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William H. J. Summerskill, D.M., M.R.C.P.; Stanley J. Wolfe, M.D.; Charles S. Davidson, M.D.

AMA Arch Intern Med. 1956;97(6):661-663.

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

AMMONIA intoxication has yet to be established as the causal factor in hepatic coma, although several observations suggest this to be the case. Nevertheless, the significance of high blood ammonia values in liver disease and the influence that recent advances in this field should exert on treatment demand critical review.

Ammonia metabolism had been intimately related to liver function even before Krebs gave precise details of the synthesis of urea from ammonia in the liver. The greatest concentration of ammonia is in portal vein blood after protein ingestion, reflecting enzymatic activity on dietary nitrogen. Values higher than in peripheral veins are found in renal vein blood, and recent work has indicated that the arterial concentration is higher than peripheral venous.¹ It is possible also that ammonia may be derived from other sources. Elevated fasting peripheral blood ammonia levels in certain patients with hepatic cirrhosis were originally attributed to shunting of portal blood through collateral vessels, an explanation in accord with observations made . . . [Full Text PDF of this Article]

Author Affiliations
From the Thorndike Memorial Laboratory and Second and Fourth (Harvard) Medical Services, Boston City Hospital, and the Department of Medicine, Harvard Medical School, Boston.

Footnotes
Submitted for publication March 9, 1956.

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