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Maternal Serum-Soluble Vascular Endothelial Growth Factor Receptor-1 in Early Pregnancy Ending in Preeclampsia or Intrauterine Growth Retardation

Departments of Obstetrics and Gynecology (K.-A.W., E.T., E.H., O.Y., P.V.) and Clinical Chemistry (U.-H.S., H.A., P.F.), Helsinki University Central Hospital, Biomedicum Helsinki, 00029 HUS, Helsinki, Finland

Address all correspondence and requests for reprints to: Professor Olavi Ylikorkala, Helsinki University Central Hospital, P.O. Box 140, 00029 HUS, Finland.

Context: Vascular endothelial growth factor (VEGF) promotes placental vascularization, which is inadequate in preeclampsia and intrauterine growth retardation (IUGR). The soluble receptor of VEGF (sVEGFR-1), also known as soluble fms-like tyrosine kinase-1, is produced in the placenta and reduces VEGF activity. Therefore, elevated sVEGFR-1 could contribute to the development of preeclampsia and IUGR.

Objective: The objective of this study was to study maternal serum sVEGFR-1 concentration in early pregnancy ending in preeclampsia and IUGR.

Design: This was a case-control study.

Setting: This study was conducted at Helsinki University Central Hospital (Helsinki, Finland), a tertiary referral center.

Patients: Patients included 124 pregnant women, of whom 49 developed preeclampsia, 16 gave birth to IUGR infants without preeclampsia, and 59 remained normotensive and gave birth to normal-sized infants. Serum samples were collected at 12–15 and 16–20 gestational weeks.

Main Outcome Measures: Serum sVEGFR-1 concentrations were determined by ELISA.

Results: Women with subsequent preeclampsia had higher [median; interquartile range (IQR)] concentrations of sVEGFR-1 at 16–20 wk gestation (436 and 282–699 ng/liter; P = 0.005) than the controls (296 and 184–508 ng/liter). The conclusion was the same if women with mild (340 and 285–750 ng/liter; P = 0.043) or severe (497 and 235–699 ng/liter; P = 0.022) preeclampsia were analyzed separately. An elevated sVEGFR-1 concentration at 16–20 wk gestation is associated with an increased risk of preeclampsia but not of isolated IUGR. Soluble VEGFR-1 concentration decreased by 15% from the first to the second sampling in the controls but not in women with preeclampsia or IUGR.

Conclusion: Elevated sVEGFR-1 concentrations at 16–20 wk gestation precede the clinical manifestations of preeclampsia. By neutralizing VEGF, sVEGFR-1 may contribute to inadequate placental vascularization.

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