title: Women with poor response to IVF have lowered circulating gonadotrophin surge-attenuating factor (GnSAF) bioactivity during spontaneous and stimulated cycles.
abstract: BACKGROUND
  Up to 13% of IVF cancellations are due to poor responses during down-regulated cycles. Because premature luteinization occurs more frequently in older or "poor responder" patients, defective production of gonadotrophin surge-attenuating factor (GnSAF) may be involved.
  
  
  METHODS
  Nine women with normal previous IVF response (NORM) and 9 with previous poor IVF response (POOR) were monitored in a spontaneous cycle (blood samples: days 2, 7, 11, 15 and 20) and then stimulated with recombinant human FSH (rFSH) under GnRH agonist (blood samples: treatment days GnRH agonist + 2, GnRH agonist + 7, day of HCG administration and days HCG + 1 and HCG + 8). LH, FSH, estradiol, progesterone and inhibin-A and -B were assayed in individual samples while GnSAF bioactivity was determined in samples pooled according to day, cycle and IVF response.
  
  
  RESULTS
  During spontaneous cycles LH, steroids and inhibins were similar between NORM and POOR women, FSH was elevated in POOR women (4.9 +/- 0.3 versus 6.7 +/- 0.6 mIU/l, P < 0.01) and GnSAF bioactivity was detectable on days 2, 7 and 11 in NORM women only. During IVF cycles inhibin-A and -B rose more markedly in NORM than POOR women. Similarly GnSAF production peaked on day GnRH agonist + 7 in NORM women, but on the day of HCG administration in POOR women.
  
  
  CONCLUSIONS
  Defects in ovarian responsiveness to FSH include reduced GnSAF production. This suggests that GnSAF should be investigated as a marker of ovarian reserve once an immunoassay becomes available.
authors.affiliation: Obstetricia y Ginecologia, Institut Universitari Dexeus, Barcelona, Spain.
authors.forename: Francisca
authors.initials: F
authors.lastname: Martinez
authors.forename: P N
authors.initials: PN
authors.lastname: Barri
authors.forename: B
authors.initials: B
authors.lastname: Coroleu
authors.forename: R
authors.initials: R
authors.lastname: Tur
authors.forename: Tarja
authors.initials: T
authors.lastname: Sorsa-Leslie
authors.forename: William J
authors.initials: WJ
authors.lastname: Harris
authors.forename: Nigel P
authors.initials: NP
authors.lastname: Groome
authors.forename: Philip G
authors.initials: PG
authors.lastname: Knight
authors.forename: Paul A
authors.initials: PA
authors.lastname: Fowler
mesh_terms: D000328:Adult; D005260:Female; D005307:Fertilization in Vitro; D005640:Follicle Stimulating Hormone / Q000627:therapeutic use*; D042341:Gonadal Hormones; D006062:Gonadotropins / Q000097:blood; D006801:Humans; D007247:Infertility, Female / Q000097:blood / Q000628:therapy*; D007265:Inhibins / Q000097:blood; D008597:Menstrual Cycle / Q000502:physiology*; D010053:Ovary / Q000187:drug effects*; D010062:Ovulation Induction; D011506:Proteins / Q000378:metabolism*; D011994:Recombinant Proteins / Q000627:therapeutic use; D013256:Steroids / Q000097:blood; D017211:Treatment Failure
chemical_list: D042341:Gonadal Hormones; D006062:Gonadotropins; D011506:Proteins; D011994:Recombinant Proteins; D013256:Steroids; C080538:attenuin; D007265:Inhibins; D005640:Follicle Stimulating Hormone