INTRODUCTION
Over the past few decades, increasing knowledge of ovarian physiology and the possibility to evaluate accurately the ovarian reserve has led progressively to individualization and tailoring of ovarian stimulation for in vitro fertilization (IVF)—treatment.
Final oocyte maturation is the crucial step in ovarian stimulation cycles for IVF to retrieve mature oocytes for further processing in the IVF laboratory. In gonadotropin-releasing hormone (GnRH) antagonist cycles, human chorionic gonadotropin (hCG) and GnRH agonist can be administered for final oocyte maturation. Meanwhile, in patients with an expected or known high response, stimulation in a GnRH antagonist protocol with the use of GnRH agonist for final oocyte maturation is the state-of-the-art treatment to avoid or at least reduce significantly the risk for the development of ovarian hyperstimulation syndrome (OHSS).
The GnRH agonist dislocates the GnRH antagonist in the pituitary from the GnRH receptors. This results in a surge of LH and FSH, inducing final oocyte maturation and ovulation (2). However, induced LH/FSH peak is shorter compared to a natural LH surge. The duration of the LH/FSH surge is critical for normal luteal function, and due to a shortened LH surge, the granulosa cells fail to complete luteinization, resulting in a corpus luteum with impaired secretory function and a shortened lifespan. Therefore, the luteal phase will be characterized by luteolysis and luteal phase insufficiency (3). Previously, it was assumed that all patients will develop severe luteolysis within a matter of 5 days after GnRH agonist trigger (3); however, recently, it was clearly demonstrated that luteolysis after GnRH agonist trigger is patient specific (4). Unfortunately, there are so far no established predictive parameters to estimate the severity of the luteolysis.