Placental angiogenic growth factors and uterine artery Doppler findings for characterization of different subsets in preeclampsia and in isolated intrauterine growth restriction - 18/08/11
, Elisa Llurba, MD a, Pilar Martín-Gallán, BSc b, Luís Cabero, MD a, Eduard Gratacós, MD a
Reprint requests: Carmen Domínguez, PhD, Biochemistry and Molecular Biology Center, Hospital Materno-Infantil Vall d’Hebron, Pg Vall d’Hebron 119-129, 08035 Barcelona, Spain.Abstract |
Objective |
The purpose of this study was to evaluate possible relationships between placental markers and endothelial dysfunction in preeclampsia and intrauterine growth restriction.
Study design |
A prospective study was conducted in 76 patients with preeclampsia and 37 patients with intrauterine growth restriction that were classified as early onset (<34 weeks of gestational age) or late onset, and 40 control subjects. Plasma levels of placental growth factor, soluble fms-like tyrosine kinase–1, vascular cell adhesion molecule–1, and uterine artery Doppler indices were measured.
Results |
In early-onset preeclampsia and intrauterine growth restriction, placental growth factor was lower and soluble fms-like tyrosine kinase–1 and vascular cell adhesion molecule–1 higher than in control subjects, although all changes were more pronounced in preeclampsia. In late-onset preeclampsia, those patients with abnormal uterine artery Doppler indices had higher soluble fms-like tyrosine kinase–1 and vascular cell adhesion molecule–1 levels.
Conclusion |
Biochemical changes in early-onset preeclampsia and intrauterine growth restriction point to a common placental disorder and a state of endothelial dysfunction, which may require interaction with other factors to explain the maternal disease in preeclampsia. Data in late-onset preeclampsia suggest that a proportion of them may occur with minimal placental involvement.
Le texte complet de cet article est disponible en PDF.Key words : Preeclampsia, Intrauterine growth restriction, Uterine artery Doppler, Soluble fms-like tyrosine kinase–1
Plan
| Supported by grants from the Fondo the Investigación Sanitaria (FIS 01/1397 and 02/0742), and Centre Network RCMN (C03/08), and Group Network (G03/054) financed by the Carlos III Institute of Health (Madrid, Spain). |
Vol 195 - N° 1
P. 201-207 - juillet 2006 Retour au numéro
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