title: Reducing the Risk of OHSS by GnRH Agonist Triggering.
abstract: BACKGROUND
  Overstimulation of follicle development in assisted reproductive technology cycles can lead to the development of life-threatening ovarian hyperstimulation syndrome (OHSS). There is evidence that administration of GnRH agonist as the trigger for final follicular maturation, instead of the usual human chorionic gonadotropin trigger, will reduce the risk of OHSS by shortening the duration of luteal stimulation, lowering estrogen levels by inducing luteolysis and reducing the secretion of vascular endothelial growth factor (VEGF).
  
  
  METHODS
  The paper by Miller et al (1) in this month's issue of the Journal of Clinical Endocrinology and Metabolism (JCEM) demonstrates that GnRH agonist may directly reduce the activity of VEGF by stimulation of granulosa cell expression and secretion of pigment epithelial-derived factor (PEDF).
  
  
  RESULTS
  The increased expression and secretion of PEDF in response to a bolus of GnRH agonist may antagonize the adverse effects of VEGF on ovarian vascular permeability and may contribute to luteolysis by reducing corpus luteum vascularity, thereby reducing the risk of OHSS. In addition, stimulation of PEDF may also be part of the protective mechanism of dopamine agonists used for prevention of OHSS.
  
  
  CONCLUSIONS
  The new data presented by Miller et al (1) propose a likely mechanism for the reduced risk of OHSS following GnRH agonist triggering of follicle maturation in assisted reproductive technology cycles.
authors.affiliation: Division of Reproductive Sciences, Department of Obstetrics and Gynecology, University of Toronto, Lunenfeld-Tanenbaum Research Institute, Mt Sinai Hospital, and TCART Fertility Partners, Toronto ON, M5S 2X9, Canada.
authors.forename: Robert F
authors.initials: RF
authors.lastname: Casper
mesh_terms: D000818:Animals; D005136:Eye Proteins / Q000819:agonists*; D005260:Female; D005300:Fertility Agents, Female / Q000009:adverse effects*; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists*; D006107:Granulosa Cells / Q000187:drug effects*; D006801:Humans; D009414:Nerve Growth Factors / Q000819:agonists*; D016471:Ovarian Hyperstimulation Syndrome / Q000378:metabolism*; D011966:Receptors, LHRH / Q000819:agonists*; D015843:Serpins / Q000819:agonists*; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors*
chemical_list: D005136:Eye Proteins; D005300:Fertility Agents, Female; D009414:Nerve Growth Factors; D011966:Receptors, LHRH; D015843:Serpins; D042461:Vascular Endothelial Growth Factor A; D007987:Gonadotropin-Releasing Hormone