Full Text
Abstract
Thrombosis is the second leading cause of death in cancer patients. Molecular mechanisms that increase thrombogenicity in can- cer patients have been poorly studied. At present two main ways to thrombosis are considered: (1) direct mechanisms through the fact that cancer cells expressed on or released several factors such as tissue factor, podoplanin, platelet agonists, phospha- tidylserine, cancer procoagulant and plasminogen activation inhibitor-1; (2) indirect mechanism activating hemocoagulation in- volves inflammatory cytokines from tumor cells, activating platelets, neutrophil stimulation and release neutrophil extracellular traps. As a result there is a pronounced activation of platelets, fibrin deposition and capture of erythrocytes that aggravates clot formation. Acting jointly these two ways lead to reduced effectiveness of antithrombotic therapy in cancer patients. Low molec- ular weight heparins (LMWH) have been the de facto standard for reducing risk of venous thromboembolic complications (VTE) for a long time and they are still considered that. However a lot of evidence from various randomized clinical trials are appeared about direct oral anticoagulants (DOAC) using for the treatment of cancer-associated thrombosis including topics on the conve- nience of their administration. Recent guidelines suggest the use of certain DOAC (rivaroxaban and edoxaban) in cancer patients with VTE in cases of low risk of bleeding and the lack of pharmacological interactions with current systemic therapy. Most of the available studies have been conducted with rivaroxaban. That allows to draw so-named ‘portrait of patient’ in order to build up individual treatment of VTE with rivaroxaban and/or with LMWH.
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