Where a clinically reliable discrimination between survivors and nonsurvivors can be derived. Other pro- and anti-inflammatory cytokines like Interleukin IL-8, IL-6, IL-1b, or Tumor necrosis factor-a were shown to hold similar AUC. Thus, it is most likely that the one particular biomarker for predicting outcome of patients with systemic inflammation may not exist due to the complexity of the immune response. One may speculate that ASM increases as a result of inflammation, as various inflammatory stimuli lead to activation of ASM mediated lipid signalling, including oxidative stress, induction by or of cytokines, platelet activating-factor -mediated pulmonary oedema formation during acute lung injury and ceramide accumulation in ischemia/reperfusion injury in mitochondria. Due to the various pathophysiological properties of ASM in mediation of inflammation and apoptosis, we may also speculate that non-declining or continuously increased ASM in critically ill patients with systemic inflammation plays a putative causative role with respect to adverse outcome. Our study has some limitations which have to be mentioned. The main limitation is the low number of patients included and that it was conducted as a single FDA-approved Compound Library inhibitor center study. Therefore, our results should be interpreted with caution as there is a high likelihood of a type II error. However, this study should be regarded in the context of a single center, pilot study aiming to gain more insight into the clinical usefulness of ASM kinetics in the course of systemic inflammation. A further limitation is that we did not perform consecutive ASM measurements in the ICU patients without systemic inflammation. This was due to financial restraints of this pilot study. Measurements of ASM are not yet comparable with established laboratory for PCT or CRP that are easier and cheaper to conduct. It is also likely that the time interval at which ASM was measured did not accurately capture an early change in ASM kinetics. Future studies on ASM kinetics may address this potential limitation choosing an even closer measurement interval. Lastly, the potential of using ASM as a prognostic marker after systemic inflammation in clinical practice warrants further improvement of the assay to become more widely available. Conclusions Our study showed that patients who underwent uncomplicated surgery exhibited a significant post-operative increase in ASM. In a mixed ICU population, ASM was significantly higher compared to these patients. While ASM did not indicate the onset of systemic inflammation earlier than PCT in our group of patients, it was able to predict ICU mortality in patients after systemic inflammation in the presence of low PCT level. ASM may hold potential as a tool for risk stratification of these patients, but the clinical value has to be further evaluated in larger studies. SPIDIA is a European Commission funded, four-year, integrated project aimed at the standardization and improvement of preanalytical procedures for in vitro diagnostics.