Successful Rechallenge with Imatinib in a Patient with Chronic Myeloid Leukemia Who Previously Experienced Imatinib Mesylate Induced Pneumonitis

Go, Seong Woo; Kim, Boo Kyeong; Lee, Sung Hak; Kim, Tae-Jung; Huh, Joo Yeon; Lee, Jong Min; Hah, Jick Hwan; Kim, Dong Whi; Cho, Min Jung; Kim, Tae Wan; Kang, Ji Young

Although the pathophysiology of imatinib-induced interstitial pneumonitis has not been identified clearly until now, the noncytotoxic or cytotoxic types are suggested as possible mechanisms 6 . The noncytotoxic type manifests as eosinophilic pneumonia, hypersensitive pneumonitis, or obstructive bronchiolitis, whereas the cytotoxic pattern manifests as interstitial edema, lymphocyte infiltration, and destruction of alveolar epithelial cells. In addition, imatinib aggravates interstitial pneumonitis by inhibiting PDGF tyrosine kinase, which leads to acute lung injury 7, 8 . The diagnosis is made based on history, clinical symptoms, radiological findings, and pathological results. Chest radiographs show diverse patterns such as a hypersensitivity reaction, interstitial pneumonitis, cryptogenic-organizing pneumonia, nodular or peribronchovascular lesions, and diffuse alveolar damage 2 . Pathologic manifestations also vary and include diffuse alveolar damage, nonspecific interstitial pneumonia, bronchiolitis obliterans organizing pneumonia, eosinophilic pneumonia, and pulmonary hemorrhage 9 . The current case was strongly suggested initially by lung histology, showing fibrous plugs in the alveoli with infiltration of inflammatory cells in the interstitium, and by exclusion of other infectious causes via microbiologic and clinical studies. Finally, he was confirmed to have druginduced interstitial pneumonitis due to improvement of the pneumonitis by discontinuing the causative drug and initiating steroid therapy.