Dynamic elevation of aromatic amino acids in Hepatitis C Virus induced cirrhosis after a standard meal.

At baseline cirrhotic patients with compensated liver disease have adequate reserve liver function to metabolize AAA and BCAA. When faced with a metabolic stressor, such as a standard meal, cirrhotic patients are less able to metabolize the increased load of AAA. This impairment correlates with porto-systemic shunting. Further evaluation of AAA in compensated liver disease might further the understanding of the liver-muscle- axis and the role it may play in development of sarcopenia in liver disease.