title: Serum inhibin A, VEGF and TNFalpha levels after triggering oocyte maturation with GnRH agonist compared with HCG in women with polycystic ovaries undergoing IVF treatment: a prospective randomized trial.
abstract: BACKGROUND
  We aimed to examine the serum levels of inhibin A, vascular endothelial growth factor (VEGF), tumour necrosis factor alpha (TNFalpha), estradiol (E2) and progesterone levels after triggering of final oocyte maturation with GnRH agonist compared with HCG in patients with polycystic ovaries (PCO) and to investigate the relationship between these markers and ovarian hyperstimulation syndrome (OHSS).
  
  
  METHODS
  Twenty-eight patients with PCO, undergoing controlled ovarian hyperstimulation with FSH and GnRH antagonist for IVF-embryo transfer treatment, were randomized for triggering of final oocyte maturation with GnRH agonist (GnRH agonist group, n = 15) or HCG (HCG group, n = 13). Blood samples were obtained on the day of randomization and thereafter every 2-7 days. Serum levels of inhibin A, VEGF, TNFalpha, E2 and progesterone, the incidence of OHSS, ovarian size and pelvic fluid accumulation were evaluated.
  
  
  RESULTS
  Serum inhibin A, E2 and progesterone levels were significantly lower in the GnRH agonist group compared with the HCG group, particularly on the day of embryo transfer (P < 0.0001). Serum VEGF and TNFalpha levels were similar between the two groups. Four patients in the HCG group developed severe OHSS, whereas no patient had any symptoms or signs of OHSS in the GnRH-agonist group (P < 0.05).
  
  
  CONCLUSIONS
  In patients with PCO treated with FSH/GnRH antagonist, final oocyte maturation with GnRH agonist instead of HCG reduces significantly inhibin A, E2 and progesterone levels during the luteal phase. This phenomenon reflects the inhibition of the corpus luteum function and may explain, at least in part, the mechanism of OHSS prevention in high-risk patients. Our results do not support a crucial role for VEGF or TNFalpha in OHSS.
authors.affiliation: IVF Unit, Department of Obstetrics and Gynecology, Shaare Zedek Medical Center, Jerusalem, Israel.
authors.forename: Rachel
authors.initials: R
authors.lastname: Babayof
authors.forename: Ehud J
authors.initials: EJ
authors.lastname: Margalioth
authors.forename: Mahmoud
authors.initials: M
authors.lastname: Huleihel
authors.forename: Alaa
authors.initials: A
authors.lastname: Amash
authors.forename: Edit
authors.initials: E
authors.lastname: Zylber-Haran
authors.forename: Michael
authors.initials: M
authors.lastname: Gal
authors.forename: Baruch
authors.initials: B
authors.lastname: Brooks
authors.forename: Tzvia
authors.initials: T
authors.lastname: Mimoni
authors.forename: Talia
authors.initials: T
authors.lastname: Eldar-Geva
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D006063:Chorionic Gonadotropin / Q000819:agonists*; D004958:Estradiol / Q000097:blood; D005260:Female; D005307:Fertilization in Vitro; D005640:Follicle Stimulating Hormone / Q000008:administration & dosage; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists* / Q000037:antagonists & inhibitors; D006801:Humans; D007265:Inhibins / Q000097:blood; D009865:Oocytes / Q000187:drug effects* / Q000254:growth & development; D016471:Ovarian Hyperstimulation Syndrome / Q000175:diagnosis* / Q000517:prevention & control*; D011085:Polycystic Ovary Syndrome / Q000378:metabolism; D011247:Pregnancy; D011374:Progesterone / Q000097:blood; D017329:Triptorelin Pamoate / Q000008:administration & dosage; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D015415:Biomarkers; D006063:Chorionic Gonadotropin; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C422362:inhibin A; D017329:Triptorelin Pamoate; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D004958:Estradiol; D007265:Inhibins; D005640:Follicle Stimulating Hormone