Artificial hepatic support - Where are we now?

The liver plays a central role in metabolic homeostasis, but also a major role in host-defence mechanisms. There is great debate as to the underlying etiology of what causes the clinical syndrome of acute liver failure, whether it represents toxin accumulation due to defective hepatocyte function, or is due to endothelial and Kupffer cell mediated inflammation secondary to hepatocyte necrosis with resultant endotoxemia, cytokine activation and recruitment of inflammatory cells. Thus, treatments designed to support the patient with liver failure must not only remove toxins, but also provide adequate hepatic function, until sufficient hepatic regeneration occurs, or transplantation. The history of treating patients with acute hepatic failure is littered with small uncontrolled series advocating one treatment after another. It is important after the debacle of charcoal perfusion that the newer treatments are carefully evaluated by randomized controlled trials. The BioLogic-DT and MARS systems will remove a varying amount of toxins, but do not provide hepatic support. Bioartificial livers, such as the ELAD and hepatocyte infusions, may prove to be the superior treatment, but the question arises as to how many hepatocytes are required.