Glial Fibrillary Acidic Protein Is Not an Early Marker of Injury in Perinatal Asphyxia and Hypoxic-Ischemic Encephalopathy

Ann-Marie Looney, Caroline Ahearne, Geraldine B Boylan, Deirdre M Murray, Ann-Marie Looney, Caroline Ahearne, Geraldine B Boylan, Deirdre M Murray

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.

Keywords: GFAP; biomaker; early diagnosis; hypoxic–ischemic encephalopathy; therapeutic interventions; umbilical cord blood.

Figures

Figure 1
Figure 1
Boxplot representing umbilical cord blood (UCB) levels of GFAP (ng/ml) following commercial ELISA analysis. Infants grouped as healthy controls (n = 83), infants with perinatal asphyxia (PA) without HIE (n = 56), and infants with clinical and electrographically confirmed HIE (n = 30). No significant alteration was detected between groups (p = 0.566).
Figure 2
Figure 2
Boxplot representing further analysis of umbilical cord blood (UCB) levels of GFAP (ng/ml) in infants which would be deemed eligible for therapeutic hypothermia (TH; moderate and severe hypoxic–ischemic encephalopathy, n = 9) and infants who would not meet the eligible criteria (Non-TH; controls, perinatal asphyxia, and mild hypoxic–ischemic encephalopathy, n = 160). No significant elevation in GFAP levels was observed (p = 0.919).
Figure 3
Figure 3
Comparison of umbilical cord blood (UCB) levels of GFAP (nanogram per milliliter) from infants with a normal outcome at 24–36 months (n = 103) compared to those with an abnormal outcome (n = 13), presented as a box plot. A significant difference was not detected between groups (p = 0.919).

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