The thrombophilic state induced by therapeutic agents in the cancer patient.

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.