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This version published online on May 10, 2005
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2004-1955
A more recent version of this article appeared on August 1, 2005
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*High Risk Pregnancy

Submitted on October 5, 2004
Accepted on May 4, 2005

Soluble fms-like Tyrosine Kinase 1 (sFlt-1) is Increased in Preeclampsia but not in Normotensive Pregnancies with Small For Gestational Age Neonates: Relationship to Circulating Placental Growth Factor (PlGF)

Eiji Shibata, Augustine Rajakumar, Robert W. Powers, Robert W. Larkin, Carol Gilmour, Lisa M. Bodnar, William R. Crombleholme, Roberta B. Ness, James M. Roberts, and Carl A. Hubel*

Magee-Womens Research Institute and Department of Obstetrics & Gynecology, and Reproductive Sciences, University of Pittsburgh, PA; Department of Pediatrics, Allegheny General Hospital, Pittsburgh, PA; Department of Epidemiology, University of Pittsburgh Graduate School of Public Health; Department of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health, Pittsburgh PA

* To whom correspondence should be addressed. E-mail: rsicah{at}mwri.magee.edu.

Context. An excess of the soluble receptor, sFlt-1 may contribute to maternal vascular dysfunction in women with preeclampsia by binding and thereby reducing concentrations of free vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) in the circulation. The putative stimulus for increased sFlt-1 during preeclampsia, placental hypoxia due to poor perfusion, is common to both preeclampsia and idiopathic intrauterine growth restriction. However, the latter condition occurs without maternal vascular disease.

Objective. We asked if, as with preeclampsia, sFlt-1 is increased and free PlGF is decreased in villous placenta and maternal serum of normotensive women with small for gestational age (SGA) neonates.

Study Design. This was a case-control study using banked samples. Groups of women with small for gestational age (SGA) neonates (birthweight centile < 10th) and women with preeclampsia were matched to separate sets of normal pregnancy controls based on gestational age at blood sampling (serum) or gestational age at delivery (placenta).

Results. sFlt-1 levels were higher in preeclamptics than controls (serum: P < 0.0001; placental protein: P = 0.03; placental mRNA: P = 0.007) but not increased in SGA pregnancies. PlGF was lower in both preeclampsia (serum: P < 0.0001; placental protein: P = 0.05) and SGA (serum: P = 0.0008; placental protein: P = 0.03) compared with their controls. PlGF in preeclampsia and SGA groups did not differ.

Conclusions. These data are consistent with a role for sFlt-1 in the maternal manifestations of preeclampsia. In contrast to preeclampsia, sFlt-1 does not appear to contribute substantially to decreased circulating free PlGF in SGA pregnancies in the absence of a maternal syndrome.
Key words: pregnancy • preeclampsia • fetal growth restriction • placental growth factor • soluble vascular endothelial growth factor receptor-1




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