From the Guidelines
There is no established causative relationship between deep vein thrombosis (DVT) and leukemia, meaning DVT does not cause leukemia. However, patients with leukemia have a significantly increased risk of developing DVT due to several factors. Leukemia creates a hypercoagulable state in the body through the release of procoagulant substances from cancer cells, increased inflammation, and disruption of normal blood cell function, as noted in studies such as 1. Additionally, treatments for leukemia such as chemotherapy, central venous catheters, and prolonged immobilization during hospitalization further increase DVT risk, as highlighted in 1.
This relationship is unidirectional - while leukemia can contribute to DVT development, developing a blood clot does not cause or lead to leukemia. The increased risk of VTE in patients with cancer, including leukemia, is supported by various studies, including those that show cancer as the cause of approximately 20% of the VTE cases seen in the community 1. Patients with leukemia often receive prophylactic anticoagulation therapy (such as low molecular weight heparin) to prevent DVT, especially during hospitalization or while using central venous catheters.
Key factors that increase the risk of DVT in leukemia patients include:
- The presence of malignancy
- Exposure to chemotherapy
- Extrinsic vascular compression from cancer-associated regional bulky lymphadenopathy
- Certain hematologic malignancies, such as lymphoma, acute leukemia, and multiple myeloma
- Treatments like thalidomide- or lenalidomide-based combination regimens
The connection between these conditions represents a complication of the underlying cancer rather than a causative relationship, emphasizing the need for vigilant monitoring and management of DVT risk in patients with leukemia, as suggested by 1 and 1.
From the Research
Causative Relationship Between Deep Vein Thrombosis and Leukemia
- The relationship between deep vein thrombosis (DVT) and leukemia is complex, with multiple factors contributing to the development of thrombosis in patients with leukemia 2, 3, 4.
- Leukemic cell procoagulant properties, cytotoxic therapies, and concomitant infections are major determinants of clotting activation in acute leukemia 2.
- Patients with acute leukemia often present with a hypercoagulable state or with evidence for chronic disseminated intravascular coagulation, even in the absence of active thrombosis and/or bleeding 2.
- The incidence of DVT in patients with acute leukemia is significant, with studies reporting cumulative incidences of upper extremity DVT ranging from 4.1% to 6.6% at 3 and 12 months, respectively 5.
Mechanisms of Thrombosis in Leukemia
- Multiple mechanisms have been implicated in the activation of coagulation in patients with leukemia, including the procoagulant properties of tumor cells, hyperleukocytosis, and increased expression of tissue factor 3, 4.
- However, studies have also shown that leukemic cell procoagulant activity is not always responsible for the hypercoagulable state, and other mechanisms should be sought to explain the pathogenesis of thrombosis in some patients 3.
Clinical Implications
- The treatment of DVT in patients with leukemia is challenging due to the high risk of hemorrhage, particularly in those with severe thrombocytopenia 2, 4.
- Anticoagulant therapy is a unique challenge in patients with acute leukemia, and careful assessment of hemorrhagic risk is required when using newer anticoagulants 2.
- The incidence of catheter-related thrombosis is higher in patients with peripherally inserted central catheters (PICC) compared to those with centrally inserted central catheters (CICC) 6.