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Arch Hellen Med, 31(3), May-June 2014, 298-315


Thrombosis and cancer

Α. Argyrou,1 A. Gialeraki,2 A. Gafou,1 E. Merkouri,2 A. Travlou2
1Blood Bank, "Aghioi Anargyroi" General Anticancer Hospital, Athens,
2Hematology Laboratory and Blood Bank, "Attikon" University and General Hospital, Athens, Greece

Cancer and hypercoagulability are two of the most common causes of morbidity and mortality worldwide. Their relationship was first reported in the mid 1800s, but it is only during the last 30 years that its mechanism has started to be elucidated. The risk of venous thromboembolism (VTE) among cancer patients is 4−6 times higher than among non-cancer patients and the likelihood of thrombosis is associated with parameters related to the patient and to the disease and its treatment. Malignancy affects all the parameters of the Virchow's triad: Blood-flow, coagulation procedure and endothelium. Cancer cells induce a hypercoagulant state by secreting procoagulant, antifibrinolytic and proaggregational factors and inflammatory mediators. Tissue factor production leads via coagulation-dependent and -independent pathways, to the creation of a vicious circle by which malignancy induces a thrombophilic state and thrombophilia, in turn, promotes tumor growth and metastasis. The spectrum of clinical and laboratory manifestations of cancer-related thrombosis is wide. In recent years efforts have been made to set up prognostic models to identify cancer patients at high risk for developing VTE, for whom the use οf thromboprophylaxis would be beneficial. Meanwhile, guidelines on thromboprophylaxis and the treatment of cancer-related thrombosis are being drawn up, and the use of anticoagulants as antineoplasmatic agents is under investigation.

Key words: Anticoagulant treatment, Cancer, Prognosis, Thrombosis.

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