6.0, P < 0.001). LH levels were higher in fPPOS cycles compared to GnRH antagonist cycles up to the trigger day (P < 0.001). After the GnRHa trigger, fPPOS cycles were associated with a steeper LH surge compared with antagonist cycles (P = 0.02). Higher endogenous gonadotropin levels through the stimulation period and an LH surge of higher magnitude following a GnRHa trigger suggest a milder pituitary suppression by fPPOS, which needs to be confirmed in larger samples. It appears that progestins do not deplete pituitary LH reserves and a GnRHa trigger is usable after PPOS in women with high ovarian reserve.

While gonadotrophin releasing hormone (GnRH) antagonists have been the standard of pituitary suppression during ovarian stimulation for ART, progestin primed ovarian stimulation (PPOS) has emerged as an alternative. Progestins can be started simultaneously with gonadotrophins (fixed PPOS) or later in the cycle depending on follicle growth (flexible PPOS). However, the flexible and fixed PPOS regimens have not been directly compared as of yet. This was a retrospective cohort study including women with diminished ovarian reserve who underwent oocyte cryopreservation. All women underwent ovarian stimulation with a fixed 300 IU daily dose of FSH. The primary outcome was the number of MII oocyte retrieved per cycle. Secondary outcome measures included the incidence of premature LH surge (>10ng/mL) and number of follicles larger than 14mm on the day of maturation trigger. During the screening period 2 out of 97 cycles were cancelled before oocyte retrieval, one in each group yielding an overall cancelation rate of 2%. Among women who had oocyte retrieval, 65 underwent flexible and 30 fixed PPOS. At baseline women on fixed and flexible PPOS had similar age (mean difference: -2.17 years, 95% CI: -4.46 to 0.11) and serum AMH levels (mean difference: 0.10 ng/mL, 95% CI: -0.24 to 0.47). Slight imbalances between the groups were rectified with propensity score matching using age and AMH levels. The incidence of premature LH surge (RR: 1.47, 95% CI: 0.51 – 5.27, p = 0.50), follicle count larger than 14mm on hCG day (RR: 1.14, 95% CI: 0.93 – 1.42, p = 0.22), number of MII oocytes retrieved (RR: 0.95, 95% CI: 0.79 – 1.15, p = 0.61) were similar between flexible and fixed PPOS. The rate of no oocyte retrieval was same between the groups (0.0% both) but no formal estimation was possible. Flexible and fixed PPOS regimens had no appreciable differences regarding MII oocyte yield and the incidence of premature LH surges. Cycles without oocyte retrieval were rare in both groups and ultrasonographic parameters of gonadotropin response were similar. Our study suggests the performances of either progestin regimen are comparable in this group of women.