Affiliations: Neonatology Unit, Department of Pediatric Faculty of
Medicine, Ain Shams University, Cairo, Egypt | Neonatology Unit, Clinical Pathology Department,
Faculty of Medicine, Ain Shams University, Cairo, Egypt
Note: [] Corresponding author: Maha Hassan Mohamed, Department of
Pediatrics, Ain Shams University, Cairo, Egypt. Tel.: +20 10528 7175; E-mail:
mahahassan1971@yahoo.com
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.
