[Hypercoagulable State in Cancer]

It has been estimated that cancer patients have a 4- to 7-fold increased risk of VTE compared with the general population. The prothrombotic state variably results from tumor- and patient-specific factors. The pathophysiology of cancer-associated thrombosis is not entirely understood. The hypercoagulable state in cancer involves several complex interdependent mechanisms, including interaction among cancer cells, host cells, and the coagulation system. Key roles in pathophysiology are played by TF, inflammatory cytokines, and platelets. Many risk factors for cancer-associated thrombosis have been identified, including patient-, cancer-, and treatment-related factors. Several biomarkers have been identified as potentially predictive of VTE in multivariate analyses. Elevations of leukocyte and platelet counts and low hemoglobin levels are all predictive of chemotherapy- associated VTE. The levels of FRMs are significantly higher in patients with than in those without malignant diseases. A recently developed risk score referred to as the Khorana Risk Score can accurately stratify cancer patients into low, intermediate, and high risk for developing VTE. Observed rates of VTE in the development and validation cohorts were 0.8 and 0.3% in the low-risk category, 1.8 and 2% in the intermedi- ate-risk category, and 7.1 and 6.7% in the high-risk category, respectively. This model has now been validated in several other studies, including the prospective Vienna CATS study, which expanded the study and improved prediction by including biomarkers.