A blood-based biomarker panel to risk-stratify mild traumatic brain injury.
Abstract
Mild traumatic brain injury (TBI) accounts for the vast majority of the nearly two
million brain injuries suffered in the United States each year. Mild TBI is commonly
classified as complicated (radiographic evidence of intracranial injury) or uncomplicated
(radiographically negative). Such a distinction is important because it helps to determine
the need for further neuroimaging, potential admission, or neurosurgical intervention.
Unfortunately, imaging modalities such as computed tomography (CT) and magnetic resonance
imaging (MRI) are costly and not without some risk. The purpose of this study was
to screen 87 serum biomarkers to identify a select panel of biomarkers that would
predict the presence of intracranial injury as determined by initial brain CT. Serum
was collected from 110 patients who sustained a mild TBI within 24 hours of blood
draw. Two models were created. In the broad inclusive model, 72kDa type IV collagenase
(MMP-2), C-reactive protein (CRP), creatine kinase B type (CKBB), fatty acid binding
protein-heart (hFABP), granulocyte-macrophage colony-stimulating factor (GM-CSF) and
malondialdehyde modified low density lipoprotein (MDA-LDL) significantly predicted
injury visualized on CT, yielding an overall c-statistic of 0.975 and a negative predictive
value (NPV) of 98.6. In the parsimonious model, MMP-2, CRP, and CKBB type significantly
predicted injury visualized on CT, yielding an overall c-statistic of 0.964 and a
negative predictive value (NPV) of 97.2. These results suggest that a serum based
biomarker panel can accurately differentiate patients with complicated mild TBI from
those with uncomplicated mild TBI. Such a panel could be useful to guide early triage
decisions, including the need for further evaluation or admission, especially in those
environments in which resources are limited.
Type
Journal articleSubject
HumansBrain Concussion
Malondialdehyde
Lipoproteins, LDL
C-Reactive Protein
Granulocyte-Macrophage Colony-Stimulating Factor
Tomography, X-Ray Computed
Glasgow Coma Scale
Prospective Studies
Predictive Value of Tests
Adult
Aged
Middle Aged
Male
Fatty Acid-Binding Proteins
Creatine Kinase, BB Form
Matrix Metalloproteinase 2
Neuroimaging
Biomarkers
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https://hdl.handle.net/10161/22424Published Version (Please cite this version)
10.1371/journal.pone.0173798Publication Info
Sharma, Richa; Rosenberg, Alexandra; Bennett, Ellen R; Laskowitz, Daniel T; & Acheson,
Shawn K (2017). A blood-based biomarker panel to risk-stratify mild traumatic brain injury. PloS one, 12(3). pp. e0173798. 10.1371/journal.pone.0173798. Retrieved from https://hdl.handle.net/10161/22424.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Shawn K. Acheson
Adjunct Assistant Professor in the Department of Psychiatry and Behavioral Sciences
In collaboration with Dr. Scott Swartzwelder, research in our lab has focused on the
neurodevelopmental effects of alcohol and other drugs of abuse. In particular, we
have been interested in how and why adolescents are more sensitive to some effects
of ethanol and THC (e.g., learning and memory) and less sensitive to other effects
(e.g., sedation). Beginning in Fall 2011, my lab will begin a new line of research
focused on potential pharmacotherapies for TBI and the basic underlying mechani
Ellen Ruth Bennett
Adjunct Assistant Professor in the Department of Neurology
Daniel Todd Laskowitz
Professor of Neurology
Our laboratory uses molecular biology, cell culture, and animal modeling techniques
to examine the CNS response to acute injury. In particular, our laboratory examines
the role of microglial activation and the endogenous CNS inflammatory response in
exacerbating secondary injury following acute brain insult. Much of the in vitro work
in this laboratory is dedicated to elucidating cellular responses to injury with the
ultimate goal of exploring new therapeutic interventions in the clinical settin
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