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Semin Thromb Hemost 2003; 29(3): 275-282
DOI: 10.1055/s-2003-40965
Copyright © 2003 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

The Blood Coagulation Mechanism in Multiple Myeloma

Maurizio Zangari1 , Fariba Saghafifar2 , Paulette Mehta3 , Bart Barlogie2 , Louis Fink3 , Guido Tricot2
  • 1Associate Professor, University of Arkansas for Medical Sciences, Myeloma Institute for Research and Therapy, Little Rock, Arkansas
  • 2Myeloma Institute for Research and Therapy, Little Rock, Arkansas
  • 3The Central Arkansas Veterans Healthcare System, Little Rock, Arkansas
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Publication History

Publication Date:
30 July 2003 (online)

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ABSTRACT

Many cancers are associated with hypercoagulability, including multiple myeloma. At least four possible reasons for hypercoagulability have been described in myeloma patients: interference of immunoglobulins on fibrin structure, procoagulant autoantibody production, effects of inflammatory cytokines on endothelium, and acquired activated protein C (APC) resistance. Moreover, injury to endothelium, either by tumor cells or by chemotherapy, may predispose to thrombosis by causing upregulation of adhesion molecules, allowing adhesion of blood cellular elements (platelets, lymphocyte, neutrophils, and tumor cells, which secrete thrombogenic as well as angiogenic substances). In most cases, the pathogenesis of a thrombotic complication in myeloma patients remains unexplained. Administration of chemotherapy may play a larger role in the thrombotic process than a specific abnormality does because thrombotic complications become more prominent after the start of treatment. The recently reported evidence of a non-factor V Leiden APC resistance has increased our understanding of the pathophysiology of this hypercoagulable state.

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