N.E. Kummer

Dual trigger of oocyte maturation with gonadotropin-releasing hormone agonist and low-dose human chorionic gonadotropin to optimize live birth rates in high responders

OBJECTIVE To compare live birth rates after dual trigger of oocyte maturation with GnRH agonist (GnRHa) and low-dose hCG versus GnRHa alone in high responders with peak E(2) <4,000 pg/mL at risk of ovarian hyperstimulation syndrome (OHSS). DESIGN Retrospective cohort study. SETTING University-based tertiary-care fertility center. PATIENT(S) Patients <40 years old with peak E(2) <4,000 pg/mL at risk of OHSS who underwent IVF/intracytoplasmic sperm injection with GnRH antagonist protocol and triggered with GnRHa alone or GnRHa plus 1,000 IU hCG (dual trigger) for oocyte maturation. INTERVENTION(S) GnRHa alone versus dual trigger. MAIN OUTCOME MEASURE(S) Live birth, implantation, and clinical pregnancy rates and OHSS. RESULT(S) The dual-trigger group had a significantly higher live birth rate (52.9% vs. 30.9%), implantation rate (41.9% vs. 22.1%), and clinical pregnancy rate (58.8% vs. 36.8%) compared with the GnRHa trigger group. One case of mild OHSS occurred in the dual-trigger group, and there were no cases of OHSS in the GnRHa trigger group. CONCLUSION(S) Dual trigger of oocyte maturation with GnRHa and low-dose hCG in high responders with peak E(2) <4,000 pg/mL improves the probability of conception and live birth without increasing the risk of significant OHSS.

Predicting successful induction of oocyte maturation after gonadotropin-releasing hormone agonist (GnRHa) trigger

STUDY QUESTION Are there factors predicting the number of total and mature oocytes retrieved after controlled ovarian hyperstimulation (COH) utilizing a gonadotropin-releasing hormone (GnRH) antagonist protocol and a GnRH agonist (GnRHa) to induce oocyte maturation? SUMMARY ANSWER Peak estradiol (E₂) level, post-trigger LH and progesterone and the magnitude of LH rise are independent predictors of the total number of oocytes and mature oocytes retrieved. WHAT IS KNOWN ALREADY Despite multiple follicular development in high responders, oocyte retrieval after a GnRHa trigger in a small subset of patients fails to obtain a substantial number of total oocytes or mature oocytes. STUDY DESIGN, SIZE AND DURATION A retrospective chart review of all autologous and oocyte donation cycles utilizing a GnRHa antagonist protocol where GnRHa was used for the induction of oocyte maturation between 1 April 2003 and 31 December 2011. PARTICIPANTS/MATERIALS, SETTING AND METHODS A total of 508 autologous and donor IVF/ICSI cycles utilizing a GnRH antagonist protocol for COH and GnRHa for the induction of oocyte maturation at a university-based tertiary fertility center. MAIN RESULTS AND THE ROLE OF CHANCE Peak E₂ on the day of trigger (r = 0.19, P < 0.001), post-trigger LH (r = 0.12, P = 0.009) and progesterone (r = 0.47, P < 001) and LH rise (r = 0.18, P < 0.001) all positively correlated with the number of total and mature oocytes retrieved. The true incidence of empty follicle syndrome was 1.4% (7/508). There was no post-trigger LH or progesterone cut-off value for the prediction of oocyte yield. However, all cases of empty follicle syndrome occurred in patients with post-trigger LH <15 IU/l and P ≤ 3.5 ng/ml. The findings of this study may also be due to chance since it was a retrospective study and not prospectively designed. LIMITATION, REASONS FOR CAUTION This is a retrospective chart review and therefore subject to bias. Serum hormone measurements were performed between 8 and 12 h after GnRHa trigger rather than a standardized time period following trigger administration. Therefore, peak levels of LH may have been missed due to the short ascending limb of LH rise lasting approximately 4 h after GnRHa trigger. WIDER IMPLICATIONS OF THE FINDINGS The results of this study can be generalized to high responders utilizing a GnRH antagonist protocol for COH and a GnRHa for the induction of oocyte maturation. The use of alternative stimulation regimens or medications will limit the ability to generalize the results of this study to other populations. STUDY FUNDING/COMPETING INTEREST(S) This study was not funded, and there are no conflicts of interest. TRIAL REGISTRATION NUMBER n/a.

Factors that predict the probability of a successful clinical outcome after induction of oocyte maturation with a gonadotropin-releasing hormone agonist.

OBJECTIVE To determine factors predicting cycle success after in vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI) in high-risk patients undergoing controlled ovarian stimulation with a gonadotropin-releasing hormone (GnRH) antagonist protocol with a GnRH agonist to induce oocyte maturation. DESIGN Retrospective cohort study. SETTING University-based tertiary fertility center. PATIENT(S) Women who underwent a GnRH antagonist protocol during IVF-ICSI cycles and received a GnRH agonist for oocyte maturation. INTERVENTION(S) GnRH-agonist trigger. MAIN OUTCOME MEASURE(S) Clinical and ongoing pregnancy rates and any occurrence of ovarian hyperstimulation syndrome (OHSS). RESULT(S) The serum luteinizing hormone (LH) level on the day of trigger of oocyte maturation was the single most important predictor of clinical pregnancy. Patients with a peak estradiol (E(2)) level ≥4,000 pg/mL also had statistically significant higher serum LH on the day of the GnRH-agonist trigger and had a higher clinical pregnancy rate compared with those with a peak E(2) level <4,000 pg/mL, although the two groups had comparable numbers of oocytes retrieved. No patients developed OHSS. CONCLUSION(S) Serum LH and E(2) levels ≥4,000 pg/mL on the day of the GnRH-agonist trigger are important predictors of success in patients at high risk of OHSS development. As none of the patients in this high-risk population developed OHSS, the GnRH-agonist trigger is effective in the prevention of this iatrogenic complication.

In vitro fertilization outcomes in patients experiencing a premature rise in luteinizing hormone during a gonadotropin-releasing hormone antagonist cycle

Patients undergoing controlled ovarian hyperstimulation and pituitary suppression with a GnRH antagonist who experienced a transient premature rise in LH were compared with those who did not have an early surge. Those experiencing a premature LH surge had equivalent clinical and ongoing pregnancy rates per ET.