Identifying biomarkers distinguishing sepsis after trauma from trauma-induced SIRS based on metabolomics data: A retrospective study

Abstract

Background Sepsis after trauma and trauma-induced SIRS may present with similar symptoms, so it is a great challenge to distinguish sepsis after trauma from trauma-induced SIRS. Besides, trauma-induced SIRS uncovers the occurrence of sepsis after trauma. Thus, there is a need for biomarkers to distinguish them. We hypothesized that sepsis after trauma leads to different changes in blood metabolism than trauma-induced SIRS and searched for metabolite biomarkers in blood to distinguish between the two conditions. Methods This study retrospectively analyzed the existing blood metabonomics data from the patients with severe trauma (100 cases), patients with sepsis after trauma (50 cases), and the non-trauma controls (50 cases). We screened out 40 patients with trauma-induced SIRS from the 100 severe trauma patients and then used a pairwise comparison between patients with sepsis after trauma and trauma-induced SIRS to screen the differential metabolites as biomarkers distinguishing sepsis after trauma from trauma-induced SIRS. Results In total, 413 metabolites could differentiate sepsis after trauma patients from the trauma-induced SIRS. Using partial least‑squares discriminant analysis, we showed that sepsis after trauma patients was metabolically distinct from the trauma-induced SIRS. The main distinguishing metabolites were LPC O-22:1, uric acid, 23-Norcholic acid, PC O-38:1, and PC O-42:3 (AUC: 0.875 to 0.910). Conclusions Our study has identified the potential of employing metabolic biomarkers for differentiation of sepsis after trauma from trauma-induced SIRS. In particular, LPC O-22:1, uric acid, 23-Norcholic acid, PC O-38:1, and PC O-42:3 demonstrated potential as important biomarkers for distinguishing sepsis after trauma from trauma-induced SIRS. These biomarkers provide a basis for further research on identifying biomarkers distinguishing sepsis after trauma from trauma-induced SIRS based on targeted metabolomics.