- Poster presentation
- Open Access
Serum S-100B protein predicts prognosis in endogenous encephalopathy
© BioMed Central Ltd. 2004
- Published: 15 March 2004
- Schwann Cell
- Glasgow Coma Scale
- Central Nervous System Damage
- Cerebral Disease
- Cerebrospinal Fluid Concentration
Cerebrospinal fluid concentrations of S-100B protein, an acidic calcium-binding protein found in astrocytes and Schwann cells, increase after central nervous system damage. Serum S-100B protein thus has potential as a biomedical marker of brain cell damage. Several reports show a relation between the severity of head injury and serum S-100B protein (S-100B) levels in trauma patients, but there are few data about S-100B in endogenous cerebral disease.
The aim of this study is to evaluate S-100B as a marker in endogenous encephalopathy.
Serum S-100B protein concentrations (pg/ml) were measured daily by ELISA until ICU discharge in 19 ICU patients (12 men, seven women; age 9–80 years [mean 57.1 ± 22.8 years]) with endogenous encephalopathy. The APACHE II score and Glasgow coma scale (GCS) were used to assess the severity; electroencephalography (EEG) and computerised tomography (CT) were also examined. Values are expressed as mean ± SD. The unpaired Student's t test, or tests of Mann–Whitney's U, Wilcoxon signed-rank, Kruskal–Wallis and Pearson's correlation coefficient were used. P < 0.05 was considered statistically significant.
There were 10 survivors and nine nonsurvivors with no significant differences in age, APACHE II score or GCS. There was no significant difference in S-100B levels on admission between survivors and nonsurvivors, but S-100B levels were significantly lower in survivors than in nonsurvivors from day 1 (1129 ± 1780 vs 465,370 ± 780,293, P < 0.05) until ICU discharge (16.5 ± 15.9 vs 231,120 ± 591,110, P < 0.05). In survivors, S-100B levels decreased from 5 day (30.1 ± 18.5) to discharge compared with admission levels (P < 0.05); in nonsurvivors, there were no significant changes in S-100B compared with admission levels. There were no correlations of S-100B levels with APACHE II score (R = 0.3, P > 0.05) or GCS (R = -0.1, P > 0.05), but EEG and CT abnormalities were correlated with S-100B levels.
Serum S-100B concentrations follow different courses in survivors and nonsurvivors in endogenous encephalopathy. Although similar on admission, differences in serum S-100B protein between survivors and nonsurvivors appeared from the first day after admission. In survivors, but not in nonsurvivors, S-100B levels decreased until discharge. There were also significant relationships with the severity of EEG or CT abnormalities and S-100B levels. Serum S-100B protein could be a useful biomedical marker for assessment of brain damage and may predict prognosis in endogenous encephalopathy.