Maternal serum-soluble vascular endothelial growth factor receptor-1 in early pregnancy ending in preeclampsia or intrauterine growth retardation.
BACKGROUND
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.


METHODS
This was a case-control study.


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


METHODS
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.


METHODS
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.


CONCLUSIONS
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.
Wathén
Katja-Anneli
KA
Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Biomedicum Helsinki, 00029 HUS, Helsinki, Finland.
Tuutti
Eija
E
Stenman
Ulf-Håkan
UH
Alfthan
Henrik
H
Halmesmäki
Erja
E
Finne
Patrik
P
Ylikorkala
Olavi
O
Vuorela
Piia
P
D000328:Adult; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D047109:Fetal Development / Q000502:physiology; D005317:Fetal Growth Retardation / Q000097:blood* / Q000453:epidemiology; D006801:Humans; D011225:Pre-Eclampsia / Q000097:blood* / Q000453:epidemiology; D011247:Pregnancy / Q000097:blood*; D011256:Pregnancy Outcome; D011261:Pregnancy Trimester, First / Q000097:blood; D011262:Pregnancy Trimester, Second / Q000097:blood; D018570:Risk Assessment; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood*
D040281:Vascular Endothelial Growth Factor Receptor-1