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Post-Traumatic Hypoxia Is Associated with Prolonged Cerebral Cytokine Production, Higher Serum Biomarker Levels, and Poor Outcome in Patients with Severe Traumatic Brain Injury
Citation
Yan, EB and Satgunaseelan, L and Paul, E and Bye, N and Nguyen, P and Agyapomaa, D and Kossmann, T and Rosenfeld, JV and Morganti-Kossmann, MC, Post-Traumatic Hypoxia Is Associated with Prolonged Cerebral Cytokine Production, Higher Serum Biomarker Levels, and Poor Outcome in Patients with Severe Traumatic Brain Injury, Journal of Neurotrauma, 31, (7) pp. 618-629. ISSN 0897-7151 (2014) [Refereed Article]
Copyright Statement
Copyright Mary Ann Liebert, Inc
DOI: doi:10.1089/neu.2013.3087
Abstract
Secondary hypoxia is a known contributor to adverse outcomes in patients with traumatic brain injury (TBI). Based on the
evidence that hypoxia and TBI in isolation induce neuroinflammation, we investigated whether TBI combined with
hypoxia enhances cerebral cytokine production. We also explored whether increased concentrations of injury biomarkers
discriminate between hypoxic (Hx) and normoxic (Nx) patients, correlate to worse outcome, and depend on blood–brain
barrier (BBB) dysfunction. Forty-two TBI patients with Glasgow Coma Scale £ 8 were recruited. Cerebrospinal fluid
(CSF) and serum were collected over 6 days. Patients were divided into Hx (n = 22) and Nx (n = 20) groups. Eight
cytokines were measured in the CSF; albumin, S100, myelin basic protein (MBP) and neuronal specific enolase (NSE)
were quantified in serum. CSF/serum albumin quotient was calculated for BBB function. Glasgow Outcome Scale
Extended (GOSE) was assessed at 6 months post-TBI. Production of granulocye macrophage-colony stimulating factor
(GM-CSF) was higher, and profiles of GM-CSF, interferon (IFN)-c and, to a lesser extent, tumor necrosis factor (TNF),
were prolonged in the CSF of Hx but not Nx patients at 4–5 days post-TBI. Interleukin (IL)-2, IL-4, IL-6, and IL-10
increased similarly in both Hx and Nx groups. S100, MBP, and NSE were significantly higher in Hx patients with
unfavorable outcome. Among these three biomarkers, S100 showed the strongest correlations to GOSE after TBI-Hx.
Elevated CSF/serum albumin quotients lasted for 5 days post-TBI and displayed similar profiles in Hx and Nx patients.
We demonstrate for the first time that post-TBI hypoxia is associated with prolonged neuroinflammation, amplified
extravasation of biomarkers, and poor outcome. S100 and MBP could be implemented to track the occurrence of post-TBI
hypoxia, and prompt adequate treatment
Item Details
Item Type: | Refereed Article |
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Keywords: | TBI; hypoxia; neuroinflammation; biomarkers |
Research Division: | Biomedical and Clinical Sciences |
Research Group: | Neurosciences |
Research Field: | Central nervous system |
Objective Division: | Health |
Objective Group: | Clinical health |
Objective Field: | Clinical health not elsewhere classified |
UTAS Author: | Bye, N (Dr Nicole Bye) |
ID Code: | 122253 |
Year Published: | 2014 |
Web of Science® Times Cited: | 49 |
Deposited By: | Pharmacy |
Deposited On: | 2017-11-07 |
Last Modified: | 2017-11-20 |
Downloads: | 0 |
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