Studies of the brain specificity of S100B and neuron-specific enolase ( NSE) in blood serum of acute care patients.
Laboratory monitoring with damage markers of brain and of non-nervous tissues in blood serum of 401 acute care patients showed increased contents of neuron-specific enolase ( NSE) and S100B besides raised levels of markers of heart, skeletal muscle, bile duct, liver, prostate, kidney, salivary gland damage or of inflammatory stress to varying frequencies. Correlation between raised NSE and S100B contents ascertained brain damage. Correlation between raised NSE and troponin I (cTnI) values indicated brain damage induced by heart failure (probably caused by hypoxia and anemia); this was assessed with correlations between NSE and other heart markers, e.g. creatine kinase (CK) isoenzymes, alpha-hydroxybutyrate dehydrogenase. S100B did not show such correlations: data indicated S100B release from non-nervous tissues having high S100B content, e.g. fat, cartilage, skin. S100B release might be triggered by inflammatory stress and tissue damage. This was further supported by low NSE/S100B concentration ratios in serum compared to cerebrospinal fluid (CSF) of patients with comatose state, convulsive status, or intracerebral hemorrhage. Our data revealed CSF to be the relevant sample to monitor brain damage with NSE and S100B, whereas in serum raised S100B levels together with normal NSE levels indicated release from non-nervous tissues of acute care patients pointing out multi-organ dysfunction.[1]References
- Studies of the brain specificity of S100B and neuron-specific enolase (NSE) in blood serum of acute care patients. Kleine, T.O., Benes, L., Zöfel, P. Brain Res. Bull. (2003) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
