Cancer and venous thromboembolism: an overview.

BACKGROUND AND OBJECTIVE

Although the relationship between malignant diseases and venous thromboembolism has been convincingly demonstrated, the clinical implications of this association still have to be thoroughly elucidated. The aim of this study was to review briefly the mechanisms by which cancer may induce the development of thrombosis and to analyze critically the most recent clinical advances in this field.

EVIDENCE AND INFORMATION SOURCES

The material examined in the present review includes articles published in journals covered by the Science Citation Index and Medline .

STATE OF THE ART

Neoplastic cells can activate the clotting system directly, thereby generating thrombin, or indirectly, by stimulating mononuclear cells to synthesize and express various procoagulants. Cancer cells and chemotherapeutic agents can injure endothelial cells, thereby intensifying hypercoagulability. Currently, primary prevention of venous thrombosis should be considered for cancer patients during and immediately after chemotherapy, when long-term indwelling central venous catheters are placed, during prolonged immobilization from any cause, and following surgical interventions. Secondary prevention of recurrent venous thromboses usually necessitates long-term anticoagulation. In some patients with cancer the condition is resistant to warfarin, and long-term adjusted high-dose heparin is required. The diagnosis of venous thromboembolism may help to uncover previously occult carcinoma by prompting a complete physical examination and a few routine tests.

PERSPECTIVES

Further investigations are required to evaluate the cost-benefit ratio of extensive diagnostic screening for occult malignancy in all patients presenting with idiopathic venous thromboembolism, and to explore the potential of low molecular weight heparins for improving survival in patients with cancer.