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Mol. Hum. Reprod. Advance Access first published online on March 3, 2006
This version published online on March 29, 2006
Molecular Human Reproduction, doi:10.1093/molehr/gal024
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received December 9, 2005
Accepted February 2, 2006

Article

Genetic polymorphisms of vascular endothelial growth factor in severe pre-eclampsia

Ilona Bányász 1 *, Szilvia Szabó 1, Géza Bokodi 1, Ádám Vannay 2, Barna Vásárhelyi 3, András Szabó 1, Tivadar Tulassay 4, and János Rigó Jr. 5

1 First Department of Pediatrics, Semmelweis University, Budapest, Hungary
2 Szentágothai János Knowledge Centre, Semmelweis University, Budapest, Hungary
3 Research Group for Pediatrics and Nephrology, Hungarian Academy of Sciences
4 First Department of Pediatrics; Szentágothai János Knowledge Centre, Semmelweis University, Budapest, Hungary; Research Group for Pediatrics and Nephrology, Hungarian Academy of Sciences
5 First Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary

* To whom correspondence should be addressed.
Ilona Bányász, E-mail: banyasz{at}gyer1.sote.hu


  Abstract

Several lines of evidence support the hypothesis that vascular endothelial growth factor (VEGF) plays an important role in the pathogenesis of pre-eclampsia (PE). VEGF is a key component in the regulation of vascular remodelling and the survival of cytotrophoblasts in the placenta. In this case-control study, we aimed to test whether VEGF genetic polymorphisms are associated with the risk of severe PE. We enrolled 84 nulliparous pregnant women with severe PE (PE group). Their VEGF G+405C and VEGF C-2578A genotypes were determined by PCR-restriction fragment length polymorphism (PCR-RFLP) from venous blood samples and were compared with the corresponding VEGF genotypes of 96 nulliparous patients with uncomplicated pregnancies (control group). Carriers of the VEGF+405G allele occurred less frequently in PE than in the control group [P = 0.039; adjusted odds ratio (aOR) = 0.28, range: 0.08-0.93]. Hypertension and proteinuria were diagnosed earlier (by 1.6 weeks and 1.9 weeks, respectively) in PE patients with VEGF-2578A only after adjustment of this association for risk factors of PE. Our results suggest that carriers of VEGF+405G allele have a decreased susceptibility to PE and that the progression of PE may be modified by the presence of VEGF-2578A allele. Nevertheless, the clinical significance of these findings remains to be determined.

Keywords: hypertension/polymorphism/proteinuria/severe pre-eclampsia/VEGF.
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