Increased levels of serum S100B protein in critically ill patients without brain injury

Objective

S100B, a calcium-binding protein produced and released predominantly by astrocytes of the central nervous system, has been established as a specific biochemical marker for brain injury [1]. However, there is increasing evidence that S100B release is also induced by other causes or even from tissue outside the brain [2]. The aim of this study was to explore the possible role and the utility of S100B in critically ill patients with respiratory failure of various etiologies, but without brain injury.

Patients and methods

Thirty-eight mechanically ventilated critically ill patients aged 62 ± 17 years, 29 males, with respiratory and/or organ failure, but with no evidence of brain injury or other neurological disorder, were prospectively studied. Blood samples for analysis of serum S100B protein were obtained from the radial artery at the time of laboratory sampling and blood gas analysis. For the determination of S100B, all samples were analyzed using a commercially available immunoluminometric assay (LIASON; Sangtec Medical, Bromma, Sweden). Blood gases and lactate were analyzed using the ABL 625 analyzer (Radiometer Copenhagen, Denmark) and then the arterial oxygen content was calculated.

Results

Serum S100B was measured in 16 medical and 22 surgical ICU patients with a SOFA score on admission of 8 ± 3.4. Compared with the normal values (< 0.15 μg/l), almost all patients exhibited increased serum S100B levels at least once (0.56 ± 1.03 μg/l, mean ± standard deviation, range 0.04–9.25). Pearson's correlation showed a statistically significant relation between S100B and Hb (P < 0.001), O₂ content (P = 0.002), and arterial lactate (P < 0.001). Multivariate analysis using a stepwise logistic regression model showed that the lactate was an independent variable (F = 9.6, P < 0.001), followed by O₂ content (F = -3.25, P = 0.02).

Conclusions

Serum levels of S100B protein are elevated in critically ill patients and correlate with increased lactate levels, low hemoglobin, and abnormal oxygen content. Further research should determine the sources of this S100B release and evaluate its significance as a possible marker of tissue hypoperfusion in the ICU setting.