Objective: To investigate if the availability of nonprotein-bound iron after birth asphyxia is related to the severity of the postasphyxial injury and neurodevelopmental outcome.
Methods: Nonprotein-bound iron (bleomycin assay) and thiobarbituric-acid-reactive species, an index of oxidative lipid damage, were measured in plasma of 50 newborn infants (gestational age > 34 weeks) between 0 to 8 hours, 8 to 16 hours, and 16 to 24 hours after birth. Three groups were compared: healthy infants (n = 20), moderately asphyxiated infants (n = 15), who were neurologically normal during the first 24 hours after birth and severely asphyxiated infants (n = 15), who developed abnormal neurological signs in the first 24 hours after birth.
Results: In the severely asphyxiated infants, liver enzymes, creatinine, urea, and uric acid concentrations were significantly elevated. Eleven severely asphyxiated infants were brain-damaged, 9 of them died during the neonatal period. Nonprotein-bound iron was detectable in 30% of the control, 60% of the moderately asphyxiated, and 80% of the severely asphyxiated infants. During the whole study period nonprotein-bound iron concentration was significantly elevated in severely asphyxiated infants as compared with controls. Three of the four severely asphyxiated infants who had a normal outcome at 1 year of age, had no detectable nonprotein-bound iron during the study period. Stepwise logistic regression analysis with neurodevelopmental outcome at 1 year of age (normal versus adverse/death) as dependent variable and all the measured parameters for organ damage as independent variables revealed that the nonprotein-bound iron concentration at 0 to 8 hours after birth was the most significant variable and at the same time the only variable that entered the model, in relation to neurodevelopmental outcome. Thiobarbituric-acid-reactive species tended to be higher in severely asphyxiated infants, suggesting oxidative lipid damage.
Conclusion: Nonprotein-bound iron may play an important role in oxidative damage-mediated postasphyxial brain injury and subsequent neurodevelopmental outcome.