Chitinase-3-Like Protein 1, Serum Amyloid A1, C-Reactive Protein, and Procalcitonin Are Promising Biomarkers for Intracranial Severity Assessment of Traumatic Brain Injury: Relationship with Glasgow Coma Scale and Computed Tomography Volumetry.

OBJECTIVE: The volume and location of intracranial hematomas are well-known prognostic factors for traumatic brain injury. The aim of this study was to determine the relationship of serum biomarkers S100ß, glial fibrillary acidic protein, neuron-specific enolase, total tau, phosphorylated neurofilament heavy chain, serum amyloid A1 (SAA1), C-reactive protein, procalcitonin (PCT), and chitinase-3-like protein 1 (YKL-40) with traumatic brain injury severity and the amount and location of hemorrhagic traumatic lesions. METHODS: A prospective observational cohort of 115 patients with a Glasgow Coma Scale (GCS) score of 3-15 were evaluated. Intracranial lesion volume was measured from the semiautomatic segmentation of hematoma on computed tomography using Analyze software. The establishment of possible biomarker cutoff points for intracranial lesion detection was estimated using the Youden Index (J) obtained from the area under the receiver operating characteristic curve. RESULTS: SAA1, YKL-40, PCT, and S100ß showed the most robust association with level of consciousness, both with total GCS and motor score. Biomarkers significantly correlated with volumetric measurements of subdural hematoma, traumatic subarachnoid hemorrhage, intraparenchymal hemorrhage, intraventricular hemorrhage, and total amount of bleeding. The type of intracranial hemorrhage was associated with various release patterns of neurobiochemical markers. CONCLUSIONS: YKL-40, SAA1, C-reactive protein, and PCT combined with S100ß were the most promising biomarkers to determine the presence, location, and extent of traumatic intracranial lesions. Combination of biomarkers further increased the discriminatory capacity for the detection of intracranial bleeding.

Serum Amyloid A1 as a Potential Intracranial and Extracranial Clinical Severity Biomarker in Traumatic Brain Injury.

Extracranial injury is frequently present in patients with traumatic brain injury (TBI). However, no reliable biomarker exists nowadays to evaluate the magnitude and extension of extracranial injury as well as the identification of patients who are at risk of developing secondary injuries. The purpose of this study was to identify new possible peptide biomarkers by mass spectrometry analysis in patients with TBI and ascertain whether the novel biomarker discovered by peptide mass fingerprinting, serum amyloid A1 (SAA1), is capable of reflecting the condition of the patient and both intracranial and extracranial injury extension. Demographic characteristics, clinical data, and serum samples were prospectively collected from 120 patients with TBI (Glasgow Coma Scale [GCS] score 3-15) on admission. Biomarkers were quantified by enzyme-linked immunosorbent assay. Intracranial lesion volume was measured from the semiautomatic segmentation of hematoma on computed tomography (CT) using Analyze software. Functional outcome was evaluated using the Glasgow Outcome Scale (GOS) at hospital discharge and GOS extended scores at 6 months. The SAA1 levels were significantly associated with intracranial (GCS score at admission, lesion load measured with cranial CT, and pupil responsiveness) and extracranial clinical severity (all Abbreviated Injury Scale regions, Injury Severity Score, major extracranial injury, polytrauma, and orthopedic fractures presence), along with systemic secondary insults and functional outcome. SAA1 was is associated with the volume of traumatic intracranial lesions. The SAA1 levels were correlated with astroglial S100ß and glial fibrillary acidic protein (GFAP), neuronal neuron-specific enolase (NSE), and axonal total tau (T-tau) and phosphorylated neurofilament heavy chain (pNF-H) injury markers. SAA1 predicts unfavorable outcome and mortality at hospital discharge (area under the curve [AUC] = 0.90, 0.82) and 6 months (AUC = 0.89). SAA1 can be established as a marker for the overall patient condition due to its involvement in the neuroendocrine axis of the systemic response to craniocerebral trauma.