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Correspondence: Charles Eby, MD, Washington University School of Medicine, 660 S. Euclid Ave., Box 8118, St Louis MO 63110; phone (314) 362–3186; fax (314) 362–1461; eby{at}labmed.wustl.edu
Abstract
Major, spontaneous bleeding is uncommon in patients with plasma cell dyscrasias despite frequent abnormal screening hemostasis tests. However, acquired von Willebrand deficiency and light-chain (AL) amyloidosis, and amyloidosis complicating multiple myeloma can present with serious hemorrhagic complications that are challenging to manage. While patients with monoclonal gammapathy of undetermined significance and multiple myeloma share an intrinsic increased risk of venous thromboembolic events (VTE), treatment with thalidomide and lenalidomide increases the incidence of VTE in certain multiple myeloma patient subsets. Our understanding of the complex interactions among malignant plasma cells, inflammatory and hemostasis pathways, and treatment modalities that combine to produce thrombotic complications is incomplete. Prospective, randomized trials are clearly needed to assist clinicians in providing optimal VTE prophylaxis to their patients with plasma cell dyscrasias.
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