Semin Thromb Hemost 1999; 25(2): 137-145
DOI: 10.1055/s-2007-994915
Copyright © 1999 by Thieme Medical Publishers, Inc.

The Thrombophilic State Induced by Therapeutic Agents in the Cancer Patient

Agnes Y.Y. Lee, Mark N. LevineDr. Lee is a recipient of a Research Fellowship from the Heart and Stroke Foundation of Canada.
  • Cancer Care Ontario Hamilton Regional Cancer Centre, Departments of Medicine, and Clinical Epidemiology and Biostatistics, McMaster University, Hamilton, Ontario, Canada.
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Publication History

Publication Date:
06 February 2008 (online)

Abstract

Multiple risk factors contribute to the hypercoagulable state in cancer patients. Antineoplastic therapy, including single- or multiagent chemotherapy, hormonal therapy, and hematopoietic growth factors, is an unavoidable and a significant precipitant of venous and arterial thromboses. The risk of thrombosis following cancer treatment also depends on the interaction between treatment agents, type and stage of cancer, and the presence of other risk factors for thrombosis such as advanced age, surgery, immobilization, and the use of central venous catheters. Therefore, although a causal role of cancer treatment in thrombosis is widely accepted, the pathogenic mechanisms are poorly understood and are difficult to investigate because of the multiple confounding factors that are involved. Alterations in coagulation factors, anticoagulant proteins, and endothelial damage have all been shown to occur following cytotoxic agents. The best-studied drugs with definite hypercoagulable effects are L-asparaginase and tamoxifen.