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Glial fibrillary acidic protein as a biomarker for brain injury in neonatal CHD

Published online by Cambridge University Press:  20 January 2016

Stephanie L. McKenney
Affiliation:
Department of Pediatrics, Division of Neonatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
Fahad F. Mansouri
Affiliation:
Department of Pediatrics, Division of Pediatric Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America Department of Gynecology and Obstetrics, Division of Maternal-Fetal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
Allen D. Everett
Affiliation:
Department of Pediatrics, Division of Pediatric Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
Ernest M. Graham
Affiliation:
Department of Gynecology and Obstetrics, Division of Maternal-Fetal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
Irina Burd
Affiliation:
Department of Gynecology and Obstetrics, Division of Maternal-Fetal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America Integrated Research Center for Fetal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
Priya Sekar*
Affiliation:
Department of Pediatrics, Division of Pediatric Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America The Helen B. Taussig Congenital Heart Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
*
Correspondence to: P. Sekar, MD, MPH, Department of Pediatrics, Division of Pediatric Cardiology, Johns Hopkins University School of Medicine, Bloomberg Children’s M2321, 1800 Orleans St., Baltimore, MD 21287-1228, United States of America. Tel: 443 287 0529; Fax: 410 955 0897; E-mail psekar1@jhmi.edu

Abstract

Neonates with critical CHD have evidence, by imaging, of preoperative brain injury, although the timing is unknown. We used circulating postnatal serum glial fibrillary acidic protein as a measure of acute perinatal brain injury in neonates with CHD. Glial fibrillary acidic protein was measured on admission and daily for the first 4 days of life in case and control groups; we included two control groups in this study – non-brain-injured newborns and brain-injured newborns. Comparisons were performed using the Kruskal–Wallis test with Dunn’s multiple comparisons, Student’s t-test, and χ2 test of independence where appropriate. In aggregate, there were no significant differences in overall glial fibrillary acidic protein levels between CHD patients (n=56) and negative controls (n=23) at any time point. By day 4 of life, 7/56 (12.5%) CHD versus 0/23 (0%) normal controls had detectable glial fibrillary acidic protein levels. Although not statistically significant, the 5/10 (50%) left heart obstruction group versus 1/17 (6%) conoventricular, 0/13 (0%) right heart, and 1/6 (17%) septal defect patients trended towards elevated levels of glial fibrillary acidic protein at day 4 of life. Overall, glial fibrillary acidic protein reflected no evidence for significant peripartum brain injury in neonates with CHD, but there was a trend for elevation by postnatal day 4 in neonates with left heart obstruction. This pilot study suggests that methods such as monitoring glial fibrillary acidic protein levels may provide new tools to optimise preoperative care and neuroprotection in high-risk neonates with specific types of CHD.

Type
Original Articles
Copyright
© Cambridge University Press 2016 

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Footnotes

*

Both the authors contributed equally to this work.

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