[The role of direct oral anticoagulants in the management of cancer-associated thrombosis in 2020]

Bull Cancer. 2020 May;107(5):574-585. doi: 10.1016/j.bulcan.2020.02.010. Epub 2020 Apr 3.
[Article in French]


Direct oral anticoagulants, anti-IIa or anti-Xa, are widely used in the treatment and prevention of venous thromboembolic disease as well as in nonvalvular atrial fibrillation. Direct oral anticoagulants are characterized by a rapid onset of activity, a predictable response and a relatively wide therapeutic window. Nevertheless, theoretical drug interactions exist since direct oral anticoagulants are substrates of the transport protein P-glycoprotein and/or of isoforms of cytochromes P450 pathway. Direct oral anticoagulants do not have a marketing authorization for the treatment of cancer-associated thrombosis unlike low-molecular-weight heparins which remain the gold standard treatment today. However, recent studies have compared low-molecular-weight heparins to direct oral anticoagulants in the treatment of cancer-associated thrombosis. Results of these studies showed a non-inferiority of direct oral anticoagulants in the prevention of recurrent thromboembolic events but at the cost of an increased hemorrhagic risk, in particular for patients with gastrointestinal and urogenital cancers. Thus, international guidelines, unlike French guidelines, integrate them in first line of the therapeutic strategy of cancer patients. We are certainly entering an era of personalized therapy for cancer-associated thrombosis, considering cancer type and also the theoretical risk of drug interactions with anti-cancer treatments or supportive care.

Keywords: Anticoagulants oraux directs; Cancer; Direct oral anticoagulants; Drug interaction; Interactions médicamenteuses; Thrombose; Thrombosis.

Publication types

  • Review

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B / metabolism
  • ATP Binding Cassette Transporter, Subfamily G, Member 2 / metabolism
  • Anticoagulants / therapeutic use
  • Antineoplastic Agents / metabolism
  • Antineoplastic Agents / therapeutic use
  • Cytochrome P-450 Enzyme System / metabolism
  • Dabigatran / metabolism
  • Dabigatran / therapeutic use
  • Drug Interactions
  • Factor Xa Inhibitors / adverse effects
  • Factor Xa Inhibitors / metabolism
  • Factor Xa Inhibitors / therapeutic use*
  • Hemorrhage / chemically induced
  • Heparin, Low-Molecular-Weight / therapeutic use
  • Humans
  • Neoplasm Proteins / metabolism
  • Neoplasms / blood
  • Neoplasms / complications*
  • Neoplasms / drug therapy
  • Pyrazoles / metabolism
  • Pyrazoles / therapeutic use
  • Pyridines / metabolism
  • Pyridines / therapeutic use
  • Pyridones / metabolism
  • Pyridones / therapeutic use
  • Recurrence
  • Rivaroxaban / metabolism
  • Rivaroxaban / therapeutic use
  • Secondary Prevention
  • Thiazoles / metabolism
  • Thiazoles / therapeutic use
  • Thrombosis / drug therapy*
  • Thrombosis / etiology
  • Venous Thromboembolism / prevention & control


  • ABCB1 protein, human
  • ABCG2 protein, human
  • ATP Binding Cassette Transporter, Subfamily B
  • ATP Binding Cassette Transporter, Subfamily G, Member 2
  • Anticoagulants
  • Antineoplastic Agents
  • Factor Xa Inhibitors
  • Heparin, Low-Molecular-Weight
  • Neoplasm Proteins
  • Pyrazoles
  • Pyridines
  • Pyridones
  • Thiazoles
  • apixaban
  • Cytochrome P-450 Enzyme System
  • Rivaroxaban
  • Dabigatran
  • edoxaban