RESUMO
Four million infants suffer from birth asphyxia allover the world each year; of them, one million dies and a similar number will develop serious sequelae; including hypoxic ischemia encephalopathy [HIE]. A better understanding of the pathogenesis of this event and its early identification is highly required. The role of non-protein bound iron [NPBI], lactate, and other laboratory and clinical criteria as diagnostic and prognostic markers were studied. This study included 25 asphyxiated neonates and 25 healthy matched neonates as a control group. Both groups were subjected to clinical assessment, routine laboratory tests, serum lactate and NPBI measurements. Clinical follow-up was done every three months till the age of 1 year. Developmental screening test was done every six months using Denver Developmental Screening Test [DDST]. Serum lactate levels were found to be significantly higher in the HIE group compared to the control group [t = 15.13, P < 0.001].HIE group [were divided into mild [10], moderate [7] and severe [8]] according to sarnat classification and there was a significant elevation in serum lactate levels in severe HIE in comparison to mild cases [P< 0.05]. Statistical analysis of serum NPBI levels in control group and HIE group revealed that there was a significant increase of NPBI in HIE group in comparison to control group [t= 7.02 P < 0.001, t= 9.89 P < 0.001, t= 13.3 P < 0.001 for mild, moderate, and severe subgroups respectively]. One way anova test revealed a significant elevation of the level of NPBI with the increase of severity in the studied subgroups [mild, moderate and severe] indicating that there is a correlation between the level of NPBI and the severity of the clinical presentation of HIE [F= 52.37, P < 0.001]. ROC curve was used to test the performance and clinical value of NPBI for predicting neurodevelopment outcome, and it indicated reliable performance for NPBI [ROC area under curve was 0.95]. We found a significant negative correlation coefficient between the level of NPBI and pH [r = -0.5794, P< 0.001], Na[+][r = -0.06084, P< 0.05], Ca[++[r = -0.7511, P < 0.001], Apgar score at 1 minute [r = -0.5766, P < 0.001], Apgar score at 5 minute,[r = -0.5248, P < 0.001] and pO-2[--] [r = -0.2668, P < 0.05]. A positive correlation coefficient was found between the level NPBI and HCO3 [r = 0.3568, P < 0.05], urea [r = 0.2681, P < 0.05], creatinine [r = 0.5552, P < 0.001], p[co][2] [r = 0.6053, P < 0.001], lactate [r = 0.5927, P < 0.001], and K[+] [r = 0.0855, P < 0.05]. All HIE cases devoid of neurological complications [manifested by seizures] had a normal development m contrast to HIE cases which complained from seizures [75%, 9 of 12 cases] after 6 months, and [81.8%, 9 of 11 cases] after 12 months had developmental delay tested by DDST. All of neurologically complicated cases [presented with seizures] had a significant elevation of the serum level of NPBI [P < 0.001. Serum NPBI assay may be a reliable early indicator of infra and extra-uterine oxidative stress and brain injury, with a prognostic value regarding HIE. use of free iron scavengers may be indicated of those cases with increased NPBI and eventual threat of HIE occurrence with its catastrophic complications