Abstract
Background: Vascular endothelial growth factor (VEGF) is a known mediator of angiogenesis. It has been shown to induce vascular proliferation and permeability via nitric-oxide-mediated mechanism during hypoxia. VEGF exerts its effects by binding to two receptors; VEGFR-1 and VEGFR-2.
Objectives: To test the hypothesis that serum concentration of the soluble receptor sVEGF-R1 is increased in infants with hypoxic ischemic encephalopathy (HIE); and such an increase correlates with the severity of encephalopathy.
Study design: Serum samples of 30 full term newborns diagnosed with HIE and 20 controls were obtained within the first 6 hours of life and kept at −70°C. Concentrations of sVEGFR-1 were measured by the enzyme-linked immunosorbent assay double sandwich method. Values were correlated with the severity of HIE at birth and with outcomes measured at 4 weeks of age.
Results: The concentrations of sVEGFR-1 in HIE patients were increased when compared to control subjects. Patients with the least Apgar scores had the most increase in sVEGFR-1. sVEGFR-1 at a cut off 11.0 ng/ml had 100% sensitivity & 100% specificity for detection of HIE. The concentrations of sVEGFR-1 did not differ among patients with different degrees of HIE nor in patients with different short term clinical outcomes. Two stepwise regression analyses showed that both degree and outcome of HIE depend upon Apgar score and the liver enzyme alanine transaminase.
Conclusion: sVEGFR1 is upregulated early in neonates with HIE. It does not correlate with the severity of encephalopathy or the short term outcomes.
Get full access to this article
View all access options for this article.