title: Controlled ovarian hyperstimulation using multi-dose gonadotropin-releasing hormone (GnRH) antagonist results in less systemic inflammation than the GnRH-agonist long protocol.
abstract: OBJECTIVE
  The aim of the study was to investigate whether controlled ovarian hyperstimulation (COH) using multi-dose gonadotropin-releasing hormone (GnRH) antagonist results in a lesser degree of systemic inflammation than the GnRH-agonist long protocol.
  
  
  METHODS
  Prospective, observational study.
  
  
  METHODS
  Blood was drawn three times during the COH cycle from patients undergoing the long GnRH-agonist protocol (agonist group) (n = 12) or the multi-dose GnRH-antagonist protocol (antagonist group) (n = 15): the day on which adequate suppression was obtained (agonist group), or day 2 or 3 of the menstrual cycle and before gonadotropin treatment (antagonist group) (Day-0); the day of or prior to administration of human chorionic gonadotropin (Day-hCG); and the day of ovum pick-up (Day-OPU). Levels of sex steroids and serum C-reactive protein (CRP) were compared between the two study groups among the three time points.
  
  
  RESULTS
  While no between-group differences were observed in patient age or ovarian stimulation characteristics, a significantly higher number of oocytes were retrieved in the antagonist compared with the agonist group. In both groups, serum CRP levels were significantly higher on Day-OPU than on Day-hCG and Day-0. While serum CRP levels were higher on Day-hCG than Day-0, the difference was statistically significant only for the agonist group (p < 0.05). Moreover, Day-OPU serum CRP levels were significantly higher in the agonist than in the antagonist subgroup.
  
  
  CONCLUSIONS
  COH using the multi-dose GnRH-antagonist protocol yields a lesser degree of systemic inflammation, as reflected by CRP levels, than the GnRH-agonist long protocol.
authors.affiliation: Department of Obstetrics and Gynecology, Barzilai Medical Center, Ashkelon, Israel. raoulo@barzi.health.gov.il
authors.forename: Raoul
authors.initials: R
authors.lastname: Orvieto
authors.forename: Michael
authors.initials: M
authors.lastname: Volodarsky
authors.forename: Eduard
authors.initials: E
authors.lastname: Hod
authors.forename: Roy
authors.initials: R
authors.lastname: Homburg
authors.forename: Jacob
authors.initials: J
authors.lastname: Rabinson
authors.forename: Efraim
authors.initials: E
authors.lastname: Zohav
authors.forename: Eyal Y
authors.initials: EY
authors.lastname: Anteby
authors.forename: Simion
authors.initials: S
authors.lastname: Meltcer
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism*; D004334:Drug Administration Schedule; D004958:Estradiol / Q000097:blood; D005260:Female; D005300:Fertility Agents, Female / Q000008:administration & dosage; D007987:Gonadotropin-Releasing Hormone / Q000008:administration & dosage / Q000031:analogs & derivatives*; D006727:Hormone Antagonists / Q000008:administration & dosage; D006801:Humans; D007247:Infertility, Female / Q000097:blood / Q000188:drug therapy*; D007249:Inflammation / Q000097:blood*; D008186:Luteolytic Agents / Q000008:administration & dosage; D054315:Oocyte Retrieval; D010062:Ovulation Induction / Q000009:adverse effects* / Q000379:methods; D018579:Patient Selection; D011374:Progesterone / Q000097:blood; D011446:Prospective Studies; D017329:Triptorelin Pamoate / Q000008:administration & dosage*
chemical_list: D005300:Fertility Agents, Female; D006727:Hormone Antagonists; D008186:Luteolytic Agents; D017329:Triptorelin Pamoate; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D004958:Estradiol; D002097:C-Reactive Protein; C062876:cetrorelix