Venous thromboembolism in multiple myeloma: current perspectives in pathogenesis
Noppacharn Uaprasert1, Peter M Voorhees, Nigel Mackman
1Department of Medicine, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. drnoppacharn@yahoo.com
Patients with multiple myeloma are at increased risk of venous thromboembolism (VTE) compared to the general population. The introduction of immunomodulatory agents, such as thalidomide and lenalidomide, substantially increases the incidence of VTE in multiple myeloma patients, especially when used in combination with high-dose dexamethasone and/or anthracycline-based chemotherapy. Thromboprophylaxis is recommended for reducing VTE in patients receiving immunomodulatory agent-based regimens. On the other hand, bortezomib, a proteasome inhibitor, is not associated with an increased risk of VTE, as observed by a very low incidence of thrombotic complications in the absence of thromboprophylaxis. Currently, the mechanisms underlying the impact of these agents on VTE are not well-understood. Further studies to investigate the pathogenesis of VTE in multiple myeloma are warranted. These studies may not only yield greater insight into the pathogenesis of disease but may also define novel targets for the prevention and treatment of thromboembolic events in patients with multiple myeloma.
Patients with multiple myeloma are at increased risk of venous thromboembolism (VTE) compared to the general population. The introduction of immunomodulatory agents, such as thalidomide and lenalidomide, substantially increases the incidence of VTE in multiple myeloma patients, especially when used in combination with high-dose dexamethasone and/or anthracycline-based chemotherapy. Thromboprophylaxis is recommended for reducing VTE in patients receiving immunomodulatory agent-based regimens. On the other hand, bortezomib, a proteasome inhibitor, is not associated with an increased risk of VTE, as observed by a very low incidence of thrombotic complications in the absence of thromboprophylaxis. Currently, the mechanisms underlying the impact of these agents on VTE are not well-understood. Further studies to investigate the pathogenesis of VTE in multiple myeloma are warranted. These studies may not only yield greater insight into the pathogenesis of disease but may also define novel targets for the prevention and treatment of thromboembolic events in patients with multiple myeloma.
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