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Patients with cancer are at risk of cancer-associated thrombosis, an event associated with poor prognosis. Various risk factors can contribute to the cancer-induced state of hypercoagulability
Risk of events in patients receiving anticoagulation therapy for VTE2
Hazard ratios for the difference in mortality per 100 patient-years in patients with VTE and/or cancer compared with patients without VTE or cancer7
Approximately 20% of all VTE cases occur in patients with cancer.3
VTE has been shown to be present in up to 50% of patients with cancer at autopsy.3
Cumulative risk of VTE in patients with cancer undergoing chemotherapy13
Although the link between cancer and thrombosis is well established, CAT is undertreated, which compounds its status as a major health issue.14
Up to 10% of patients with VTE that appears to have no cause are diagnosed with cancer within a year after the thrombotic event, suggesting that occult cancer was the cause of thrombosis.5
Occult cancer as an underlying cause of unprovoked VTE5
A recently published consensus suggests that patients with unprovoked VTE should undergo:5
Malignant tissue, chemotherapy and other contributing factors (e.g. surgery-induced endothelia damage and venous stasis from immobility) can induce a hypercoagulable state through the activation of inflammatory cytokines, the coagulation pathway and inhibition of fibrinolytic activity.15
Pathophysiology of CAT.15 Tumour cells can activate the coagulation pathway and induce a hypercoagulable state through the release of procoagulant factors (e.g. TF) and pro-inflammatory cytokines. Tumour cells can also inhibit fibrinolysis (not shown). Chemotherapy can create a hypercoagulable state via endothelial cell damage and inducing inflammation