Abstract
Brain-specific glial fibrillary acidic protein (GFAP) has been suggested as a potential biomarker for hypoxic ischemic encephalopathy (HIE) in newborns (1, 2). Previous studies have shown increased levels in post-natal blood samples. However, its ability to guide therapeutic intervention in HIE is unknown. Therapeutic hypothermia for HIE must be initiated within 6 h of birth, therefore a clinically useful marker of injury would have to be available immediately following delivery. The goal of our study was to examine the ability of GFAP to predict grade of encephalopathy and neurological outcome when measured in umbilical cord blood (UCB). Infants with suspected perinatal asphyxia (PA) and HIE were enrolled in a single, tertiary maternity hospital, where UCB was drawn, processed, and bio-banked at birth. Expression levels of GFAP were measured by ELISA. In total, 169 infants (83 controls, 56 PA, 30 HIE) were included in the study. GFAP levels were not increased in UCB of case infants (PA/HIE) when compared to healthy controls or when divided into specific grades of HIE. Additionally, no correlation was found between UCB levels of GFAP and outcome at 36 months.
Highlights
Perinatal asphyxia (PA) occurs when there is a disruption of oxygen delivery or blood supply to the fetus around time of birth
Any infant with suspected perinatal asphyxia or hypoxic–ischemic encephalopathy (HIE) in Cork University Maternity Hospital (CUMH), Ireland born between May 2009 and June 2011, was recruited as previously described [8]
When case infants were grouped as perinatal asphyxia (PA) without HIE (n = 56) and infants with HIE (n = 30), no difference was observed (p = 0.566, Figure 1)
Summary
Perinatal asphyxia (PA) occurs when there is a disruption of oxygen delivery or blood supply to the fetus around time of birth. PA, when severe, leads to hypoxic–ischemic encephalopathy (HIE) in the neonatal period. HIE remains one of the leading clinical challenges faced in the neonatal period and the greatest cause of acquired brain injury in term infants. To optimize outcomes in neonatal HIE, early and accurate prediction of the degree of encephalopathy is vital. 20 per 1000 live births will require significant resuscitation at birth, and 10% of these infants will go on to have moderate-to-severe encephalopathy. Using currently available assessment methods, it is estimated that 20% of infants with significant hypoxic injury are clinically misclassified in the first hours of life and do not receive hypothermia [4]. There is a critical need for improved biomarkers for prediction of grade of HIE and outcome [5]
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