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Interphase Fluorescence in situ Hybridization of Bone Marrow Smears of Multiple Myeloma
Published on: April 15, 2022
Thrombosis in multiple myeloma
Maurizio Zangari1, Francesca Elice, Louis Fink
1Myeloma Institute, University of Arkansas for Medical Sciences, 4301 W. Markham Street, Slot 776, Little Rock, Arkansas 72205, USA. zangarimaurizio@uams.edu
Abstract:
Multiple myeloma, as with other malignancies, has been associated with the development of venous thromboembolic events. Chemotherapy or steroids in combination with antiangiogenic agents can further enhance this risk. The identification of measurable factors associated with this prothrombotic state could help in the selection of patients who need antithrombotic prophylaxis. Malignancy-associated thrombophilic state, paraprotein-specific mechanisms and treatment-induced changes can explain the high rate of thrombosis in this cancer population. While the release of inflammatory cytokines induces high levels of factor VIII, von Willebrand factor and downregulate the protein C system, elevated plasma immunoglobulin can impair fibrinolysis. Strategies of thromboprophylaxis with low molecular weight heparin, warfarin or aspirin in patients treated with thalidomide/chemotherapy or lenalidomide and dexamethasone have shown efficacy. Early data indicate that the effect of low molecular weight heparin on multiple myeloma is not confined to the anticoagulant effect but could extend to survival; a similar positive trend in overall survival has also been reported in patients treated with aspirin.
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