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Genetic polymorphisms of vascular endothelial growth factor in severe pre-eclampsia
Author(s) -
I. Bányász,
S. Szabo,
Géza Bokodi,
Ádám Vannay,
Barna Vásárhelyi,
Attila J. Szabó,
Tivadar Tulassay,
János Rigó
Publication year - 2006
Publication title -
molecular human reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.143
H-Index - 122
eISSN - 1460-2407
pISSN - 1360-9947
DOI - 10.1093/molehr/gal024
Subject(s) - vascular endothelial growth factor , biology , genotype , allele , medicine , odds ratio , restriction fragment length polymorphism , pathogenesis , endocrinology , eclampsia , preeclampsia , placenta , vascular endothelial growth factor a , case control study , immunology , gastroenterology , pregnancy , vegf receptors , genetics , fetus , cancer research , gene
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(+405)C and VEGF C(-2578)A 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(+405)G 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(-2578)A only after adjustment of this association for risk factors of PE. Our results suggest that carriers of VEGF(+405)G allele have a decreased susceptibility to PE and that the progression of PE may be modified by the presence of VEGF(-2578)A allele. Nevertheless, the clinical significance of these findings remains to be determined.

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