Relationship between maternal and cord blood hemostatic disturbances in preeclamptic pregnancies.
Thromb Res
; 123(2): 219-24, 2008.
Article
em En
| MEDLINE
| ID: mdl-18384840
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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Pré-Eclâmpsia
/
Sangue Fetal
/
Hemostasia
/
Mães
Tipo de estudo:
Observational_studies
/
Risk_factors_studies
Limite:
Adult
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Female
/
Humans
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Newborn
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Pregnancy
Idioma:
En
Revista:
Thromb Res
Ano de publicação:
2008
Tipo de documento:
Article
País de afiliação:
Portugal
País de publicação:
Estados Unidos