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INTERPRETATION : Current therapeutic recommendations on protein restriction, use of antibiotics and lactulosis to patients with hepatic failure are not sufficiently documented. There is a need for development of novel ammonia lowering strategies. RESULTS : Under normal conditions the intestines and the kidneys are the main ammonia producing organs, whereas the liver and skeletal muscles are the major ammonia consuming organs. Small and large intestines contribute equally to the release of ammonia. Development of intra- and extra hepatic portasystemic shunts, impaired urea synthesis, and reduced hepatic perivenous glutamine synthesis capacity, contribute to the development of hyperammonaemia with hepatic failure. The kidneys are quantitatively as important as the portal drained viscera in ammonia production, but can adapt to hyperammonaemia by reducing the production of ammonia to the blood and at the same time increase its excretion in urine. Furthermore, the lungs are metabolically active, but their role in hyperammonaemia remains unsettled. Skeletal muscle contributes to reducing the ammonia level in the body through synthesis of glutamine from equimolar quantities of glutamate and ammonia. MATERIAL AND METHODS : The present paper is based on experimental research performed in a porcine model of acute liver failure and a literature search in Pubmed. BACKGROUND : Serious hepatocellular dysfunction leads to disturbances in the ammonia metabolism and increases the risk for development of hepatic encephalopathy. The present paper describes pathophysiological patterns for development of hyperammonemia in patients with liver diseases and discusses the rationale for novel ammonia lowering strategies.

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