Is procalcitonin a new surrogate marker for hypoxic brain damage?

Objective

Procalcitonin is so far known as a marker of severe sepsis mostly caused by Gram-negative bacteria. But recent literature provided hints for its elevation after mechanic or hypoxic tissue damage, too. In a pilot study we therefore investigated the possibility whether PCT could serve as a neurological outcome marker after out-of-hospital cardiac arrest.

Methods

S100 protein and PCT serum levels were serially analyzed on hospital admission and on the following 3 days in 23 patients resuscitated after out-of-hospital cardiac arrest. At day 14 patients were divided in two groups applying the Glasgow Outcome Scale (GOS): 16 patients in the group with bad neurological outcome (GOS 1–3); seven patients in the group with good neurological outcome (GOS 4–5). If present signs of sepsis or systemic inflammatory response syndrome (SIRS) were documented at the different time points. The diagnostic performance of S100 and PCT levels to differentiate between the both groups was performed with the use of receiver operating characteristics (ROC). Both parameters were measured on the LIA-mat using the assays from Byk-Sangtec and Brahms.

Results

Patients with bad neurological outcome had significantly higher S100 levels than those with a good neurological outcome at all time points and significantly elevated PCT levels at days 1–3. Highest levels for S100 were found immediately after hospitalization and for PCT at day 1. The brain-originated S100 showed best performance immediately after hospitalization with an area under the curve of 0.89 (sensitivity of 62.5% and specificity of 100% at a cut-off value of 1.25 μg/l), while the non-brain-originated PCT was the best predictor for bad neurological outcome at day 1 (AUC = 0.98; sensitivity of 92% and specificity of 100% at a cutoff value of 0.5 μg/l). None of the patients revealed signs of sepsis or SIRS at the investigated time points.

Conclusion

Although we only investigated a small number of patients our results are promising and show that PCT is not only induced in severe bacterial infection, SIRS, septic shock or multiorgan dysfunction syndrome. Further investigations on larger patient populations have to follow. Nevertheless we recommend that S100 and PCT serum levels in the case of patients with out-of hospital cardiac arrest can be used as reliable and, because of their different liberation kinetics, to each other complementary parameters for the prediction of neurological outcome in successfully resuscitated patients.