2019
DOI: 10.1007/s12288-019-01085-x
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Hematological Malignancies and Arterial Thromboembolism

Abstract: Established guidelines exist for prevention and treatment of venous thromboembolism in hematological malignancies, but none for arterial thromboembolism. However, arterial and venous thromboembolism share the same provoking features—including altered procoagulant factors and defective fibrinolytic system. The morbidity for arterial thromboembolism is increasing in hematological malignancies, with the advent of immunomodulatory and targeted therapy. However, survival rate for hematological malignancy is improvi… Show more

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Cited by 8 publications
(11 citation statements)
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References 132 publications
(154 reference statements)
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“…Moreover, the KRS system does not include other clinical parameters-such as female sex, older age, number of chronic comorbidities, and presence of a central venous catheter-that were previously shown to be associated with an increased risk of thrombosis among AML patients [22]. Hematopoietic growth factors (erythropoietin, granulocyte colony-stimulating factor, and granulocytemacrophage colony-stimulating factor) play a role in activating coagulation factors and cytokines that alter coagulation, modulate hemostasis, and cause platelet aggregationall of which contribute to thrombotic events [23][24][25][26][27]. In addition, the KRS does not stratify by type of thrombosis, and arterial thromboembolism may be associated with greater morbidity and mortality than venous thromboembolism [27,28].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Moreover, the KRS system does not include other clinical parameters-such as female sex, older age, number of chronic comorbidities, and presence of a central venous catheter-that were previously shown to be associated with an increased risk of thrombosis among AML patients [22]. Hematopoietic growth factors (erythropoietin, granulocyte colony-stimulating factor, and granulocytemacrophage colony-stimulating factor) play a role in activating coagulation factors and cytokines that alter coagulation, modulate hemostasis, and cause platelet aggregationall of which contribute to thrombotic events [23][24][25][26][27]. In addition, the KRS does not stratify by type of thrombosis, and arterial thromboembolism may be associated with greater morbidity and mortality than venous thromboembolism [27,28].…”
Section: Discussionmentioning
confidence: 99%
“…The pathophysiology of arterial and venous thrombosis both follow the principles of Virchow's Triad: alterations in flow, abnormal cell and molecular properties, and altered blood vessel walls [27]. The multifactorial pathogenesis of thrombosis in leukemia involves blast cells secreting prothrombotic tissue factor, cancer procoagulants, and cytokines.…”
Section: Discussionmentioning
confidence: 99%
“…For the peculiar characteristics of arterial thrombosis related to acute leukemia, including acute promyelocytic leukemia, we refer the readers to other comprehensive recent reviews. 12,15,16…”
Section: Search Methods and Inclusion Criteriamentioning
confidence: 99%
“…Malignancies are associated with the development of thromboembolic event, approximately up to six-fold higher than the general population. The pathogenesis of cancer-associated thrombosis (CAT) is multifactorial and complex, mainly related to components of Virchow’s triad [ 1 , 2 ]. Cancer cells may alter hemostasis by secreting procoagulant factors and interacting with endothelial cells to trigger a coagulation cascade [ 3 ].…”
Section: Introductionmentioning
confidence: 99%