The role of activated protein C resistance in the pathogenesis of venous thrombosis

Venous thromboembolism (VTE) is the third most common cardiovascular disease in the United States. VTE is usually a consequence of either acquired or inherited alterations in hemostatic regulatory proteins. These regulatory proteins are predominantly those of the protein C/protein S natural anticoagulant pathway. Acquired deficiencies in this pathway are frequently a consequence of other clinical entities leg, cancer, AIDS, and diabetes), while inherited deficiencies can be responsible for venous thrombosis in an otherwise healthy individual. The purpose of this article is to briefly describe the pathobiology of the anticoagulant protein system and to review the clinical implications of activated protein C resistance.