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Prepublished online as a Blood First Edition Paper on August 8, 2002; DOI 10.1182/blood-2002-01-0329. This Article Full Text (PDF) All Versions of this Article: 2002-01-0329v1 100/12/4232    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Simmelink, M. J A Articles by Griffin, J. H Search for Related Content PubMed PubMed Citation Articles by Simmelink, M. J A Articles by Griffin, J. H Social Bookmarking                   What's this? Submitted February 1, 2002 Accepted July 13, 2002 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, Jose A Fernandez, and John H Griffin Department of Haematology, University Medical Center, Utrecht, The Netherlands; Department of Rheumatology & Clinical Immunology, University Medical Center, Utrecht, The Netherlands; Institute of Biomembranes, Utrecht, The Netherlands Department of Haematology, University Medical Center, Utrecht, The Netherlands; Institute of Biomembranes, Utrecht, The Netherlands Department of Rheumatology & Clinical Immunology, University Medical Center, Utrecht, The Netherlands Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA, USA * Corresponding author; email: m.simmelink{at}lab.azu.nl. 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 significantly 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, as suggested by Smirnov et al (Blood 94:3839, 1999), but also because there is a disproportionately higher level of circulating activated protein C. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. J. Schurgers, M. J. Shearer, K. Hamulyak, E. Stocklin, and C. Vermeer Effect of vitamin K intake on the stability of oral anticoagulant treatment: dose-response relationships in healthy subjects Blood, November 1, 2004; 104(9): 2682 - 2689. [Abstract] [Full Text] [PDF] U. Derhaschnig, R. Reiter, P. Knobl, M. Baumgartner, P. Keen, and B. Jilma Recombinant human activated protein C (rhAPC; drotrecogin alfa [activated]) has minimal effect on markers of coagulation, fibrinolysis, and inflammation in acute human endotoxemia Blood, September 15, 2003; 102(6): 2093 - 2098. [Abstract] [Full Text] [PDF]

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