使用GnRHa破卵仍需小心其會影響黃體期子宮內膜功能
http://humrep.oxfordjournals.org/content/20/5/1213.full
GnRH agonist (buserelin) or hCG for ovulation induction in GnRH antagonist IVF/ICSI cycles: a prospective randomized study
- P. Humaidan1,5,
- H. Ejdrup Bredkjær2,
- L. Bungum1,
- M. Bungum1,
- M.L. Grøndahl2,
- L. Westergaard3 and
- C. Yding Andersen4
+Author Affiliations
- 5To whom correspondence should be addressed. Email:peter.humaidan@sygehusviborg.dk
- Received September 7, 2004.
- Revision received December 22, 2004.
- Accepted January 7, 2005.
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 dayper 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.
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