Serum vascular endothelial growth factor and Doppler blood flow velocities in in vitro fertilization: relevance to ovarian hyperstimulation syndrome and polycystic ovaries

1998 ◽  
Vol 70 (4) ◽  
pp. 651-658 ◽  
Author(s):  
Rina Agrawal ◽  
Gerard Conway ◽  
Povilas Sladkevicius ◽  
Seang Ling Tan ◽  
Lawrence Engmann ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Blood Flow ◽  
Ovarian Hyperstimulation Syndrome ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Polycystic Ovaries ◽  
Vitro Fertilization ◽  
Blood Flow Velocities ◽  
Endothelial Growth Factor

scholarly journals A Unique Human Chorionic Gonadotropin Antagonist Suppresses Ovarian Hyperstimulation Syndrome in Rats

Endocrinology ◽  
2009 ◽  
Vol 150 (8) ◽  
pp. 3807-3814 ◽  
Author(s):  
Pratibhasri A. Vardhana ◽  
Martin A. Julius ◽  
Susan V. Pollak ◽  
Evan G. Lustbader ◽  
Rhonda K. Trousdale ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Ovarian Hyperstimulation Syndrome ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Physiological Changes ◽  
Lh Receptor ◽  
Glycosylation Sites ◽  
Endothelial Growth Factor

Ovarian hyperstimulation syndrome (OHSS) is a complication of in vitro fertilization associated with physiological changes after hCG administration to induce final oocyte maturation. It presents as widespread increases in vascular permeability and, in rare cases, results in cycle cancellation, multi-organ dysfunction, and pregnancy termination. These physiological changes are due primarily to activation of the vascular endothelial growth factor (VEGF) system in response to exogenous human chorionic gonadotropin (hCG). An hCG antagonist (hCG-Ant) could attenuate these effects by competitively binding to the LH/CG receptor, thereby blocking LH activity in vivo. We expressed a form of hCG that lacks three of its four N-linked glycosylation sites and tested its efficacy as an antagonist. The hCG-Ant binds the LH receptor with an affinity similar to native hCG and inhibits cAMP response in vitro. In a rat model for ovarian stimulation, hCG-Ant dramatically reduces ovulation and steroid hormone production. In a well-established rat OHSS model, vascular permeability and vascular endothelial growth factor (VEGF) expression are dramatically reduced after hCG-Ant treatment. Finally, hCG-Ant does not appear to alter blastocyst development when given after hCG in mice. These studies demonstrate that removing specific glycosylation sites on native hCG can produce an hCG-Ant that is capable of binding without activating the LH receptor and blocking the actions of hCG. Thus hCG-Ant will be investigated as a potential therapy for OHSS.

scholarly journals Human Chorionic Gonadotropin-Induced Ovarian Hyperstimulation Syndrome Is Associated with Up-Regulation of Vascular Endothelial Growth Factor

2002 ◽  
Vol 87 (7) ◽  
pp. 3300-3308 ◽  
Author(s):  
Tzu-Hao Wang ◽  
Shang-Gwo Horng ◽  
Chia-Lin Chang ◽  
Hsien-Ming Wu ◽  
Yi-Ju Tsai ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Granulosa Cells ◽  
Ovarian Hyperstimulation Syndrome ◽  
Elevated Serum ◽  
Tyrosine Kinase Receptor ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Ovarian hyperstimulation syndrome (OHSS), a life-threatening complication occurring in stimulated ovarian cycles, arises from treatment with gonadotropin for induction of follicular maturation in infertile women. Clinical characteristics of OHSS include ascites and pleural effusion induced by increased vascular permeability, where vascular endothelial growth factor (VEGF) was suspected to be the culprit. To test whether the effects of human CG (hCG) on the pathogenesis of OHSS were mediated through the VEGF produced by luteinized granulosa cells, we measured estradiol, VEGF, IGF-II levels in serum, and follicular fluid and analyzed their mRNA expression in luteinized granulosa cells obtained from 101 women (58 with OHSS and 43 controls) who underwent in vitro fertilization and embryo transfer. This study presents the first evidence that hCG up-regulated VEGF expression of granulosa cells in the OHSS, not the control groups, and that follicular VEGF worked through an autocrine mechanism using its kinase insert domain-containing receptor, not the fms-like tyrosine kinase receptor. We calculated total follicular production of VEGF, by multiplying follicular concentrations by follicular volumes, and verified that an increase in total follicular production of VEGF accounted for elevated serum levels of VEGF, which was associated with the development of OHSS. These findings demonstrate that through up-regulation of VEGF, hCG plays a significant role in the pathogenesis of OHSS.

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