UCL Institute for Liver and Digestive Health, University College of London, Royal Free Campus, London, UK.
PURPOSE OF REVIEW:
Hyperammonemia is thought to be central in the pathophysiology of hepatic encephalopathy in patients suffering from liver failure. The purpose of this article is to explore existing treatment options that help lower ammonia levels in patients and alleviate symptoms of hepatic encephalopathy.
There are two ways to approach modulating ammonia levels and its effect on the brain. The first targets ammonia levels itself and the second targets inflammation, which makes the brain susceptible to the deleterious effect of ammonia. Recent studies provide new evidence for the use of lactulose, probiotics and rifaximin, as well as closure of large portosystemic shunts in the treatment of hepatic encephalopathy.
Over the past 20 years or so, many new approaches to treat hepatic encephalopathy have been developed based upon better understanding of interorgan ammonia metabolism. Reduction in ammonia can be achieved by targeting its production, absorption or elimination. This review will primarily focus on these strategies that reduce ammonia levels in liver failure patients.