In patients with malignant diseases, venous thromboembolism (VTE) remains a significant cause of morbidity and mortality(1). According to the latest epidemiological data, the risk of VTE is up to 9 times higher in cancer patients compared to the general population, regardless of age(1,2). Furthermore, patients with malignant neoplasms and thrombotic complications have a 2-3 times greater mortality rate than those with cancer but no associated thrombosis(3). In addition, the anticoagulant treatment that is mandated by a thrombotic event in patients with malignant tumours is a challenge, as these patients are at an elevated risk of hemorrhagic complications (incidence of 12.4%) and thrombotic relapses (20% at 12 months after discontinuing the anticoagulant treatment)(1,2). Patients with cancer frequently exhibit abnormalities in one or more coagulation tests, regardless of whether they have thrombotic complications, suggesting a correlation between malignant diseases and procoagulant status(4). VTE can be the first manifestation of an occult malignancy(5). In cancer patients, the risk for these complications is also influenced by the tumour type and stage, as well as the oncological therapies used, in addition to the general risk factors for VTE (age, history of VTE, recent surgical interventions, immobility, etc.)(4). Thus, the greatest risk of thrombotic complications is associated with pancreatic, gastric, lung cancer, and primary brain tumours1. The inflammatory response of the host, in conjunction with the specific prothrombotic properties of the cancer cell, are the primary factors contributing to the pathogenesis of hypercoagulability in cancer(4). Malignant cells synthesize and secrete procoagulant and fibrinolytic proteins, as well as inflammatory cytokines and procoagulant microparticles4. Furthermore, cancer cells express adhesion molecules that attach to endothelial cells, platelets, and leukocytes, therefore promoting the prothrombotic characteristics of these cells(4). Of interest, most of these mechanisms, besides activating the hemostatic system, also promote the local and distant extension of the tumour(5). The molecular studies of recent years have demonstrated that the oncogenes responsible for neoplastic cell transformation also control the expression of hemostatic proteins and the release of microparticles by cancer cells(5). Up to 50% of VTEs diagnosed in oncology centers are detected incidentally, during imaging evaluation for cancer staging, assessment of response to treatment, or routine monitoring(2). The reason is related to non-specific symptoms, frequently attributed to malignancy or the side effects of therapy(2). The prevention of VTE in cancer patients, through pharmacological and non-pharmacological measures, is a key element in order to reduce the morbidity and mortality of these patients(1). Cancer-associated VTE treatment remains a challenge. In these patients, anticoagulant therapies must be tailored to the type and stage of the cancer, the risk of bleeding, the risk of drug interactions, and the patient’s preferences(2).
Full text sources https://doi.org/10.31688/ABMU.2024.59.3.257
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Camelia C. DIACONU
E-mail: drcameliadiaconu@gmail.com
