Activated Protein C Resistance: What Have We Learned Now That the Dust Has Settled?

References

• Dahlbäck B, Carlsson M, Svensson P J. Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C. Proc Natl Acad Sci USA 1993; 90: 1004–8
   PubMed Web of Science ®Google Scholar
• Dahlbäck B. Molecular genetics of venous thromboembolism. Ann Med 1995; 27: 187–92
   Web of Science ®Google Scholar
• Kalafatis M, Mann K G. Factor VLeiden and thrombophilia. Arteriosc/er Thromb Vase Biol 1997; 17: 620–7
   Google Scholar
• Bertina R M, Koeleman B PC, Koster T, et al. Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature 1994; 369: 64–7
   PubMed Web of Science ®Google Scholar
• Greengard J S, Sun X, Xu X, Fernandez J A, Griffin J H, Evatt B. Activated protein C resistance caused by Arg506Gln mutation in factor Va. Lancet 1994; 343: 1361–2
   PubMed Web of Science ®Google Scholar
• Voorberg J, Roelse J, Koopman R, et al. Association of idiopathic venous thromboembolism with single point-mutation at Arg506 of factor V. Lancer 1994; 343: 1535–6
   PubMed Web of Science ®Google Scholar
• Zivelin A, Griffin J H, Xu X, et al. A single genetic origin for a common Caucasian risk factor for venous thrombosis. Blood 1997; 89: 397–402
   PubMed Web of Science ®Google Scholar
• Ridker P M, Miletich J P, Stampfer M J, Goldhaber S Z, Lindpaintner K, Hennekens C H. Factor V Leiden and risks of recurrent idiopathic venous thromboembolism. Circulation 1995; 92: 2800–2
   PubMed Web of Science ®Google Scholar
• Simioni P, Pradoni P, Lensing A WA, et al. The risk of recurrent venous thromboembolism in patients with an Arg506 to Gin mutation in the gene for factor V (factor V Leiden). N Engl J Med 1997; 336: 399–400
   PubMed Web of Science ®Google Scholar
• Rintelen C, Pabinger I, Knobl P, Lechner K, Mannhalter C. Probability of recurrence of thrombosis in patients with and without factor V Leiden. Thromb Haemost 1995; 75: 229–32
   Google Scholar
• Koeleman B PC, Reitsma P H, Allaart C F, Bertina R M. Activated protein C resistance as an additional risk factor for thrombosis in protein C-deficient families. Blood 1994; 84: 1031–6
   PubMed Web of Science ®Google Scholar
• Zoller B, Berntsdotter A, Garcia de Frutos P, Dahlback B. Resistance to activated protein C as an additional genetic risk factor in hereditary deficiency of protein S. Blood 1995; 85: 3518–23
   PubMed Web of Science ®Google Scholar
• Ridker P M, Hennekens C H, Lindpaintner K, Stampfer M J, Eisenberg P R, Miletich J P. Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men. N Engl J Med 1995; 332: 912–7
   PubMed Web of Science ®Google Scholar
• Vandenbroucke J P, Koster T, Briet E, Reitsma P H, Bertina R M, Rosendaal F R. Increased risk of venous thrombosis in oral-contraceptive users who are carriers of factor V Leiden mutation. Lancet 1994; 344: 1453–7
   PubMed Web of Science ®Google Scholar
• Hellgren M, Svensson P J, Dahlbäck B. Resistance to activated protein C as a basis for venous thromboembolism associated with pregnancy and oral contraceptives. Am J Obstet Gynecol 1995; 173: 210–3
   PubMed Web of Science ®Google Scholar
• Bokarewa M L, Bremme K, Blomback M. Arg506-Gln mutation in factor V and risk of thrombosis during pregnancy. Br J Haematol 1996; 92: 473–8
   PubMed Web of Science ®Google Scholar
• Halbmayer W-M, Haushofer A, Schön R, Fischer M. The prevalence of poor anticoagulant response to activated protein C (APC resistance) among patients suffering from stroke or venous thrombosis and among healthy subjects. Stood Coagul Fibrinolysis 1994; 5: 51–7
   PubMed Web of Science ®Google Scholar
• Fisher M, Fernändez J A, Ameriso S F, et al. Activated protein C resistance in ischemic stroke not due to factor V arginine506 glutamine mutation. Stroke 1996; 27: 1163–6
   PubMed Web of Science ®Google Scholar
• van der Bom J G, Bots M L, Haverkate F, et al. Reduced response to activated protein C is associated with increased risk for cerebrovascular disease. Ann Intern Med 1996; 125: 265–9
   PubMedGoogle Scholar
• Sakata T, Kario K, Katayama Y, Matsuyama T, Kato H, Miyata T. Clinical significance of activated protein C resistance as a potential marker for hypercoagulable state. Thromb Res 1996; 82: 235–44
   Google Scholar
• Potzsch B, Kawamura H, Preissner K T, Schmidt M, Seelig C, Muller-Berghaus G. Acquired protein C dysfunction but not decreased activity of thrombomodulin is a possible marker of thrombophilia in patients with lupus anticoagulant. J Lab Clin Med 1995; 125: 56–65
   PubMedGoogle Scholar
• Poort S R, Rosendaal F R, Reitsma P H, Bertina R M. A common genetic variation in the 3′-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood 1996; 88: 3698–703
   PubMed Web of Science ®Google Scholar