Anti-S100B monoclonal antibody, clone 2C3

Background: S100-beta protein has been introduced as a sensitive biomarker of silent cerebral injury. This study compares its serum levels before, during, and 24 hours after carotid artery stenting (CAS) and carotid endarterectomy (CEA). Methods: We measured serum level of S100-beta in arterial blood before (S100Ba), during (S100Bb), and 24 hours after (S100Bc) CAS and CEA. We assessed differences in S100-beta levels using non-parametric tests. We analyzed the relationship between carotid plaque type (echolucency) and S100-beta protein level. We also examined its relation to the oximetry results in the CEA group (ipsilateral and contralateral). Results: Thirty patients were enrolled, including 15 CAS and 15 CEA patients, with no significant differences in baseline atherosclerotic characteristics. There was no significant difference in S100Ba or S100Bb levels between CAS and CEA patients. However, a significant difference was found in S100Bc: 331.3 pg/mL (IQ range 56.4-583.5) for CAS vs. 76.3 pg/mL (IQ range 29.7-117.4) for CEA (P=0.01). Type I and II plaques were associated with the higher S100Bc levels in CAS (P=0.048). S100Bc was higher in CEA patients when the contralateral cerebral hemisphere had oximetry values less than 60% (P=0.043). Conclusions: Our study suggests that CAS might produce silent brain injury. Moreover, vulnerable plaques might be associated with higher levels of S100-beta protein, especially in CAS. This pilot study demonstrates that S100-beta is a useful biomarker for silent brain injury in carotid revascularization. Large scale studies are still needed to confirm these findings.

Introduction The aim of this study was the assessment of neuron-specific enolase (NSE) and S-100 concentration in serum and cerebrospinal fluid (CSF) in patients with different clinical forms of tick-borne encephalitis (TBE). Material and Methods The serum and CFS concentrations of S100B and NSE of 43 patients with TBE were measured with ELISA method using commercial kits: NSE and S100B Elisa Kit (DRG, Germany). Subjects were divided into: Group I-patients with meningoencephalitis (n = 17) and Group II-patients with meningitis (n = 26). None of the patients reported any neurodegenerative disorder that could affect the results of the study. The control group (CG) consisted of 13 patients. These patients were admitted to the hospital because of headache, and the CSF examination excluded inflammatory process. Samples were collected on admission (sample 1) and after treatment (sample 2). Results Neuron-specific enolase concentration in CSF was higher in group I than in group II (p = 0.0002) and controls (p = 0.04). NSE concentration was higher in the second serum and CSF sample in both groups. S100B concentration did not differ between TBE patients and controls. NSE concentration in serum after 14 days was higher in the sequelae group (34.3 +/- 9.7 vs. 16.7 +/- 15, p = 0.04). Also, NSE serum sample 2/serum sample 1 ratio was significantly higher in the sequelae group (3.57 +/- 0.92 vs. 1.53 +/- 1.99, p = 0.04). Receiver Operating Characteristic curve analysis indicated that NSE concentration in serum II differentiates sequelae group from other meningoencephalitis patients (p = 0.0001). S100B serum sample 2/CSF sample 2 ratio was lower in the sequelae group (0.05 +/- 0.1 vs. 0.37 +/- 0.28, p = 0.02). Conclusions (a) Neurodegeneration process is present in TBE encephalitis. (b) NSE concentration correlates with inflammatory parameters in CSF in TBE. (c) Neurodegeneration is present even after clinical recovery of TBE. (d) NSE could be used in the prediction of TBE course. (e) S-100 did not differ between TBE patients and controls.