Venous Thromboembolism in Patients with Glioblastoma: Molecular Mechanisms and Clinical Implications.

Nevertheless, Yust-Katz et al demonstrated that the majority of VTE events developed after the start of adjuvant chemotherapy with temozolomide in a cohort of glioblastoma patients. 8 In line, our research group recently demonstrated increased TF-mediated procoagulant activity following treatment with temozolomide or lomustine in three well-established glioblastoma cell lines in vitro. 39 Furthermore, treatment with bevacizumab may increase the risk of pulmonary embolism in glioblastoma patients, as a trend toward significance was observed in bevacizumab-treated glioblastoma patients compared to glioblastoma patients who did not receive bevacizumab ( p = 0.07). 40 The risk of VTE may also be increased by high-dose glucocorticoid therapy such as dexamethasone, which directly affects the vascular endothelium. 41 In

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In a study with high-grade glioma patients ( n = 141), of which 68.1% with glioblastoma, three potential biomarkers were identified: low platelet count, elevated D-dimer, and high soluble P (sP)-selectin. 125 In addition, FVIII activity and leukocyte count both showed borderline significance.

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