Abstract
The introduction of immunomodulatory drugs (IMiDs) has improved clinical outcome in
patients with multiple myeloma (MM). However, their use has been associated with a
higher risk of cardiovascular complications. The use of IMiDs with dexamethasone,
chemotherapy, or in combination with erythropoietic agents enhances the risk of venous
thromboembolism (VTE) up to 25%. The pathogenesis of this increased risk of VTE seen
with IMiD-based combination therapy is not yet fully understood, but several mechanisms
have been proposed to explain the development of this hypercoagulable state. In cancer
patients, prothrombotic factors include age, chemotherapy, immobility, enhanced expression
of tissue factor of malignant cells, circulating microparticles, and increased vascular
endothelial growth factor (VEGF). In patients with paraproteinemias, immunoglobulin-specific
mechanisms may also be involved and include hypofibrinolysis, hyperviscosity, procoagulant
autoantibody production, effects of inflammatory cytokines, and acquired activated
protein C resistance (APCR). In this review we will focus on IMiD-associated effects
on specific thrombotic mechanisms.
Keywords
immunomodulatory drugs - paraproteinemias - venous thrombosis