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Cited by 332Traumatic Brain Injury ResearchTraumatic Brain Injury and Neurovascular DisturbancesTrauma and Emergency Care Studies

Elevated levels of serum glial fibrillary acidic protein breakdown products in mild and moderate traumatic brain injury are associated with intracranial lesions and neurosurgical intervention

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Papa, Linda, Lewis, Lawrence M., Falk, Jay L., Zhang, Zhiqun, Silvestri, Salvatore, Giordano, Philip, Brophy, Gretchen M., Demery, Jason A. +11 more·2012·Annals of Emergency Medicine
DOI 10.1016/j.annemergmed.2011.08.021PMC PMC3830977
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Abstract

Objective This study examined whether serum levels of GFAP breakdown products (GFAP-BDP) were elevated in mild and moderate TBI compared to controls and if they were associated with traumatic intracranial lesions on CT scan (+CT) and having a neurosurgical intervention (NSI). Methods This prospective cohort study enrolled adult patients presenting to three Level 1 Trauma Centers following blunt head trauma with loss of consciousness, amnesia, or disorientation and a GCS 9–15. Control groups included normal uninjured controls and trauma controls presenting to the ED with orthopedic injuries or an MVC without TBI. Blood samples were obtained in all patients within 4 hours of injury and measured by ELISA for GFAP-BDP (ng/ml). Results Of the 307 patients enrolled, 108 were TBI patients (97 with GCS 13–15, and 11 with GCS 9–12) and 199 were controls (176 normal controls and 16 MVC controls and 7 orthopedic controls). ROC curves demonstrated that early GFAP-BDP levels were able to distinguish TBI from uninjured controls with an AUC of 0.90 (95%CI 0.86–0.94) and differentiated TBI with a GCS 15 with an AUC 0.88 (95%CI 0.82–0.93). Thirty two TBI patients (30%) had lesions on CT. The AUC for discriminating those patients with CT lesions versus those without CT lesions was 0.79 (95%CI 0.69–0.89). Moreover, the ROC curve for distinguishing NSI from no NSI yielded an AUC of 0.87 (95%CI 0.77–0.96). Conclusions GFAP-BDP is detectable in serum within an hour of injury and is associated with measures of injury severity including the GCS score, CT lesions and neurosurgical intervention. Further study is required to validate these findings before clinical application.

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  • Antibodies may form after TBI due to disruption of the blood-brain barrier, allowing brain proteins to leak into the circulation and evoke an immune response.

    “Antibodies may form after TBI due to the disruption of the blood-brain barrier, which allows brain proteins (especially the release of sequestered pituitary and hypothalamic antigens from injured/ necrotic tissue) to leak into the circulation, evoking an immune response (164, 165).”

    From Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach (2015) · cites this paper as [165]

    The Results report that GFAP breakdown products appeared rapidly in serum after TBI, and the Discussion describes their release from injured glial cells. The paper does not attribute that appearance to blood–brain barrier disruption or discuss antibody formation, an immune response, or pituitary and hypothalamic antigens. No page numbers were provided for these passages. (LLM, conf=0.84)

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  1. [59]Zhang Z Yang B Glushakova O Alterations in the expression of glial fibrillary acidic protein and fragmentation in the subacute phase of brain injury [Abstract] The 28th National Neurotrauma Society Symposium Vol suppl Las Vegas, Nevada J Neurotrauma 2010

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Authors
Papa, L., Lewis, L. M., Falk, J. L., Zhang, Z., Silvestri, S., Giordano, P., Brophy, G. M., Demery, J. A., Dixit, N. K., Ferguson, I., Liu, M. C., Mo, J., Akinyi, L., Schmid, K., Mondello, S., Robertson, C. S., Tortella, F. C., Hayes, R. L., & Wang, K. K. W.
Affiliations
  • Orlando Regional Medical Center (US)
  • Washington University in St. Louis (US)
  • Orlando Health (US)
  • Banyan Biomarkers (United States) (US)
  • Virginia Commonwealth University (US)
  • University of Florida Health (US)
  • North Florida/South Georgia Veterans Health System (US)
  • Walter Reed Army Institute of Research (US)
  • Baylor College of Medicine (US)
ORCID
Venue
Annals of Emergency Medicine
Publisher
Elsevier BV
Published
2012-06
Volume
59
Issue
6
Pages
471-483
ISSN
0196-0644 (ISSN-L)
DOI
10.1016/j.annemergmed.2011.08.021
PMC
PMC3830977
OpenAlex
W2033297074
Semantic Scholar
12ff89b6596ae97b6f490939d5ade9cf2c3f7f3a
Cited by
332
References
73
Citations by year
2026: 14 · 2025: 12 · 2024: 22 · 2023: 19 · 2022: 20 · 2021: 17 · 2020: 24 · 2019: 18 · 2018: 19 · 2017: 32 · 2016: 27 · 2015: 36 · 2014: 29 · 2013: 26 · 2012: 13
FWCI
16.80
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Annals of Emergency Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Neurological Disorders and Stroke (R01NS057676)
Topics
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Emergency Medicine › Trauma and Emergency Care Studies
Keywords
traumatic brain injury, serum biomarkers, mild traumatic brain injury, moderate traumatic brain injury, intracranial lesions, neurosurgical treatment, Glasgow Coma Scale, blunt head trauma, injury severity, diagnostic biomarkers, motor vehicle crash injuries, orthopedic trauma, neuroinflammation, neurodegeneration
MeSH terms
Adolescent, Adult, Aged, Aged, 80 and over, Brain, Brain Injuries, Female, Glial Fibrillary Acidic Protein, Humans, Male, Middle Aged, Prospective Studies, ROC Curve, Trauma Centers, Glasgow Coma Scale, Case-Control Studies, Young Adult

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