S100B is not a reliable prognostic index in paediatric TBI.
ABSTRACT As far as paediatric traumatic brain injury is concerned, it is difficult to quantify the extent of the primary insult, to monitor secondary changes and to predict neurological outcomes by means of the currently used diagnostic tools: physical examination, Glasgow Coma Scale (GCS) score and computed tomography. For this reason, several papers focused on the use of biochemical markers (S100B, neuron-specific enolase) to detect and define the severity of brain damage and predict outcome after traumatic head injury or cardiac arrest.
The aim of this paper is measuring the range of S100B serum concentrations in children affected by traumatic brain injury and describing the possible roles of this protein in the reaction to trauma.
Fifteen children aged 1-15 years were included in the study. Traumatic brain injury severity was defined by paediatric GCS score as mild (9 patients), moderate (2 patients) or severe (4 patients). Blood samples for S100B serum measurement were taken at emergency department admission and after 48 h.
The serum S100B concentration was higher in the group of severe trauma patients, who scored the lowest on the GCS at admission, and among them, the highest values were reported by the children with concomitant peripheral lesions.
The role of S100B in paediatric traumatic brain injury has not been clarified yet, and the interpretation of its increase when the head trauma is associated with other injuries needs the understanding of the physiopathological mechanisms that rule its release in the systemic circulation. The levels of S100B in serum after a brain injury could be related to the mechanical discharge from a destroyed blood-brain barrier, or they could be due to the active expression by the brain, as a part of its involvement in the systemic inflammatory reaction. Early increase of this protein is not a reliable prognostic index of neurological outcome after pediatric traumatic brain injury, since even very elevated values are compatible with a complete neurological recovery.
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ABSTRACT: This paper describes the pilot phase of the National Traumatic Coma Data Bank, a cooperative effort of six clinical head-injury centers in the United States. Data were collected on 581 hospitalized patients with severe non-penetrating traumatic head injury. Severe head injury was defined on the basis of a Glasgow Coma Scale (GCS) score of 8 or less following nonsurgical resuscitation or deterioration to a GCS score of 8 or less within 48 hours after head injury. A common data collection protocol, definitions, and data collection instruments were developed and put into use by all centers commencing in June, 1979. Extensive information was collected on pre-hospital, emergency room, intensive care, and recovery phases of patient care. Data were obtained on all patients from the time of injury until the end of the pilot study. The pilot phase of the Data Bank provides data germane to questions of interest to neurosurgeons and to the lay public. Questions are as diverse as: what is the prognosis of severe brain injury; what is the impact of emergency care; and what is the role of rehabilitation in the recovery of the severely head-injured patient?Journal of Neurosurgery 09/1983; 59(2):276-84. · 3.15 Impact Factor
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ABSTRACT: Levels of the neurotrophic cytokine S100β and the proinflammatory cytokine interleukin-6 (IL-6) are both elevated in Alzheimer’s brain, and both have been implicated in β-amyloid plaque formation and progression. We used RT-PCR and electrophoretic mobility shift assay to assess S100β induction of IL-6 expression and the role of κB-dependent transcription in this induction in neuron-enriched cultures and in neuron-glia mixed cultures from fetal rat cortex. S100β (10 or 100 ng/ml × 24 h) increased IL-6 mRNA levels two- and fivefold, respectively (p < 0.05 in each case), and S100β (100-1,000 ng/ml) induced increases in medium levels of biologically active IL-6 (30-80%). Combined in situ hybridization and immunohistochemistry preparations localized IL-6 mRNA to neurons in these cultures. S100β induction of IL-6 expression correlated with an increase in DNA binding activity specific for a κB element and was inhibited (75%) by suppression of κB binding with double-stranded “decoy” oligonucleotides. The low levels of S100β required to induce IL-6 overexpression in neurons, shown here, suggest that overexpression of S100β induces neuronal expression of IL-6 and of IL-6-induced neurodegenerative cascades in Alzheimer’s disease.Journal of Neurochemistry 12/2001; 74(1):143 - 150. · 3.97 Impact Factor
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ABSTRACT: To compare S-100B and interleukin-8 serum values on scene/at admission and 12 hrs later with respect to neurologic long-term outcome 12 months after cardiac arrest and return of spontaneous circulation, as well as after severe traumatic brain injury. Prospective comparative cohort study. On scene; intensive care units of a university hospital. Twenty patients with out-of-hospital cardiac arrest. Twenty patients with severe traumatic brain injury. Therapy was adjusted to the standards of modern prehospital and intensive care management by physicians who were not involved in the study. First median S-100B values of the cardiac arrest group (4.42 ng/mL) mounted as high as those of the traumatic brain injury group (4.11 ng/mL). Within 12 hrs, S-100B levels significantly decreased to 0.75 ng/mL in cardiac arrest patients and to 0.68 ng/mL in traumatic brain injury patients but remained significantly elevated compared with the controls (0.04 ng/mL). Interleukin-8 levels of the cardiac arrest patients on scene (30.33 pg/mL) were clearly elevated above normal (12.60 pg/mL) and increased significantly to 101.40 pg/mL after 12 hrs. They showed no significant difference compared with those of the traumatic brain injury patients (78.75 pg/mL and 96.00 pg/mL, respectively). Multivariate Cox regression analysis in cardiac arrest patients identified only the S-100B level measured 12 hrs after study entry as an independent predictor for unfavorable neurologic outcome according to the Glasgow Outcome Scale score. In contrast, S-100B as well as interleukin-8 levels quantified 12 hrs after admission significantly predicted an unfavorable neurologic course in the traumatic brain injury group. Significantly elevated S-100B and interleukin-8 serum levels 12 hrs after cardiac arrest suggest that primary brain damage and systemic inflammatory response are comparably serious with that of traumatic brain injury. In both collectives, increased S-100B values measured 12 hrs after insult correlated well with an unfavorable neurologic outcome after 12 months.Critical Care Medicine 01/2003; 30(12):2669-74. · 6.12 Impact Factor