Amino acid metabolism in infectious hepatitis.

Although Mann (1) clearly demonstrated the key role of the liver in the deamination process nearly three decades ago, it is only since the development of such techniques as the quantitative measurements of free alpha amino acids in the plasma and urine, and their separation by means of either paper and starch column chromatography or microbiological assay that more definitive studies on the metabolism of amino acids in diseases of the liver can be carried out. Using microbiological methods, Frankl, Martin, and Dunn (2) first demonstrated considerable variations in the excretion of cystine, tryptophane, and histidine in patients with various types of liver disease. Dunn, Akawaie, Yeh, and Martin estimated that approximately 20 per cent of the patients with liver disease showed increased excretion of amino acids (3). In studies on patients with cirrhosis of the liver, Gabuzda, Eckhardt, and Davidson (4) found only minor disturbances of urine amino acid excretion, the most constant abnormality consisting of increased excretion of methionine and tryptophane, and a decreased excretion of isoleucine. Kinsell, Harper, Barton, Hutchin, and Hess (5) have reported an impaired methionine tolerance in patients with liver disease as compared with normal controls, but Wheeler and Gybrgy (6) were unable to confirm this. More recently, Dent and Walshe (7) and Walshe (8, 9) have suggested that because of the enormous reserve of the liver, a study of the total amino nitrogen concentration would not reveal any significant abnormality until the liver is extensively damaged. Using paper partition chromatography techniques, they found gross aminoaciduria in patients with acute yellow atrophy of the liver and hepatic coma, but only minor changes in patients with hepatitis and cirrhosis.