title: Recombinant luteinizing hormone supplementation to recombinant follicle-stimulating hormone induced ovarian hyperstimulation in the GnRH-antagonist multiple-dose protocol.
abstract: BACKGROUND
  Suppression of endogenous LH production by mid-follicular phase GnRH-antagonist administration in controlled ovarian hyperstimulation protocol using recombinant (rec) FSH preparations void of LH activity may potentially affect ovarian response and the outcome of IVF treatment. The present study prospectively assessed the effect of using a combination of recFSH and recLH on ovarian stimulation parameters and treatment outcome in a fixed GnRH-antagonist multiple dose protocol.
  
  
  METHODS
  127 infertile patients with an indication for IVF or ICSI were recruited and randomized (using sealed envelopes) to receive a starting dose of either 150 IU recFSH (follitropin alpha) or 150 IU recFSH plus 75 IU recLH (lutropin alpha) for ovarian hyperstimulation. GnRH-antagonist (Cetrorelix) 0.25 mg was administered daily from stimulation day 6 onwards up to and including the day of the administration of recombinant HCG (chorion gonadotropin alpha). Gonadotropin dose adjustments were allowed from stimulation day 6 onwards, HCG was administered as soon as three follicles > or =18 mm were present. The primary outcome parameter was treatment duration until administration of HCG.
  
  
  RESULTS
  Exogenous LH did not shorten the time necessary to reach ovulation induction criteria. Serum estradiol (E(2)) and LH levels were significantly higher on the day of HCG administration in the recLH-supplemented group (1924.7 +/- 1256.4 vs 1488.3 +/- 824.0 pg/ml, P < 0.03), and 2.1 +/- 1.4 vs 1.4 +/- 1.5 IU/l, P < 0.01, respectively).
  
  
  CONCLUSIONS
  Except for higher E(2) and LH levels on the day of HCG administration, no positive trend in favour of additional LH was found as defined by treatment outcome parameters.
authors.affiliation: University Clinic of Schleswig Holstein, Campus Luebeck, Germany. georg.griesinger@frauenklinik.uni-luebeck.de
authors.forename: G
authors.initials: G
authors.lastname: Griesinger
authors.forename: A
authors.initials: A
authors.lastname: Schultze-Mosgau
authors.forename: K
authors.initials: K
authors.lastname: Dafopoulos
authors.forename: A
authors.initials: A
authors.lastname: Schroeder
authors.forename: A
authors.initials: A
authors.lastname: Schroer
authors.forename: S
authors.initials: S
authors.lastname: von Otte
authors.forename: D
authors.initials: D
authors.lastname: Hornung
authors.forename: K
authors.initials: K
authors.lastname: Diedrich
authors.forename: R
authors.initials: R
authors.lastname: Felberbaum
mesh_terms: D000328:Adult; D006063:Chorionic Gonadotropin / Q000627:therapeutic use; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000097:blood; D005260:Female; D005307:Fertilization in Vitro / Q000379:methods; D005640:Follicle Stimulating Hormone / Q000627:therapeutic use*; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000627:therapeutic use; D006727:Hormone Antagonists / Q000627:therapeutic use; D006801:Humans; D007247:Infertility, Female / Q000628:therapy; D007986:Luteinizing Hormone / Q000009:adverse effects* / Q000097:blood / Q000627:therapeutic use; D016471:Ovarian Hyperstimulation Syndrome / Q000139:chemically induced*; D010062:Ovulation Induction / Q000379:methods*; D011247:Pregnancy; D018873:Pregnancy Rate; D011994:Recombinant Proteins / Q000009:adverse effects / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D006063:Chorionic Gonadotropin; D006727:Hormone Antagonists; D011994:Recombinant Proteins; D007987:Gonadotropin-Releasing Hormone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; C062876:cetrorelix