Safe and successful gut-restricted adsorbent strategy against cirrhosis and acute-on-chronic liver failure

Abstract

Cirrhosis marks the advanced stage of chronic liver disease characterised by sustained inflammation leading to the loss of hepatocytes and the progression of fibrosis. These structural and functional alterations profoundly impact blood flow within the hepatic microcirculation, potentially culminating in portal hypertension over time. Traditionally, the evolution of cirrhosis has been divided into two clinical phases: An initial asymptomatic stage known as compensated cirrhosis followed by decompensated cirrhosis, marked by the emergence of complications such as ascites, variceal bleeding, hepatic encephalopathy, jaundice, coagulopathy and bacterial infections. Decompensated cirrhosis typically signals a more aggressive disease course with patients susceptible to hepatic and extrahepatic organ dysfunction, complications or necessitating liver transplantation.1 It is imperative to recognise that decompensated cirrhosis transcends hepatic manifestations representing a systemic disorder. Recent observational studies in Europe, including chronic liver failure acute-on-chronic liver failure (CANONIC) and PREDICTing Acute-on-chronic liver failure (PREDICT), have further classified decompensated cirrhosis into non-acute and various forms of acute decompensation, potentially leading to acute-on-chronic liver failure (ACLF). However, the precise factors determining the trajectory towards decompensation in cirrhosis remain elusive. Accumulating evidence suggests that specific preceding events play pivotal roles in this progression. Notably, clinically significant portal hypertension, systemic inflammation and failure of the intestinal barrier leading to bacterial product translocation through the portal circulation are key events interdependently influencing each …