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Hum. Reprod. Advance Access published online on March 10, 2005

Human Reproduction, doi:10.1093/humrep/deh765
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Human Reproduction © European Society of Human Reproduction and Embryology 2005; all rights reserved
Received September 7, 2004
Revised December 22, 2004
Accepted January 7, 2005

Article

GnRH agonist (buserelin) or hCG for ovulation induction in GnRH antagonist IVF/ICSI cycles: a prospective randomized study

P. Humaidan 1*, H. Ejdrup Bredkjær 2, L. Bungum 1, M. Bungum 1, M.L. Grøndahl 2, L. Westergaard 3, and C. Yding Andersen 4

1 The Fertility Clinic, Viborg Hospital (Skive), DK 7800 Skive, Denmark
2 The Fertility Clinic, Hvidovre Hospital, DK 2650, Hvidovre, Denmark
3 The Fertility Clinic Trianglen, Lundevangsvej 12, DK 2900 Hellerup, Denmark
4 Laboratory of Reproductive Biology, Section 5712, University Hospital of Copenhagen, DK 2100 Copenhagen, Denmark

* To whom correspondence should be addressed.
P. Humaidan, E-mail: peter.humaidan{at}sygehusviborg.dk


   Abstract

BACKGROUND: We aimed to determine the efficacy of ovarian hyperstimulation protocols employing a GnRH antagonist to prevent a premature LH rise allowing final oocyte maturation and ovulation to be induced by a single bolus of either a GnRH agonist or hCG. METHODS: A total of 122 normogonadotrophic patients following a flexible antagonist protocol was stimulated with recombinant human FSH and prospectively randomized (sealed envelopes) to ovulation induction with a single bolus of either 0.5 mg buserelin s.c. (n=55) or 10 000 IU of hCG (n=67). A maximum of two embryos was transferred. Luteal support consisted of micronized progesterone vaginally, 90 mg a day, and estradiol, 4 mg a day per os. RESULTS: Ovulation was induced with GnRH agonist in 55 patients and hCG in 67 patients. Significantly more metaphase II (MII) oocytes were retrieved in the GnRH agonist group (P<0.02). Significantly higher levels of LH and FSH (P<0.001) and significantly lower levels of progesterone and estradiol (P<0.001) were seen in the GnRH agonist group during the luteal phase. The implantation rate, 33/97 versus 3/89 (P<0.001), clinical pregnancy rate, 36 versus 6% (P=0.002), and rate of early pregnancy loss, 4% versus 79% (P=0.005), were significantly in favour of hCG. CONCLUSIONS: Ovulation induction with a GnRH agonist resulted in significantly more MII oocytes. However, a significantly lower implantation rate and clinical pregnancy rate in addition to a significantly higher rate of early pregnancy loss was seen in the GnRH agonist group, most probably due to a luteal phase deficiency.

Keywords: agonist; antagonist; IVF; ovulation induction.
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