Citation

Suehiro E, Fujiyama Y, Kiyohira M, Motoki Y, Nojima J, Suzuki M. Neurol. Med. Chir. 2019; 59(2): 63-67.

Affiliation

Department of Neurosurgery, Yamaguchi University Graduate School of Medicine.

Copyright

(Copyright © 2019, Japan Neurosurgical Society)

DOI

10.2176/nmc.oa.2018-0254

PMID

30674749

Abstract

d-dimer is a potential biomarker for the detection of traumatic brain injury (TBI). However, the mechanisms that trigger elevation of d-dimer in TBI remain unclear. The purpose of this study was to evaluate the reliability of d-dimer in blood as a biomarker for TBI and to determine the mechanisms involved in regulating its blood levels. Nine patients with moderate to severe isolated TBI (Glasgow Coma Scale [GCS] score 7-13) were admitted to our hospital from May 2013 to June 2014. Blood samples were collected from systemic arteries on arrival and at 1, 3, 5, and 7 days after injury. Blood levels of neuron specific enolase (NSE), d-dimer, and soluble tissue factor (sTF) were measured. NSE (33.4 ng/ml: normal <12.0 ng/ml) and d-dimer (56.1 μg/ml: normal <1.0 μg/ml) were elevated at admission and declined on day 1 after injury. At admission, there were significant correlations of d-dimer levels with NSE (R = 0.727, P = 0.026) and sTF (R = 0.803, P = 0.009) levels. The blood level of d-dimer accurately reflects the degree of brain tissue damage indicated by NSE levels. Our data suggest that release of sTF induced by brain tissue damage may activate the coagulation cascade, leading to elevation of d-dimer.

Language: en

Keywords

D-dimer; biomarker; neuron specific enolase; tissue factor; traumatic brain injury