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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
Cancer-associated thrombosis (CAT) is a highly prevalent complication of cancer.1 CAT adds to the emotional and symptomatic burden of cancer , with patients experiencing:
Risk of events in patients receiving anticoagulation therapy for VTE2
VTE is also a leading cause of mortality in patients with cancer.5,6
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
VTE is also associated with a threefold increase in hospitalizations and higher healthcare costs in patients with cancer compared with patients without cancer3,5
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
Previous studies have reported that VTE occurs in 0.5-20% of patients with cancer, with highly variable risk depending on factors such as cancer type.8-12
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
The risk of VTE also varies over the natural history of cancer; it is highest during hospitalization, chemotherapy and metastasis.1,17
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
The multifactorial pathogenesis of CAT involves various overlapping pathways influenced by a multitude of risk factors for disease.15
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