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Reducing the Risk of OHSS by GnRH Agonist Triggering

Context: 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 u... Full description

Journal Title: The journal of clinical endocrinology and metabolism 2015, Vol.100 (12), p.4396-4398
Main Author: Casper, Robert F
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: United States: Endocrine Society
ID: ISSN: 0021-972X
Link: https://www.ncbi.nlm.nih.gov/pubmed/26513003
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recordid: cdi_proquest_miscellaneous_1747331486
title: Reducing the Risk of OHSS by GnRH Agonist Triggering
format: Article
creator:
  • Casper, Robert F
subjects:
  • Abridged Index Medicus
  • Animals
  • Eye Proteins - agonists
  • Female
  • Fertility Agents, Female - adverse effects
  • Gonadotropin-Releasing Hormone - agonists
  • Granulosa Cells - drug effects
  • Humans
  • Nerve Growth Factors - agonists
  • Ovarian Hyperstimulation Syndrome - metabolism
  • Receptors, LHRH - agonists
  • Serpins - agonists
  • Vascular Endothelial Growth Factor A - antagonists & inhibitors
ispartof: The journal of clinical endocrinology and metabolism, 2015, Vol.100 (12), p.4396-4398
description: Context: 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). Evidence Acquisition: 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). Evidence Synthesis: 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.
language: eng
source:
identifier: ISSN: 0021-972X
fulltext: no_fulltext
issn:
  • 0021-972X
  • 1945-7197
url: Link


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descriptionContext: 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). Evidence Acquisition: 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). Evidence Synthesis: 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.
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subjectAbridged Index Medicus ; Animals ; Eye Proteins - agonists ; Female ; Fertility Agents, Female - adverse effects ; Gonadotropin-Releasing Hormone - agonists ; Granulosa Cells - drug effects ; Humans ; Nerve Growth Factors - agonists ; Ovarian Hyperstimulation Syndrome - metabolism ; Receptors, LHRH - agonists ; Serpins - agonists ; Vascular Endothelial Growth Factor A - antagonists & inhibitors
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descriptionContext: 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). Evidence Acquisition: 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). Evidence Synthesis: 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.
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abstractContext: 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). Evidence Acquisition: 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). Evidence Synthesis: 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.
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