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Article
January 1959

Relation of Azotemia to Blood "Ammonium" in Patients with Hepatic Cirrhosis

Author Affiliations

Cleveland

From the Department of Medicine, Western Reserve University School of Medicine, and Cuyahoga County Hospital (formerly City Hospital). Russell M. Wilder Fellow of the National Vitamin Foundation, Instructor in Medicine and Research Associate in Biochemistry, Western Reserve University School of Medicine (Dr. Webster); Associate Professor of Medicine, Western Reserve University School of Medicine, Visiting Physician, Department of Medicine, Cuyahoga County Hospital (Dr. Gabuzda).

AMA Arch Intern Med. 1959;103(1):15-22. doi:10.1001/archinte.1959.00270010021004
Abstract

Oliguria and azotemia may accompany the development of hepatic coma in patients with severe liver disease, and they are frequently ominous prognostic signs. Since urea from the circulating blood enters the gastrointestinal tract where it can be degraded to ammonium by the action of bacterial urease,1 urea may be capable of contributing indirectly to the increased concentration of ammonium found in the blood of some patients with liver disease. Increased circulating urea might then be considered with other nitrogenous substances capable of inducing impending hepatic coma in patients with severe hepatic disease.2-7 This investigation was done to determine the influence of azotemia upon the blood ammonium levels in patients with hepatic disease and to evaluate the relation of azotemia to hepatic coma.

Materials and Methods  Four groups of patients were studied. One group consisted of six patients with azotemia but without liver disease (Table 1). A second group

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