The gonadotrophin-releasing hormone (GnRH) antagonist binds competitively t
o the receptors and thereby prevents endogenous GnRH from exerting its stim
ulatory effect on the pituitary cells. This causes suppression of gonadotro
phin secretion which occurs immediately after administration of the antagon
ist. When using GnRH antagonist in controlled ovarian stimulation, ovulatio
n or maturation of the oocyte can, therefore, be induced by a variety of dr
ugs, e.g. native GnRH, recombinant LH or short-acting GnRH agonists. Short-
acting GnRH agonists were recommended for triggering ovulation in cases wit
h a high risk of developing ovarian hyperstimulation syndrome (OHSS). Since
it is evident that GnRH is required to initiate the LH surge and the oestr
adiol rise, a single administration of GnRH antagonist during the late foll
icular phase delays the LH surge. Studies show ed that a single s.c. admini
stration of 3 or 5 mg of Cetrorelix in the late follicular stage was suffic
ient to prevent the LH surge for 6-17 days. This phenomenon can be used in
high responder patients who are prone to OHSS. The question whether this de
lay has any effect on oocyte quality and maturation still remains unanswere
d, Overall, there are four uses for GnRH antagonist: (i) using short-acting
GnRH agonists for triggering ovulation in cases in which the GnRH antagoni
st is part of the protocol for ovarian stimulation. Recombinant LW and nati
ve LHRH could also be used as triggers of LH surge; (ii) delaying the LH su
rge in cases prone to OHSS by treatment with GnRH antagonist; (iii) to admi
nister GnRH antagonist during the luteal phase to decrease the activity of
corpora lutea; (iv) in polycystic ovarian disease with elevated LH the LH/F
SH ratio can be corrected with the injection of GnRH antagonist prior to an
d during ovarian stimulation.