Increased S100B serum levels in dilated cardiomyopathy patients.

BACKGROUND: The S100B protein is considered a biochemical marker for brain injuries. However, our group demonstrated that the isolated rat heart releases S100B. In this study, we investigated the serum levels of S100B in dilated cardiomyopathy (DCM) patients to evaluate its levels in heart disease. METHODS AND RESULTS: We selected DCM patients, excluding any condition that could influence S100B serum levels. Control individuals were sex and age matched. Both groups were submitted to clinical evaluation and echocardiography. We measured the S100B and NT-proBNP serum levels (expressed as median [interquartile range]). NT-proBNP levels in patients group (1462 pg/mL [426-3591]) were higher than in controls (35 pg/mL [29-55]), P < .001. S100B serum levels were higher in patients group (0.051 microg/L [0.022-0.144]) than in controls (0.017 microg/L [0.003-0.036]), P = .009. Additionally, we found a positive correlation between S100B and NT-proBNP serum levels only in patients group (Spearman's coefficient r = 0.534; P = .013). CONCLUSIONS: Although we cannot rule out the influence of S100B from brain, the positive correlation between S100B and NT-proBNP levels in DCM patients points to the myocardium as the main source for the rise in S100B serum levels.

The ischemic rat heart releases S100B.

S100B is an astrocytic protein assessed in cerebrospinal fluid and serum as a biochemical marker of cerebral injuries. However, increasing evidences suggest the influence of extra cerebral sources on its serum levels. Since it was reported that the injured myocardium expresses S100B, we investigated whether the isolated heart releases this protein. The rat hearts were excised and perfused by the Langendorff technique of isolated heart perfusion. After stabilization, 10 hearts (ischemic group) were submitted to 20 minutes of ischemia and 30 minutes of reperfusion, and 5 hearts (control group) were submitted to 50 minutes of perfusion. The perfusion fluid was collected at pre-ischemia, and 0, 5, 10, 15 and 30 min after ischemia (or equivalent in controls) for S100B and cardiac troponin T (a heart injury marker) assays. In the ischemic group, S100B and troponin T levels increased significantly at time 0 min: S100B values [mug/L, median (IQ25/IQ75)] increased from < or = 0.02 (< or = 0.02/0.03) to 0.38 (0.22/0.84), while troponin T values [mug/L, median (IQ25/IQ75)] increased from 0.31 (0.15/0.45) to 2.84 (2.00/3.63). Our results point to the ischemic heart as an extra cerebral source of S100B.

S100B and NSE serum levels in patients with Parkinson's disease.

We evaluated S100B protein and neuron-specific enolase (NSE) serum levels in Parkinson's disease (PD) patients and their correlation with the severity of disease. The levels of S100B (P=0.16) and NSE (P=0.39) between PD and controls were similar. However, S100B levels correlated positively with the Hoehn and Yahr scale (r=0.368; P=0.02) and negatively with the Activities of Daily Living (ADL) scale (r=-0.431; P=0.006). Therefore, S100B and NSE may not have a diagnostic role in PD, but S100B may have a potential role as a marker of disease progression. The study of S100B may also contribute to elucidate the controversial role of glial cells in PD.

Increase in serum S100B protein level after a swimming race.

Physical activity has been shown to be a beneficial stimulus to the central and peripheral nervous systems. The S100B is a cytokine physiologically produced and released predominantly by astrocytes on the central nervous system (CNS). In order to study the possible influence of a nonimpact exercise on S100B serum levels, we measured this protein serum level after a 7,600-meter swimming race. We observed an increase in S100B levels in athletes post-race compared with their baseline values, pointing to a potential acute influence of physical exercise on serum S100B levels not related with CNS injury. We discuss this result and emphasize the possible central and peripheral origins of S100B serum levels.