JOURNAL ARTICLE

Gonadotropin-releasing hormone agonist versus human chorionic gonadotropin as a trigger of ovulation in polycystic ovarian disease gonadotropin hyperstimulated cycles

A Lanzone, A M Fulghesu, P Villa, C Guida, M Guido, M C Nicoletti, A Caruso, S Mancuso
Fertility and Sterility 1994, 62 (1): 35-41
8005301

OBJECTIVE: To compare the use of GnRH agonist (GnRH-a) versus hCG in triggering the follicular rupture in patients with polycystic ovarian disease (PCOD) in whom ovulation was induced by gonadotropins.

DESIGN: Polycystic ovarian disease gonadotropin hyperstimulated cycles outcome was investigated in a prospective study.

PATIENTS AND INTERVENTIONS: Thirty-three PCOD patients (40 cycles) with gonadotropin-induced mild to moderate degree of ovarian hyperstimulation received 5,000 IU IM hCG or 200 microg [corrected] SC GnRH-a. A subgroup of GnRH-a-treated patients received P for luteal support. Five GnRH-a-treated patients underwent a GnRH test during luteal phase.

MAIN OUTCOME MEASURES: Echographic and endocrine characteristics both during the therapy and the luteal phase.

RESULTS: There was a similar percentage of ovulation and pregnancy rate in both groups of patients. The ovarian enlargement during the luteal phase in the GnRH-a-treated patients was lower than in the hCG group. Progesterone plasma levels (at midluteal phase) and the length of luteal phase was significantly lower in GnRH-a-treated patients with respect to the hCG-treated group. These differences disappeared in patients receiving luteal support. After GnRH injection, LH secretion decreased in GnRH-a-treated patients with respect to controls; however, corpus luteum was able to respond with a normal increase of P production.

CONCLUSION: The GnRH-a appears to be an effective alternative to hCG for inducing the follicular rupture in stimulated cycles in women who are at risk for developing ovarian hyperstimulation syndrome. However, GnRH-a administration can induce short luteal phase. This defect may be ascribed to the pituitary desensitization rather than to a direct effect on corpus luteum. Luteal phase support is needed to prevent luteal phase deficiency.

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