الفهرس 
Introduction and Aim of the workOnly 14 pages are availabe for public view
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Abstract
Hematological malignant disorders are associated with a perturbed haemostatic system, and patients are at risk for bleeding and thrombotic complications. The latter are at least as frequent as in patients with solid tumours, but are often overshadowed by the significant morbidity and high mortality associated with bleeding and infections. As in the case of solid tumours, the rate of thromboembolic events is increased even before diagnosis, thus indicating the presence of a prothrombotic state in the earliest phase. Furthermore, the risk of thrombosis persists after remission, as cumulative incidence increases with the length of observation. The pathogenesis of thromboembolic disease in hematological malignancies is complex and multifactorial, and can be due to the underlying disorder or can be a result of therapy. Prothrombotic factors include hyperleukocytosis, increased tissue factor expression and activation in leukaemic cells, and the prothrombotic effects of therapeutic agents and vascular access catheters. In addition, comorbid conditions, including hereditary thrombophilia, infections, cytokine- induced endothelial cell activation, antiphospholipid syndrome and acquired activated protein C resistance, are major contributory factors. In patients with Philadelphia chromosome– negative chronic myeloproliferative disorders (i.e., essential thrombocythemia [ET] and polycythemia vera [PV]), a thrombosis rate as high as 40% has been recorded. A hypercoagulable state is present in virtually all of these patients, even without clinical manifestations. Patients with multiple myeloma (MM) are at an increased risk of venous and arterial thrombosis. The pathogenesis involves several factors such as activation of procoagulant factors, acquired activated protein C resistance, and inflammation. In addition to general risk factors for venous thromboembolism, such as older age, immobility, surgery, and inherited thrombophilia, there are some MM-specific and treatment-related factors that contribute to the increased risk. The risk for venous thromboembolism is high when patients are treated with thalidomide or lenalidomide in combination with dexamethasone or multi-agent chemotherapy. In patients with lymphoma in addition to routine clinical factors (immobility, infection, catheters, etc.) and the effect of chemotherapy and hematopoietic growth factors, tumor mass effect may also predispose to thrombosis. Increased TF expression in the mononuclear cells of patients with advanced lymphoma and suggested this resulted from cytokines secreted from the lymphoma cells. In myelodysplastic syndromes thrombocytopenia and platelet dysfunction contribute to hemorrhagic complications observed. Several markers have been found to be elevated in patients with hematological malignancies include FDP, FVIII, TAT complex, prothrombin fragments 1+2, vWF antigen, fibrinogen and D-dimer. Patients with hematological malignancies are at high risk of thrombotic and hemorrhagic complications. Clinical manifestations range from localized thrombosis to diffuse, life threatening bleeding. The malignant cell procoagulant properties, cytotoxic therapies, and concomitant infections are important players in the pathogenesis of clotting activation in hematologic malignancies. As the molecular basis for this phenomenon becomes better elucidated, it is possible to predict the development of drugs that will target both the malignant process and the associated thrombotic/hemorrhagic disorders.