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Kallikrein-Bradykinin System in Chronic Alcoholic Liver Disease

PATRICK WONG, M.D.; ROBERT W. COLMAN, M.D., F.A.C.P.; RICHARD C. TALAMO, M.D.; and BERNARD M. BABIOR, M.D., Ph.D.
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Supported in part by grants HE-13206, AM-13348, AM-09115, and AM-05413, and by Career Development Awards HE-48075 (Dr. Colman), AM-31937 (Dr. Talamo), and AM-19950 (Dr. Babior), National Institutes of Health, Bethesda, Md.

▸Requests for reprints should be addressed to Bernard M. Babior, M.D., Thorndike Memorial Laboratory, Boston City Hospital, Boston, Mass. 02118.


Boston, Massachusetts


Ann Intern Med. 1972;77(2):205-209. doi:10.7326/0003-4819-77-2-205
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The kallikrein-bradykinin system was studied in patients with chronic alcoholic liver disease. Kallikreinogen levels were depressed in patients with cirrhosis when compared with levels in normal control subjects (18.8 ± 4.3 SD µmoles/ml·hr and 97 ± 24 SD µmoles/ml·hr, respectively). Levels in cirrhotics with long prothrombin times (7.8 ± 2.8 SD µmoles/ml·hr) were lower than levels in cirrhotics with normal prothrombin times (35.2 ± 20 SD µmoles/ml·hr). The lowest levels (1.5 ± 1.2 SD µmoles/ml·hr) were in three patients with hepatorenal syndrome. In contrast, Hageman factor, kallikrein inhibitor, and bradykinin levels were normal or only moderately depressed. Free kallikrein was not detected. We conclude that kallikreinogen production is impaired in alcoholic liver disease, the degree of impairment correlating well with the severity of the liver disease, and that kallikreinogen levels therefore are a sensitive index of liver dysfunction. Strong evidence was presented that the hepatorenal syndrome is not caused by elevated plasma bradykinin levels.

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