The Kallikreinogen-Kallikrein Enzyme System of Human Plasma
Assay of Components and Observations in Disease States
- ROBERT W. COLMAN, M.D.;
- JOHN W. MASON, M.D.; and
- SOL SHERRY, M.D., F.A.C.P.
- Requests for reprints should be addressed to Sol Sherry, M.D., Temple University School of Medicine, 3400 N. Broad St., Philadelphia, Pa. 19140
SUMMARY
Biochemical methods have been developed for the assay of kallikreinogen, kallikrein inhibitor, and spontaneous arginine esterase activity in human plasma which have permitted investigation of alterations in these components in health and disease. Kallikreinogen is not activated by kaolin in Hageman factor deficiency plasma, is reduced in severe liver disease, and is elevated during administration of estrogens. Plasma kallikrein inhibitor is permanently decreased in hereditary angioneurotic edema and is transiently depressed in resolving pancreatitis. Plasma kallikreinogen and kallikrein inhibitor are elevated in allergic states. In carcinoid syndrome evidence of in vivo activation of plasma kallikreinogen, that is, increased spontaneous arginine esterase activity resembling plasma kallikrein with associated decreases in plasma kallikreinogen and kallikrein inhibitor, was present during spontaneous flushes and absent during asymptomatic intervals. A spontaneous arginine esterase activity that did not resemble plasma kallikrein was present in acute pancreatitis.
Article and Author Information
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From the Departments of Medicine and Pathology, Harvard Medical School, the Massachusetts General Hospital, Boston, Mass.; and the Department of Medicine, Temple University School of Medicine, Philadelphia, Pa.
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Supported by grants HE 11519 and HE 12148, National Institutes of Health, Bethesda, Md.
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*The International Union of Biochemistry recommends the use of prekallikrein instead of kallikreinogen; however this term is not yet widely accepted. In this report, we adhere to the more common usage, kallikreinogen.
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- Received June 17, 1969.
- Accepted July 3, 1969.
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