Document Detail

Maternal serum-soluble vascular endothelial growth factor receptor-1 in early pregnancy ending in preeclampsia or intrauterine growth retardation.
MedLine Citation:
PMID:  16263826     Owner:  NLM     Status:  MEDLINE    
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.
Katja-Anneli Wathén; Eija Tuutti; Ulf-Håkan Stenman; Henrik Alfthan; Erja Halmesmäki; Patrik Finne; Olavi Ylikorkala; Piia Vuorela
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-11-01
Journal Detail:
Title:  The Journal of clinical endocrinology and metabolism     Volume:  91     ISSN:  0021-972X     ISO Abbreviation:  J. Clin. Endocrinol. Metab.     Publication Date:  2006 Jan 
Date Detail:
Created Date:  2006-01-10     Completed Date:  2006-01-31     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  180-4     Citation Subset:  AIM; IM    
Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Biomedicum Helsinki, 00029 HUS, Helsinki, Finland.
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MeSH Terms
Case-Control Studies
Enzyme-Linked Immunosorbent Assay
Fetal Development / physiology
Fetal Growth Retardation / blood*,  epidemiology
Pre-Eclampsia / blood*,  epidemiology
Pregnancy / blood*
Pregnancy Outcome
Pregnancy Trimester, First / blood
Pregnancy Trimester, Second / blood
Risk Assessment
Vascular Endothelial Growth Factor Receptor-1 / blood*
Reg. No./Substance:
EC Endothelial Growth Factor Receptor-1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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