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Interstitial pneumonia induced by imatinib mesylate: pathologic study demonstrates alveolar destruction and fibrosis with eosinophilic infiltration

Leukemia volume 18, pages 645–646 (2004)Cite this article

TO THE EDITOR

Imatinib mesylate (Gleevec, Glivec, formerly, STI571) is an inhibitor of the BCR-ABL tyrosine kinase that is central to the pathogenesis of chronic myelogenous leukemia (CML). A recent large-scale prospective randomized trial, comparing imatinib vs interferon plus cytarabine for chronic phase CML, demonstrated the impressive therapeutic superiority of imatinib.1 The current therapeutic strategy for CML was reviewed by Hehlmann.2 Although imatinib is a well-tolerated drug, various adverse events such as superficial edema, nausea, muscle cramps, and skin rash were reported. These events were grades 1–2 in most cases, and medical treatment appears to be feasible.3 With respect to the respiratory complications, dyspnea and cough have been reported to occur in 7–10 and 10–14% of patients receiving imatinib, respectively,1,3 although they were ascribed to pulmonary edema. Their causes have not been clearly described. We report a case of an imatinib-induced interstitial pneumonia and its pathologic findings obtained by transbronchial lung biopsy (TBLB) in a patient with CML.

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References

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Authors and Affiliations

  1. First Department of Internal Medicine, Tokyo Medical University, Japan

    T Yokoyama, K Miyazawa, E Kurakawa, A Nagate, T Shimamoto, M Aoshima & K Ohyashiki

  2. Division of Surgical Pathology, Tokyo Medical University, Japan

    K Iwaya & H Serizawa

  3. Department of Radiology, Tokyo Medical University, Japan

    S Akata

Authors
  1. T Yokoyama
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  2. K Miyazawa
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  3. E Kurakawa
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  4. A Nagate
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  5. T Shimamoto
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  6. K Iwaya
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  7. S Akata
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  8. M Aoshima
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  9. H Serizawa
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  10. K Ohyashiki
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Corresponding author

Correspondence to T Yokoyama.

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Yokoyama, T., Miyazawa, K., Kurakawa, E. et al. Interstitial pneumonia induced by imatinib mesylate: pathologic study demonstrates alveolar destruction and fibrosis with eosinophilic infiltration. Leukemia 18, 645–646 (2004). https://doi.org/10.1038/sj.leu.2403251

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  • DOI: https://doi.org/10.1038/sj.leu.2403251

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