Plasma exchange combined with hemofiltration influences serum levels of IL-17 and IL-6 in patients with HBV related acute-on-chronic liver failure

Objective To determine whether plasma exchange combined with hemofiltration influences the peripheral blood levels of interleukin(IL)-17 and/or IL-6 in patients with hepatitis B virus(HBV)-related acute-on-chronic liver failure(ACLF) and investigate its clinical significance.Methods Thirty patients diagnosed with HBV-related ACLF received a single treatment of plasma exchange combined with hemofiltration.This group was subdivided according to 72 h outcomes of improvement(n = 19) or deterioration(n = 11).Control groups were composed of chronic hepatitis B patients(CHB;n = 19) and healthy individuals(HC;n = 20).Blood samples were collected from all study participants to measure concentrations of IL-17 and IL-6 by enzyme-linked immunosorbent assay and biochemical parameters with an automatic analyzer.Intergroup differences were statistically analyzed for significance.Results IL-17 and IL-6 were markedly up-regulated in the HBV-related ACLF group compared with the CHB and HC groups.The plasma exchange combined with hemofiltration treatment significantly reduced the serum concentrations of IL-17 and IL-6(vs.pre-treatment levels: t = 35.1,P 0.001 and t = 33.4,P 0.001,respectively).In addition,the indexes of extracorporeal removal of IL-17 and IL-6 were higher in the improved subgroup than in the deterioration subgroup(t = 3.8,P 0.05 and t = 3.9,P 0.05,respectively) and were negatively associated with the MELD score of the HBV-related ACLF patients in both subgroups(r = 0.53,P 0.05 and r = 0.43,P 0.05,respectively).Conclusion The enhanced serum concentrations of IL-17 and IL-6 in HBV-related ACLF patients were markedly reduced by a single treatment of plasma exchange combined with hemofiltration.The removal efficiency of plasma exchange combined with hemofiltration for serum IL-17 and IL-6 may be a short-term prognostic indicator of HBV-related ACLF patients,possibly due to the reduced risk of inflammation-related damage mediated by these two cytokines.