The prognostic value of neuron-specific enolase in head trauma patients.
ABSTRACT In recent years, in addition to neurological examination and neuroradiologic examinations, attempts have been made to assess the severity of post-traumatic brain injury and to obtain an early idea of patient prognosis using biochemical markers with a high degree of brain tissue specificity. One such enzyme is neuron-specific enolase (NSE). This study investigates the correlation between serum NSE levels, Glasgow Coma Score, and prognosis measured by Glasgow Outcome Scores in head trauma patients. This was a prospective study conducted with 80 trauma patients presenting to the Emergency Department. Patients were divided into four groups. The first group consisted of patients with general body trauma, but no head trauma. The second group had minor head trauma. The third group had moderate head trauma, and the fourth group had severe head trauma. The relationship between subjects' admission NSE levels and admission and discharge Glasgow Coma Scores (GCS) and Glasgow Outcome Scores (GOS) 1 month later was examined. A receiver operating characteristic (ROC) analysis was performed using a serum NSE cutoff level of 20.52 ng/mL and a GOS of 3 or less as the definition of poor neurologic outcome. There was a significant difference in the NSE levels between group 1 (general trauma) and group 3 (moderate head trauma). There was also a statistically significant difference in NSE levels between group 1 (general trauma) and group 4 (severe head trauma) (p < 0.05). There was a statistically significant inverse relationship between NSE levels and GOS as determined within groups 3 (moderate) and 4 (severe head trauma) (p < 0.05). When NSE levels were compared with admission GCS, it was found that GCS fell as NSE levels rose. There was no significant correlation between NSE and GCS within groups 3 (moderate) or 4 (severe). There was a statistically significant correlation within group 2 (mild) (p < 0.05). By ROC analysis, serum NSE was 87% sensitive and 82.1% specific in predicting poor neurologic outcome in the study patients. The area under the curve was 0.931. This study shows that initial serum NSE levels in moderate and severe head trauma patients correlate inversely with GOS 1 month later, but only within the moderate and severe head trauma groups. However, serum NSE was 87% sensitive and 82.1% specific in predicting poor neurologic outcome in all of the study patients. This derived cutoff value now needs to be prospectively validated.
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ABSTRACT: Although several publications concerning the use of the biomarkers S100B and NSE in vertebral spine fractures in animal experimental studies have proven their usefulness as early indicators of injury severity, there are no clinical reports on their effectiveness as indicators in patients with spinal injuries. As these biomarkers have been examined-with promising results-in patients with traumatic brain injury (TBI), there is a potential for their implementation in patients with vertebral spine fractures. To investigate the early serum measurement of S100B and NSE in patients with vertebral spine fractures as compared to those in patients with acute fractures of the proximal femur. Prospective longitudinal cohort study. A cohort of 34 patients admitted over an 18-month period to a single medical center for suspected vertebral spine trauma. 29 patients were included in the control group. S100B and NSE serum levels were assessed in different types of vertebral spine fractures. We included patients over 16 years of age with vertebral spine fractures whose injuries were sustained within 24 hours prior to admission to the emergency room, and who had undergone a brief neurological examination. Spinal cord injuries were classified as being either paraesthesias, incomplete paraplegias or complete paraplegias. Blood serum was obtained from all patients within 24 hours after time of injury. Serum levels of S100B and NSE were statistically analyzed using Wilcoxon tests. S100B serum levels were significantly higher in patients with vertebral spine fractures (p=0.01). In these patients, the mean S100B serum level was 0.75 μg/L (SD 1.44) [95% CI 0.24; 1.25]. The mean S100B serum level in control group patients was 0.14 μg/L (SD 0.11) [0.10; 0.19]. The 10 patients with neurological deficits had significantly higher S100B serum levels when compared to the patients with vertebral fractures but without neurological deficits (p=0.02). The mean S100B serum level in these patients was 1.18 μg/L (SD 1.96). In the 26 patients with vertebral spine fractures but without neurological injury, the mean S100B serum level was 0.42 μg/L (SD 0.91) [95% CI 0.08; 0.76]. The analysis revealed no significant difference in NSE levels. Not only did we observed a significant correlation between S100B serum levels and vertebral spine fractures, a significant correlation was also seen between S100B serum levels and spinal cord injuries with neurological deficit. These results may be meaningful in clinical practice, and to future studies as well.The spine journal: official journal of the North American Spine Society 04/2014; · 2.90 Impact Factor
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ABSTRACT: Several studies have suggested that neuron-specific enolase (NSE) in serum may be a biomarker of traumatic brain injury. However, whether serum NSE levels correlate with outcomes remains unclear. The purpose of this review was to evaluate the prognostic value of serum NSE protein after traumatic brain injury.PLoS ONE 01/2014; 9(9):e106680. · 3.53 Impact Factor
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ABSTRACT: Traumatic brain injury (TBI) is frequently associated with abnormal blood-brain barrier function, resulting in the release of factors that can be used as molecular biomarkers of TBI, among them GFAP, UCH-L1, S100B, and NSE. Although many experimental studies have been conducted, clinical consolidation of these biomarkers is still needed to increase the predictive power and reduce the poor outcome of TBI. Interestingly, several of these TBI biomarkers are oxidatively modified to carbonyl groups, indicating that markers of oxidative stress could be of predictive value for the selection of therapeutic strategies. Some drugs such as corticosteroids and progesterone have already been investigated in TBI neuroprotection but failed to demonstrate clinical applicability in advanced phases of the studies. Dietary antioxidants, such as curcumin, resveratrol, and sulforaphane, have been shown to attenuate TBI-induced damage in preclinical studies. These dietary antioxidants can increase antioxidant defenses via transcriptional activation of NRF2 and are also known as carbonyl scavengers, two potential mechanisms for neuroprotection. This paper reviews the relevance of redox biology in TBI, highlighting perspectives for future studies.BioMed research international. 01/2014; 2014:723060.