In assisted reproductive technology (ART), the freeze-all strategy has become increasingly used to prevent ovarian hyperstimulation syndrome (OHSS). In a GnRH antagonist cycle, a GnRH agonist trigger is used instead of hCG trigger to prevent OHSS. This GnRH agonist trigger works by which mechanism?
- A Directly binds to LH receptors on granulosa cells, bypassing the flare effect and causing a short, self-limiting LH surge
- B Inhibits pituitary LH release via upregulation of inhibin B, preventing the mid-cycle LH surge from being too high
- C Causes an initial flare of endogenous LH and FSH sufficient for oocyte maturation, but this surge is shorter and lower than an hCG trigger, reducing luteal phase support ✓
- D Acts directly on cumulus cells to promote final oocyte maturation independent of LH receptor stimulation
Explanation
In GnRH antagonist protocols, the pituitary is not downregulated; therefore, a GnRH agonist trigger can be used to produce an initial 'flare' of endogenous gonadotropins (both LH and FSH) via stimulation of the agonist's own receptor — this provides sufficient LH surge amplitude and duration to complete oocyte maturation and trigger ovulation. However, unlike hCG (which has a prolonged luteal phase effect due to its 36-hour half-life), the endogenous LH surge from a GnRH agonist trigger is shorter (~24 hours), preventing the sustained ovarian hyperstimulation that leads to OHSS. Luteal phase support must then be supplemented.
Reference: Shaw's Textbook of Gynaecology, 17th ed.
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Written and medically reviewed by the StethoPrep medical team.