We sincerely thank Duane et al. for their valuable contribution and for highlighting the critical role of immunomodulatory drugs (IMiD) in the context of venous thromboembolism (VTE) risk.1 IMiD are approved for the treatment of certain hematologic cancers or conditions affecting blood cells and bone marrow, such as multiple myeloma (MM), myelodysplastic syndromes, and mantle cell or follicular lymphomas. In our review, published in Haematologica in September 2024, we focused the topic to targeted therapies approved for solid tumors. As they correctly pointed out, the VTE risk associated with IMiD, particularly when combined with dexamethasone, is well-documented and remains significant despite current thromboprophylaxis strategies.2
We agree that the precise mechanisms linking IMiD to increased thrombotic risk need further characterization. Emerging data on the regulation of pro-coagulant factors and the potential influence of genetic variability on VTE susceptibility represent important areas of research that warrant further investigation.3
Furthermore, as rightly emphasized, the lack of international consensus on optimal thromboprophylaxis strategies for MM patients receiving IMiD remains a major clinical challenge. While recent recommendations advocate for a shift from aspirin to low-molecular-weight heparin (LMWH) or direct oral anticoagulants (DOAC), comparative efficacy data on these approaches are still limited. Future studies should, therefore, focus on identifying the most effective and safest thromboprophylaxis regimen for this patient population.4
We believe that broader adoption of risk stratification tools, such as the SAVED, IMPEDE, and PRISM models, could help tailor VTE risk management in MM patients, thereby improving preventive strategies. However, to facilitate their widespread clinical implementation, further validation in real-world settings is necessary.5
In conclusion, we appreciate the insights provided by Duane et al. and fully agree on the need for additional research to optimize VTE risk management in MM patients treated with IMiD. A multidisciplinary approach that integrates clinical trials, real-world data, and advancements in precision medicine will be essential to improving clinical outcomes for this patient group.
We thank the authors for their thoughtful perspective and look forward to further discussions on this critical issue.
Footnotes
- Received April 9, 2025
- Accepted April 10, 2025
Correspondence
Disclosures
No conflicts of interest to disclose.
Contributions
References
- Duane C, Glavey S, Ǫuinn J, Murphy P. Significant risk of venous thromboembolism associated with targeted anti-myeloma immunomodulatory drugs. Comment on: Targeted anti-cancer agents and risk of venous thromboembolism. Haematologica. 2025; 101(10):2552-2553. Google Scholar
- Rajkumar SV, Jacobus S, Callander NS. Lenalidomide plus high-dose dexamethasone versus lenalidomide plus low-dose dexamethasone as initial therapy for newly diagnosed multiple myeloma: an open-label randomised controlled trial. Lancet Oncol. 2010; 11(1):29-37. Google Scholar
- Johnson DC, Corthals S, Ramos C. Genetic associations with thalidomide-mediated venous thrombotic events in myeloma identified using targeted genotyping. Blood. 2008; 112(13):4924-4934. Google Scholar
- Palumbo A, Rajkumar SV, Dimopoulos MA. International Myeloma Working Group, prevention of thalidomide- and lenalidomide-associated thrombosis in myeloma. Leukemia. 2008; 22(2):414-423. Google Scholar
- Kapur S, Feehan K, Mosiman S. Real-world validation of VTE risk models in newly diagnosed multiple myeloma in a community setting. Blood. 2021; 138(S1):2971. Google Scholar
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