title: Gonadotropin-releasing hormone agonist versus human chorionic gonadotropin as a trigger of ovulation in polycystic ovarian disease gonadotropin hyperstimulated cycles.
abstract: 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.
  
  
  METHODS
  Polycystic ovarian disease gonadotropin hyperstimulated cycles outcome was investigated in a prospective study.
  
  
  METHODS
  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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Oasi Institute for Research, Catholic University, Rome, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Lanzone
authors.forename: A M
authors.initials: AM
authors.lastname: Fulghesu
authors.forename: P
authors.initials: P
authors.lastname: Villa
authors.forename: C
authors.initials: C
authors.lastname: Guida
authors.forename: M
authors.initials: M
authors.lastname: Guido
authors.forename: M C
authors.initials: MC
authors.lastname: Nicoletti
authors.forename: A
authors.initials: A
authors.lastname: Caruso
authors.forename: S
authors.initials: S
authors.lastname: Mancuso
mesh_terms: D000328:Adult; D002064:Buserelin / Q000627:therapeutic use*; D006063:Chorionic Gonadotropin / Q000627:therapeutic use*; D004958:Estradiol / Q000097:blood; D005260:Female; D006801:Humans; D016471:Ovarian Hyperstimulation Syndrome / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D010062:Ovulation Induction; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D011374:Progesterone / Q000097:blood; D011446:Prospective Studies
chemical_list: D006063:Chorionic Gonadotropin; D011374:Progesterone; D004958:Estradiol; D002064:Buserelin