الفهرس 
Introduction 1Only 14 pages are availabe for public view
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Abstract
Perinatal asphyxia is the consequence of impaired blood
supply between mother and fetus , leading to insufficient
delivery of oxygen , glucose and other blood-borne fuels to fetal
organs , including the brain. It is a global problem resulting
in neonatal morbidity and mortality.
There is an urgent need to understand its pathophysiology
and to identify as early as possible reliable indices of brain
injury in the asphyxiated newborns to apply potential
therapeutic interventions at the optimal time and to identify
those infants at high risk for developmental delays and
disabilities.
Neuron Specific Enolase (NSE), a homodimer of the
gamma form of enolase, is localized in the cytoplasm of neurons
and cells of neuronal origin. It is an enzyme which catalyzes the
conversion of 2-phosphoglycerate to phosphoenolpyruvate in the
glycolytic pathway, and also the reverse reaction in
gluconeogenesis.
After irreversible hypoxic ischemic cellular injury, brain
cells die by necrotic lyses or apoptosis, which releases
intracellular enzymes, such as NSE into CSF and circulation.
The aim of this study was to evaluate the utility of neuron
specific enolase (NSE) serum level as a diagnostic marker in full
term neonates with perinatal asphyxia.