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Prepublished online as a Blood First Edition Paper on August 8, 2002; DOI 10.1182/blood-2002-01-0329.
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Blood, 1 December 2002, Vol. 100, No. 12, pp. 4232-4233
BRIEF REPORT
Oral anticoagulation reduces activated protein C less than
protein C and other vitamin K-dependent clotting
factors
Marleen J. A. Simmelink,
Philip G. de Groot,
Ronald H. W. M. Derksen,
José A. Fernández, and
John H. Griffin
From the Thrombosis and Haemostasis Laboratory,
Department of Haematology, and Department of Rheumatology & Clinical
Immunology, University Medical Center, Utrecht, The Netherlands; the
Institute of Biomembranes, Utrecht University, Utrecht, The
Netherlands; and the Department of Molecular and Experimental Medicine,
The Scripps Research Institute, La Jolla, CA.
Oral anticoagulant therapy, which is used for prophylaxis and
management of thrombotic disorders, causes similar reductions in plasma
levels of vitamin K-dependent procoagulant and anticoagulant clotting
factor zymogens. When we measured levels of circulating activated
protein C, a physiologically important anticoagulant and
anti-inflammatory agent, in patients on oral anticoagulant therapy,
the results unexpectedly showed that such therapy decreases levels of
activated protein C substantially less than levels of protein
C, prothrombin, and factor X, especially at lower levels of
prothrombin and factor X. Thus, we suggest that oral anticoagulant therapy results in a relatively increased expression of the protein C
pathway compared with procoagulant pathways not only because there is
less prothrombin to inhibit activated protein C anticoagulant activity,
but also because there is a disproportionately higher level of
circulating activated protein C.
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