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Submitted on May 16, 2005
Accepted on October 20, 2005
Departments of Obstetrics and Gynecologyand Clinical Chemistry, Helsinki University Central Hospital, Biomedicum Helsinki
* To whom correspondence should be addressed. E-mail: olavi.ylikorkala{at}hus.fi.
Context. Vascular endothelial growth factor (VEGF) promotes placental vascularization, which is inadequate in pre-eclampsia 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 pre-eclampsia and IUGR.
Objective. To study maternal serum sVEGFR-1 concentration in early pregnancy ending in pre-eclampsia and IUGR.
Design. A case-control study.
Setting. University hospital, a tertiary referral center.
Patients. 124 pregnant women of whom 49 developed pre-eclampsia, 16 gave birth to IUGR-infants without pre-eclampsia, 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 determined by enzyme-linked immunosorbent assay.
Results: Women with subsequent pre-eclampsia had higher (median; IQR) concentrations of sVEGFR-1 at 16-20 weeks of gestation (436 ng/L, 282-699 ng/L, P = 0.005) than the controls (296 ng/L, 184-508 ng/L). The conclusion was the same if women with mild (340 ng/L, 285-750 ng/L, P = 0.043) or severe (497 ng/L, 235-699 ng/L, P = 0.022) pre-eclampsia were analyzed separately. An elevated sVEGFR-1 concentration at 16-20 weeks of gestation is associated with an increased risk of pre-eclampsia, 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 pre-eclampsia or IUGR.
Conclusion: Elevated sVEGFR-1 concentrations at 16-20 weeks of gestation precede the clinical manifestations of pre-eclampsia. By neutralizing VEGF, sVEGFR-1 may contribute to inadequate placental vascularization.
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