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Alfred L. Baker, MD

JAMA. 1979;242(4):355-356.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Patients with chronic liver disease often have elevations in plasma levels of aromatic amino acids, including tyrosine, phenylalanine, and tryptophan, as well as methionine, glutamate, aspartate, and ornithine; branched-chain amino acids, leucine, isoleucine, and valine, are usually depressed.^1,2 Fischer et al³ have focused the interest of clinicians and investigators alike on the pathogenesis and treatment of hepatic encephalopathy by suggesting that the depressed ratio of branched-chain to aromatic amino acids may have etiologic importance in hepatic coma.⁴ A corollary of this hypothesis is that restoration of this ratio to normal should not only provide specific treatment for hepatic encephalopathy but should also allow administration of enough protein equivalents of amino acids to attain nitrogen balance without precipitating hepatic coma. Nutritional repletion may also prevent further deterioration of hepatic structure and function. A recent dietary survey reported substantially less protein consumption in patients with alcoholic hepatitis and cirrhosis . . . [Full Text PDF of this Article]

Author Affiliations
Liver Study Unit University of Chicago Chicago

Footnotes
Address editorial communications to the Editor, 535 N Dearborn St, Chicago, IL 60610.

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