RESUMO
Few studies evaluated angiogenic/anti-angiogenic factors and endothelial (dys)function in both maternal and umbilical cord blood (UCB) in preeclampsia (PE). We aimed to clarify the role of placental growth factor (PlGF), vascular endothelial growth factor (VEGF), soluble vascular endothelial growth factor receptor 1 (VEGFR-1) and tissue plasminogen activator (tPA), by evaluating them in maternal and UCB in 42 normal and 46 preeclamptic (PEc) cases. In PE, maternal and UCB PlGF were significantly lower; maternal VEGF, sVEGFR-1 and tPA were significantly higher. In UCB, sVEGFR-1 and tPA were significantly higher in PEc cases, while VEGF and PlGF were significantly lower. A significant correlation between maternal and UCB sVEGFR-1, and between sVEGFR-1 and tPA both in maternal and UCB, was observed in PEc cases. In maternal and UCB circulation in PE, a close interaction seems to exist between endothelial dysfunction and angiogenesis disturbance, and sVEGFR-1 seems to play a central role in those disturbances.
Assuntos
Feto/irrigação sanguínea , Pré-Eclâmpsia/fisiopatologia , Proteínas da Gravidez/sangue , Ativador de Plasminogênio Tecidual/sangue , Fator A de Crescimento do Endotélio Vascular/sangue , Receptor 1 de Fatores de Crescimento do Endotélio Vascular/sangue , Adulto , Estudos de Casos e Controles , Feminino , Sangue Fetal/metabolismo , Feto/metabolismo , Feto/fisiopatologia , Idade Gestacional , Humanos , Recém-Nascido , Recém-Nascido Pequeno para a Idade Gestacional , Neovascularização Fisiológica/fisiologia , Fator de Crescimento Placentário , Pré-Eclâmpsia/sangue , Pré-Eclâmpsia/metabolismo , Gravidez , Ativador de Plasminogênio Tecidual/genética , Ativador de Plasminogênio Tecidual/metabolismo , Adulto JovemRESUMO
Endothelial cell activation or damage is believed to play a key role in preeclampsia (PE) and may underlie the hemostatic changes observed in this syndrome. The aim of this study was to evaluate a relationship between maternal and cord blood hemostatic disturbances in preeclamptic pregnancies. We measured the plasma levels of tissue plasminogen activator (tPA) antigen and of plasminogen activator inhibitor type 1 (PAI-1) antigen, both markers of hemostatic and endothelial function, and fibrin fragment D-dimer. Maternal blood from uncomplicated (n=42) and PEc pregnancies (n=44) were collected before delivery, and umbilical cord blood (UCB) immediately after delivery. In preeclamptic cases, UCB presented significantly higher tPA values and significantly lower PAI-1/tPA ratio. Preeclamptic women also presented significantly higher tPA, as well as PAI-1 values, when compared with normal pregnant women; no significant difference was found for D-dimer. In preeclamptic women, proteinuria (a marker of PE severity) correlated positively and significantly with tPA and PAI-1 antigen levels. An inverse relationship between maternal tPA antigen levels and fetal birth weigh in PE was also observed. Our data show that the hemostatic maternal disturbances observed in preeclamptic women have similarities with the UCB circulation, and that endothelial dysfunction is the most plausible underlying cause. Moreover, maternal hemostatic disturbances seem to be associated with the severity of PE. Further studies are needed to strength the values of tPA and PAI-1 as markers of severity in PE.