Abstract
Glioblastoma is among the tumor entities with an extreme thrombogenic potential and patients are at very high risk of developing a venous thromboembolism (VTE) over the course of the disease, with an incidence of up to 30% per year. Major efforts are currently being made to understand and gain novel insights into the underlying pathomechanisms of the development of VTE in patients with glioblastoma and to find appropriate biomarkers. Yet, patients with glioblastoma not only face a high thromboembolic risk but are also at risk of bleeding events. In the case of VTE, a therapeutic anticoagulation with low molecular weight heparin or, in the case of low bleeding risk, treatment with a direct oral anticoagulant, is recommended, according to recently published guidelines. With respect to an elevated bleeding risk in glioblastoma patients, therapeutic anticoagulation remains challenging in this patient group and prospective data for this vulnerable patient group are scarce, particularly with regard to direct oral anticoagulants.
Highlights
Cancer patients have a four- to seven-fold increased risk of developing a venous thromboembolism, and there is a close relationship between malignancy, abnormal coagulation parameters and thrombosis [1]
The incidence of cancer-associated thrombosis varies according to the tumor site, yet glioblastoma is among the tumor entities with an extreme thrombogenic potential, and patients are at very high risk of developing a venous thromboembolism (VTE) over the course of the disease, with an incidence of up to 30% per year [3,4,5]
Is thrombosis associated with hemostatic disorders in glioblastoma but it is associated with hemorrhage, which occurs both locally and systemically [6,7,8]
Summary
Cancer patients have a four- to seven-fold increased risk of developing a venous thromboembolism, and there is a close relationship between malignancy, abnormal coagulation parameters and thrombosis [1]. The prevention of thromboembolic events is highly relevant, as venous thromboembolism is a dominant cause of death in patients with cancer and is associated with a poor prognosis [2]. The incidence of cancer-associated thrombosis varies according to the tumor site, yet glioblastoma is among the tumor entities with an extreme thrombogenic potential, and patients are at very high risk of developing a venous thromboembolism (VTE) over the course of the disease, with an incidence of up to 30% per year [3,4,5]. Current research aiming to gain novel insights into the thrombophilic state of patients with glioblastoma is endeavoring to understand its underlying pathomechanisms and how the aggressiveness of the tumor entity is linked to the high incidence of VTE in this patient group
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