The role and indications of albumin in advanced liver disease

Low serum albumin is common in cirrhosis and is associated with a reduced survival. Moreover, in this setting, the native isoform of albumin can be severely reduced due to several posttranscriptional changes that impair the non-oncotic properties of the molecule. Due to its oncotic power, albumin acts as a powerful plasma expander. As such, it can antagonize the consequences of effective hypovolemia deriving from the systemic hemodynamics abnormalities that characterize advanced cirrhosis. Indeed, the current established indications to the use of albumin in this context pertain to conditions deriving from an acute drop of effective volemia. Recent advances have shown that the pathophysiological background of decompensated cirrhosis is characterized by a sustained systemic inflammatory and pro-oxidant state deriving by an abnormal bacterial translocation from the gut. These abnormalities ultimately lead to the multiorgan dysfunction. In this cascade of events, long-term albumin administration could act against several pathogenic factors through its non-oncotic properties, thus representing a potential multi-target mechanistic treatment. Over the last year, two randomized clinical trials on this topic were published. The ANSWER Trial demonstrated that the long-term albumin administration in patients with decompensated cirrhosis improves overall survival, reduces the incidence of complications and the need of hospitalizations and ameliorates the quality of life, being cost-effective. The MACHT trial challenged these results, but the differences between the two studies (sample size, baseline severity of cirrhosis, length of follow-up and amount of albumin administered) could explain its variant results, providing the basis for further insights into this matter.