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Prepublished online as a Blood First Edition Paper on May 1, 2003; DOI 10.1182/blood-2003-02-0620. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-02-0620v1 102/5/1686    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Koenen, R. R. Articles by Hackeng, T. M. Search for Related Content PubMed PubMed Citation Articles by Koenen, R. R. Articles by Hackeng, T. M. Related Collections Clinical Trials and Observations Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 September 2003, Vol. 102, No. 5, pp. 1686-1692 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY The APC-independent anticoagulant activity of protein S in plasma is decreased by elevated prothrombin levels due to the prothrombin G20210A mutation Rory R. Koenen, Guido Tans, René van Oerle, Karly Hamulyák, Jan Rosing, and Tilman M. Hackeng From the Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, the Netherlands. Protein S exhibits anticoagulant activity independent of activated protein C (APC). An automated factor Xa–based one-stage clotting assay was developed that enables quantification of the APC-independent activity of protein S in plasma from the ratio of clotting times (protein S ratio [pSR]) determined in the absence and presence of neutralizing antibodies against protein S. The pSR was 1.62 ± 0.16 (mean ± SD) in a healthy population (n = 60), independent of plasma levels of factors V, VIII, IX, and X; protein C; and antithrombin, and not affected by the presence of factor V Leiden. The pSR strongly correlates with the plasma level of protein S and is modulated by the plasma prothrombin concentration. In a group of 16 heterozygous protein S–deficient patients, the observed mean pSR (1.31 ± 0.09) was significantly lower than the mean pSR of the healthy population, as was the pSR of plasma from carriers of the prothrombin G20210A mutation (1.47 ± 0.21; n = 46). We propose that the decreased APC-independent anticoagulant activity of protein S in plasma with elevated prothrombin levels may contribute to the thrombotic risk associated with the prothrombin G20210A mutation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. F. A. Maurissen, M. C. L. G. D. Thomassen, G. A. F. Nicolaes, B. Dahlback, G. Tans, J. Rosing, and T. M. Hackeng Re-evaluation of the role of the protein S-C4b binding protein complex in activated protein C-catalyzed factor Va-inactivation Blood, March 15, 2008; 111(6): 3034 - 3041. [Abstract] [Full Text] [PDF] K. M. Sere, J. Rosing, and T. M. Hackeng Inhibition of thrombin generation by protein S at low procoagulant stimuli: implications for maintenance of the hemostatic balance Blood, December 1, 2004; 104(12): 3624 - 3630. [Abstract] [Full Text] [PDF]

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