2013年6月7日

誘導排卵有17%提早黃體化

人工授孕誘導排卵過程有17%病患有提早黃體化現象 (LH≥10 IU/l, progesterone>1 ng/ml)

http://humrep.oxfordjournals.org/content/21/3/632.full



Treatment with the GnRH antagonist ganirelix prevents premature LH rises and luteinization in stimulated intrauterine insemination: results of a double-blind, placebo-controlled, multicentre trial*

  1. B. Mannaerts 11
+Author Affiliations
  1. 1C.B.Lambalk, Department of Reproductive Medicine, Vrije Universiteit Medical Centre, Amsterdam, the Netherlands, 2A Leader, Civic Parkdale Clinic, Ottawa, Ontario, Canada, 3F Olivennes, CHU Antoine Beclere, Clamart, France, 4MR Fluker, Genesis Fertility Center, Vancouver, Canada, 5A Nyboe Andersen, Juliane Marie Centret Fertilitetsklinikken, Kopenhagen, Denmark, 6J Ingerslev, Fertilitetsklinikken, Skejby Sygehus, Arhus, Denmark, 7Y Khalaf, Assisted conception Unit, Guy’s Hospital, London, UK, 8Avril C, Clinique Saint Antoine, Bois Guillaume, France, 9J Belaisch-Allart, Hopital Jean Rostand, Sevres, France, 10R Roulier, Institut Medical de la Reproduction, Marseille, France and 11B Mannaerts, Organon, Oss, The Netherlands
  1. 12To whom correspondence should be addressed at: Department of Reproductive Medicine, Vrije Universiteit Medical Centre (Vumc), de Boelelaan 1117, 1081 HV, Amsterdam, the Netherlands. E-mail: cb.lambalk@vumc.nl
  • Received April 22, 2005.
  • Revision received October 11, 2005.
  • Accepted October 18, 2005.

Abstract

BACKGROUND: This study was designed to assess whether the use of ganirelix in women undergoing stimulated IUI could prevent the occurrence of premature LH rises and luteinization (LH + progesterone rises). METHODS: Women of infertile couples, diagnosed with unexplained or male factor infertility, were randomized to receive either ganirelix (n = 103) or placebo (n = 100) in a double-blind design. All women were treated with an individualized, low-dose rFSH regimen started on day 2–3 of cycle. Ganirelix (0.25 mg/day) was started if one or more follicles ≥14 mm were visualized. Ovulation was triggered by HCG injection when at least one follicle ≥18 mm was observed and a single IUI was performed 34–42 h later. The primary efficacy outcome was the incidence of premature LH rises (± progesterone rise). RESULTS: In the ganirelix group, four subjects had a premature LH rise (value ≥10 IU/l), one LH rise prior to the start of ganirelix and three LH rises during ganirelix treatment, whereas in the placebo group 28 subjects had a premature LH rise, six subjects prior to the start of placebo and 22 subjects during placebo treatment. The incidence of LH rises was significantly lower in ganirelix cycles compared to placebo cycles (3.9 versus 28.0%; P = 0.003 for ITT analysis). When excluding subjects with an LH value ≥10 IU/l before the start of ganirelix/placebo the incidence of LH rises was also significantly lower in ganirelix cycles compared to placebo cycles (2.9 versus 23.4%; P= 0.003 for ITT analysis). Premature luteinization (LH rise with concomitant progesterone rise ≥1 ng/ml) was observed in one subject in the ganirelix group and in 17 subjects in the placebo group of which three subjects had a premature spontaneous ovulation. Ongoing pregnancy rates per attempt were 12.6 and 12.0% for the ganirelix and placebo groups respectively. CONCLUSIONS: Treatment with ganirelix effectively prevents premature LH rises, luteinization in subjects undergoing stimulated IUI. Low-dose rFSH regimen combined with a GnRH antagonist may be an alternative treatment option for subjects with previous proven luteinization or in subjects who would otherwise require insemination when staff are not working.

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