الفهرس | Only 14 pages are availabe for public view |
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. |