Abstract

Acute-on-chronic liver failure (ACLF) is an acute syndrome accompanied with decompensation of cirrhosis, organ failure with high 28-day mortality rate. Systemic inflammation is the main feature of ACLF, and poor outcome is closely related with exacerbated systemic inflammatory responses. It is well known that severe systemic inflammation is an important event in chronic hepatitis B (CHB)-ACLF, which eventually leads to liver injury. However, the initial CHB-ACLF events are unclear; moreover, the effect of these events on host immunity as well as that of immune imbalance on CHB-ACLF progression are unknown. Here, we investigate the initial events of ACLF progression, discuss possible mechanisms underlying ACLF progression, and provide a new model for ACLF prediction and treatment. We review the characteristics of ACLF, and consider its plausible immune predictors and alternative treatment strategies.

Highlights

  • Acute-on-chronic liver failure (ACLF) is defined as the exacerbation of chronic liver disease initiated by a precipitating event, typically resulting in elevated short-term mortality (Alam et al, 2017)

  • Since chronic hepatitis B (CHB)-ACLF is a dynamic disease, patient data originating from different phases of the disease lead to different tolllike receptor (TLR) recognition. These results suggest that TLR expression varies among different CHB-ACLF stages

  • The anti-inflammatory cytokine IL-10 was significantly increased in CHB-ACLF patients, as was the pro-inflammatory IL-6 compared to that in No-ACLF patients. This indicated increased reparative inflammation. These results suggest an excessive host immune response mediated by increased expression of anti-bacterial immunity genes, indicating an increased microbial burden (Wu et al, 2018)

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Summary

Introduction

Acute-on-chronic liver failure (ACLF) is defined as the exacerbation of chronic liver disease initiated by a precipitating event, typically resulting in elevated short-term mortality (Alam et al, 2017). TLR4 mRNA levels have been reported to be up-regulated in the peripheral blood mononuclear cells (PBMCs) of ACLF patients compared to those in healthy individuals and CHB patients.

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