Venous thromboembolism in patients with acute leukemia, lymphoma, and multiple myeloma
Division of Hematology and Oncology, UC Davis School of Medicine, Sacramento, CA 95670, USA. Thrombosis Research
(Impact Factor: 2.45).
04/2010; 125 Suppl 2(Suppl. 2):S96-102. DOI: 10.1016/S0049-3848(10)70024-4
The association of malignancies and venous thromboembolism (VTE) is a long held axiom in medicine. A growing number of studies have demonstrated that the risk of VTE associated with the hematological malignancies acute leukemia, lymphoma, and multiple myeloma is considerable. In fact, the incidence associated with these malignancies exceeds that for many solid tumors. Contributing factors include malignancy associated hypercoagulable factors; antineoplastic therapies such as high dose corticosteroids, L-asparaginase, and new immunomodulatory agents; central venous catheters; and hematopoietic growth factors. Primary and secondary pharmacological prophylaxis can be problematic in these patients who are often thrombocytopenic. Strategies to prevent VTE, especially upper extremity catheter-associated thrombosis need to be developed.
Available from: François Mullier
- "At first, solid tumours were thought to induce more thrombotic events than haematological malignancies (59). However, comparable thrombotic rates between these 2 types of cancer have been reported (60). Furthermore, new treatments with immunomodulatory drugs such as thalidomide and the use of central vein catheter have increased the incidence of thrombotic events in haematological cancers. "
[Show abstract] [Hide abstract]
ABSTRACT: Extracellular vesicles (EVs) generated during tumourigenesis are thought to play a major role in the hypercoagulant
state observed in cancer patients. They exhibit negatively charged phospholipids and tissue factor
(TF) that promote coagulation cascade activation. In addition, they contain surface proteins and cytoplasmic
molecules, both originating from the producing cell that can impact target cells’ expression. By targeting
endothelial cells of blood vessels, these EVs could disturb the physiological anticoagulant properties of these
cells and be partly responsible for the vascular endothelium activation observed in cancer patients. Indeed,
vascular endothelium naturally exhibits heparin-like proteoglycan, TF pathway inhibitor and protein C
anticoagulant pathway that prevent thrombosis in physiological condition. An overexpression of TF and a
decreased expression of coagulation cascade inhibitors have been reported after EVs’ treatment of endothelial
cells. The induction of apoptosis and an increased expression of platelet adhesion molecules have also been
highlighted. These events may promote thrombus formation in cancer. The aim of this paper is to provide a
targeted review on the current evidence and knowledge of roles and impact of EVs on endothelial surface
anticoagulant and procoagulant factors and cellular adhesion molecules expression.
07/2014; 3(24400). DOI:10.3402/jev.v3.24400
Available from: Pezhman Mirshahi
- "The clinical course of cancer is characterized by a thrombophilic state, manifested by venous thromboembolism and microcirculatory disturbances. Solid tumors and leukemias share many thrombogenic factors; however, the incidence of thrombotic complications is higher in malignant hemopathies [1–3] than in solid tumors. Additional prothrombotic factors, such as hyperleukocytosis, increased expression of tissue factor, and excessive fibrinolysis may be responsible 2008a. "
[Show abstract] [Hide abstract]
ABSTRACT: Elevated plasma level of soluble endothelial protein C receptor (sEPCR) may be an indicator of thrombotic risk. The present study aims to correlate leukemia-associated hypercoagulability to high level plasma sEPCR and proposes its measurement in routine clinical practice. EPCR expressions in leukemic cell lines were determined by flow cytometry, immunocytochemistry, and reverse transcription polymerase chain reaction (RT-PCR). EPCR gene sequence of a candidate cell line HL-60 was also determined. Plasma samples (n = 76) and bone marrow aspirates (n = 72) from 148 patients with hematologic malignancies and 101 healthy volunteers were analyzed by enzyme-linked immunosorbent assay (ELISA) via a retrospective study for sEPCR and D-dimer. All leukemic cell lines were found to express EPCR. Also, HL-60 EPCR gene sequence showed extensive similarities with the endothelial reference gene. All single nucleotide polymorphisms (SNPs) originally described and some new SNPs were revealed in the promoter and intronic regions. Among these patients 67% had plasma sEPCR level higher than the controls (100 ± 28 ng/mL), wherein 16.3% patients had experienced a previous thrombotic event. These patients were divided into: group-1 (n = 45) with amount of plasmatic sEPCR below 100 ng/mL, group-2 (n = 45) where the concentration of sEPCR was between 100 and 200, and group-3 (n = 20) higher than 200 ng/mL. The numbers of thrombotic incidence recorded in each group were four, six, and eight, respectively. These results reveal that EPCR is expressed not only by a wide range of human malignant hematological cells but also the detection of plasma sEPCR levels provides a powerful insight into thrombotic risk assessment in cancer patients, especially when it surpasses 200 ng/mL.
Cancer Medicine 10/2012; 1(2):261-7. DOI:10.1002/cam4.11 · 2.50 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Budd-Chiari syndrome (BCS) is the constellation of clinical signs and symptoms resulting from occlusion of two or more hepatic veins, often due to an underlying thrombophilic disorder. Acute myeloid leukemia has been rarely reported to be associated with hepatic vein thrombosis due to hyperleukocytosis, hyperfibrinolysis and disseminated intravascular coagulation. We report a case of acute promyelocytic leukemia where the clinical onset of the hematological disease was with acute BCS.
Journal of cancer research and therapeutics 10/2010; 6(4):567-9. DOI:10.4103/0973-1482.77077 · 0.79 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.