Send to

Choose Destination
See comment in PubMed Commons below
Brain Res Bull. 2003 Aug 15;61(3):265-79.

Studies of the brain specificity of S100B and neuron-specific enolase (NSE) in blood serum of acute care patients.

Author information

  • 1Department of Neurochemistry, Centre of Nervous Diseases, D-35033 Marburg, Germany.


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.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center