Eiwitstofwisseling bij levercirrhose

This thesis describes a study of protein metabolism in patients with cirrhosis of the liver. The incentive to start this study was the clinical observation that protein malnutrition is often found in cirrhotic patients. It is likely that this malnutrition will influence the outcome of the disease unfavourably. However, when the disease is complicated by portosyst:emic encephalopathy, dietary protein has to be restricted. This only serves to make the malnutrition problem worse. The second reason hypothesis that to start this study of protein metabolism was portosystemic encephalopathy could be considered the a consequence of protein catabolism in the body. A catabolic state would result in a disturbance of the plasma aminoacid pattern. This t.rould lead to the formation in the brain of false neurotransmitters. These were considered to be the cause of the encephalopathy. Promotion of anabolic conditions would therefore be essential to prevent and treat encephalopathy. In addition it was proposed that encephalopathy should be treated with intravenous aminoacid solutions enriched with branched chain aminoacids. A study was performed to find whether patients with cirrhosis of the liver on a protein restricted diet were in a catabolic state as a result of the diet. A second question was whether this metabolic state indeed had an influence on their encephalopathy