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HENRY BROWN, M.D.; JULIE BROWN, B.S.

AMA Arch Surg. 1962;85(5):771-775.

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

One of the very puzzling aberrations that occurs in liver disease is the elevation of blood ammonia.¹ Though this is not a constant finding it is often seen in patients with liver failure, especially those suffering from cirrhosis who have had portasystemic vein shunt operations.² Here the ammonia level may rise to several times the normal value and is thought to be at least in part responsible for symptoms of hepatic coma. This has been documented both in the laboratory and clinically where tremors, lethargy, staggering gait, coma, and death have been caused by elevating the blood ammonia and where such symptoms may be ameliorated before the terminal stages by lowering it.^1,3

Of the several methods currently used to lower blood ammonia, one of great theoretical interest is the administration of arginine.⁴ The amino acid plays an important role in the Krebs-Henseleit cycle in which ammonia . . . [Full Text PDF of this Article]

Author Affiliations
MADISON, WIS.

From the Department of Surgery, The University of Wisconsin. This work was supported by grants from the National Institute of Arthritis and Metabolic Diseases, U.S. Public Health Service (A-5995) and the Wisconsin Alumni Research Foundation.

Footnotes
Presented at the 19th Annual Meeting of the Central Surgical Association, Cincinnati, Feb. 21-24, 1962.

With the technical assistance of Wilbert Heimann.

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