Ambulatory therapy of patients with free-floating proximal deep vein thrombosis is safe

1. Osman K, Comenzo R, Rajkumar SV. Deep venous thrombosis and thalidomide therapy for multiple myeloma. N Engl J Med 2001; 344: 1951–2. 2. Zangari M, Siegel E, Barlogie B et al. Thrombogenic activity of doxorubicin in myeloma patients receiving thalidomide: implications for therapy. Blood 2002; 100: 1168–71. 3. Minnema MC, Fijnheer R, de Groot PG et al. Extremely high levels of von Willebrand factor antigen and of procoagulant factorVIII found in multiple myeloma patients are associated with activity status but not with thalidomide treatment. J Thromb Haemost 2003; 1: 445–9. 4. Zangari M, Saghafifar F, Mehta P et al. The blood coagulation mechanism in multiple myeloma. Semin Thromb Hemost 2003; 29: 275–82. 5. Deitcher SR, Choueiri T, Srkalovic G et al. Acquired activated protein C resistance in myeloma patients with venous thromboembolic events. Br J Haematol 2003; 123: 959. 6. Carr ME, Jr., Dent RM, Carr SL. Abnormal fibrin structure and inhibition of fibrinolysis in patients with multiple myeloma. J Lab Clin Med 1996; 128: 83–8. 7. YagciM, SucakGT,Haznedar R. Fibrinolytic activity in multiple myeloma. Am J Hematol 2003; 74: 231–7. 8. Lisman T, de Groot PG, Meijers JC et al. Reduced plasma fibrinolytic potential is a risk factor for venous thrombosis. Blood 2005; 105: 1102–5. 9. MinnemaMC, Breitkreutz I, Auwerda JJ et al. Prevention of venous thromboembolismwith lowmolecular-weight heparin in patients with multiple myeloma treated with thalidomide and chemotherapy. Leukemia 2004; 18: 2044–6. 10. Francis CW. Plasminogen activator inhibitor-1 levels and polymorphisms. Arch Pathol Lab Med 2002; 126: 1401–4. 11. Ridker PM,Vaughan DE, Stampfer MJ et al. Baseline fibrinolytic state and the risk of future venous thrombosis. A prospective study of endogenous tissuetype plasminogen activator and plasminogen activator inhibitor. Circulation 1992; 85: 1822–7. 12. PrinsMH, Hirsh J.A critical review of the evidence supporting a relationship between impaired fibrinolytic activity and venous thromboembolism. Arch Intern Med 1991; 151: 1721–31. 13. Lisman T, Leebeek FW, Mosnier LO et al. Thrombin-activatable fibrinolysis inhibitor deficiency in cirrhosis is not associated with increased plasma fibrinolysis. Gastroenterology 2001; 121: 131–9. 14. LismanT,Adelmeijer J, Nieuwenhuis HK et al. Enhancement of fibrinolytic potential in vitro by anticoagulant drugs targeting factorXa, but not by those inhibiting thrombin or tissue factor. Blood Coag Fibrinol 2003; 14: 557–62. vels of lowmolecular weight heparin (as measured by an anti Xa assay, data not shown). In conclusion, in this study we found an induction of hypofibrinolysis in patients with multiple myeloma during VAD and TAD treatment.These results may explain the elevated thrombosis risk in patients receiving induction chemotherapy with VAD or TAD. However, it does not explain the extra increased risk of VTE during thalidomide treatment, as hypofibrinolysis was observed both during VAD and TAD treatment. Presumably other haemostatic alterations are responsible for the thrombotic risk in myeloma patients during thalidomide therapy. Acknowledgements