Introduction to Cancer-Associated Thrombosis

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

In this section:

Epidemiology of cancer-associated thrombosis

Previous studies have reported that VTE occurs in 2–20% of patients with cancer. Approximately 20% of all VTE cases occur in patients with cancer, and VTE has been shown to be present in up to 50% of patients with cancer at autopsy.

High incidences of first VTE and recurrent VTE have recently been reported in a large population-based cohort study of 6592 patients with active cancer in the UK.

  • The incidence of first VTE was 5.8 per 100 patient-years, which is 54 times higher than the previously reported incidence in patients without cancer
  • For recurrent VTE, an incidence rate of 9.6 per 100 patient-years was observed, which peaked within the first 6 months; this incidence was twice as high as the previously reported incidence in patients without cancer

Disease burden of cancer-associated thrombosis

VTE in patients with cancer, also referred to as cancer-associated thrombosis (CAT), is associated with high recurrence and morbidity rates:

  • Patients with cancer experience higher rates of bleeding and VTE recurrence than patients without cancer, and can experience discontinuation or delay of cancer therapy because of CAT
    • A 12-month cumulative incidence of 12.4% for major bleeding has been observed in patients with cancer, compared with 4.9% in patients without cancer
    • A higher 12-month cumulative incidence of recurrent VTE in patients with cancer (20.7%) versus patients without cancer (6.8%) has also been reported
  • VTE is associated with a threefold increase in hospitalizations and higher healthcare costs in patients with cancer than in patients without cancer

VTE and PE are also leading causes of mortality in patients with cancer:

  • Of note, VTE is a significant predictor of increased mortality during the first year of cancer diagnosis for several types and stages of cancer (median overall relative risk 3.7, hazard ratio range 1.3–14.4)
    • Icreased mortality due to VTE in patients with cancer is consistent throughout the literature and multiple cancer databas

Although the link between cancer and thrombosis is well established, CAT is undertreated, which compounds its status as a major health issue.

  • Oncologists are faced with complex treatment decisions regarding anticoagulation therapy in the setting of CAT, with the need to consider bleeding risks, appropriate duration of therapy, potential interactions with cancer therapies and impact on quality-of-life
  • Provision of better information on thrombosis and its causes/treatments would be of benefit to oncologists to assist in clinical decision-making

Risk factors and screening

Overall, patients with cancer have a four- to sevenfold higher risk of developing VTE compared with patients without cancer.

There are numerous risk factors for VTE in patients with cancer, including risk factors related to the patient, tumour and treatment, as well those indicated by elevated biomarker levels.

Risk factors for venous thromboembolism in patients with cancer

Risk factors for VTE in patients with cancer.

Up to 10% of patients with unprovoked VTE are diagnosed with cancer within a year after their thrombotic event, suggesting that occult cancer was the cause of thrombosis.

  • A recently published consensus suggests that patients with unprovoked VTE should undergo a thorough medical history and physical examination, basic laboratory investigations (complete blood counts, metabolic profile and liver function tests) and chest X-ray

Pathogenesis of cancer-associated thrombosis

The multifactorial pathogenesis of CAT involves multiple overlapping pathways.

  • Increased immobility, chemotherapy- and surgery-induced endothelial damage, and a cancer-induced state of hypercoagulability play a role
    • Several factors create a hypercoagulable state, such as the induction of inflammatory cytokines, activation of the coagulation pathway, inhibition of fibrinolytic activity and chemotherapy
Pathophysiology of cancer-associated thrombosis

Pathophysiology of CAT. 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.

Recommended links to content within the website:

www.thrombosisadvisor.com/knowledge-base/cancer-associated-thrombosis/prevention

www.thrombosisadvisor.com/knowledge-base/cancer-associated-thrombosis/treatment

Approval No.: G.COM.GM.XA.12.2017.2017

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