Protein Malnutrition in Chronic Liver Disease: Corrective Measures

Abstract

Malnutrition and nutrient abnormalities are often associated with chronic liver disease, and may contribute to the development of several complications. The liver’s role being central in nitrogen metabolism, hepatic damage frequently causes derangements in protein metabolism (Mezey 1978). In most patients with chronic liver disease, protein requirements for maintenance of nitrogen balance (NB) are no different from those of normal individuals. It follows that the accuracy of either oral or parenteral protein equivalent administration can play a major role in liver disease progress. Besides, one must take into consideration the fact that an increased requirement of protein, in order to repair the hepatic damage, leads to deficiencies in other organs; specifically, it causes muscle wasting, since amino acids are continuously deaminated so as to provide a source of energy (Soeters and Fischer 1976). This picture is characteristic of chronic liver disease, with a trend to: (a) an increase in plasma concentrations of amino acids normally removed by the liver, i. e., essential and nonessential aromatic and sulfurated amino acids; (b) a decrease in the amino acids preferentially taken up by extrahepatic tissues, i.e., essential branched-chain amino acids (BCAA) such as valine, leucine, and isoleucine. Therefore, the most common amino acid pattern observed in chronic liver disease consists of increases in the aromatic amino acids (AAA) tyrosine and phenylalanine, glutamic acid, methionine, and sometimes cystine, and a decrease in the BCAA valine, leucine, and isoleucine (Rosen et al. 1977).