Increased level of presepsin in patients with acutely decompensated cirrhosis predicts development of acute-on-chronic liver failure

Introduction The clinical course of acutely decompensated cirrhosis (AD) is heterogeneous. Presepsin (PSP) is a soluble CD14-subtype biomarker that reflects Toll-like receptor activity as the immune response to endotoxaemia and bacterial infections, and it has regulatory properties of the adaptive immune system. Aim We conducted a prospective study to assess whether, in hospitalized patients with AD, plasmatic PSP could predict development of ACLF. Material and Methods AD patients were recruited at admission and underwent determination of PSP (chemiluminescent immunoassay). All patients were followed for 1 year, and predictors of ACLF were assessed by Cox analysis. Results 99 AD patients were included (median age: 61 years; 65% had alcohol-related cirrhosis). The main reasons for AD were infections and alcoholic hepatitis (52% and 22%, respectively). Median MELD and CLIF-C AD scores were 18 and 54, respectively. Median PCP was 674 U/L (308-1700). Thirty-six patients developed ACLF. PSP was higher in patients who experienced ACLF vs those who did not (1253 [670-2562] vs 375 [245-722], respectively; p<0.0001). Among patients who didn't develop ACLF, PSP was comparable between those who were re-hospitalized due to cirrhosis complications and those who were not re-hospitalized (432 vs 355, respectively). Cox analysis demonstrated that PSP was independently associated with ACLF (Table). PSP AUROC was good and comparable to CLIF-C AD score (0.78 vs 0.79, respectively). A PSP value > 660 had 77% sensitivity and 70% specificity for the development of ACLF. In a sub-analysis including patients at lower risk of ACLF (i.e. CLIF-C AD score ≤50 and Child B), PSP was significantly higher in those who developed ACLF than in those who did not (1054 vs 250, respectively). Conclusion PSP can be a useful, single and independent biomarker to identify trajectories of AD, even in patients at lower risk of ACLF, if this is confirmed in larger cohorts.