Transition to decompensation and acute-on-chronic liver failure: Role of predisposing factors and precipitating events

Abstract

The transition from compensated to decompensated cirrhosis results from a complex interplay of predisposing and precipitating factors and represents an inflection point in the probability of a patient surviving. With the progression of cirrhosis, patients accumulate multiple disorders (e.g. altered liver architecture, portal hypertension, local and systemic inflammation, bacterial translocation, gut dysbiosis, kidney vasoconstriction) that predispose them to decompensation. On the background of these factors, precipitating events (e.g. bacterial infection, alcoholic hepatitis, variceal haemorrhage, drug-induced liver injury, flare of liver disease) lead to acute decompensation (ascites, hepatic encephalopathy, variceal bleeding, jaundice) and/or organ failures, which characterise acute-on-chronic liver failure. In this review paper, we will discuss the current hypotheses and latest evidences regarding predisposing and precipitating factors associated with the transition to decompensated liver disease.

Plasticity of monocytes and macrophages in cirrhosis of the liver

“…Along cirrhosis progression patients develop multiple complications (PH, inflammation, BT, gut dysbiosis) that predispose them to decompensation and subsequent precipitating events (infection, variceal haemorrhage) lead to AD (Gustot et al, 2021).…”

Harnessing reactive oxygen/nitrogen species and inflammation: Nanodrugs for liver injury

“…However, available treatments are limited, mainly involving methods targeting etiology (including diet control, abstinence from alcoholic drink, drug withdrawal, and antiviral and antilipemic therapy) [ [17] , [18] , [19] ]. Liver injury can rapidly progress to acute liver failure, fibrosis, or even cancer if not treat effectively [ [20] , [21] , [22] ]. In cases where liver injury develops into acute liver failure and cirrhosis, transplantation is the only feasible option.…”

Oral Intake of L-Ornithine-L-Aspartate Is Associated with Distinct Microbiome and Metabolome Changes in Cirrhosis

“…Since oral LOLA comes into contact with the human gut microbiome and the intestinal barrier, effects on the gut microbiome and intestinal permeability may play a role in the clinical effects of LOLA. The gut microbiome is not only involved in ammonia generation and thereby in the pathogenesis of HE, but it is today also understood as a key driver of complications of cirrhosis [10]. The gut microbiome is severely altered in liver cirrhosis in general, with a reduction in bacterial diversity and an increase in potential pathogens [11].…”