Document: A 43-year-old man was admitted to the hospital for 2 weeks of dyspnea. He was diagnosed with CML 3 months ago and took 400 mg of imatinib/day for 2 months. His vital signs were blood pressure, 110/80 mm Hg; pulse rate, 72/min; respiratory rate, 20/min; and body temperature, 36.4°C. He presented with an acute ill-looking appearance but no specific findings were noted on neck and abdominal examinations. Heart beat was regular and breathing sounds were clear. The laboratory findings were as follows: white blood cells, 3,630/mL (segmented neutrophils, 54%; lymphocytes, 25%; eosinophils, 12%); hemoglobin, 12.4 g/dL; platelets, 136,000/mL, C-reactive protein, 0.31 mg/dL (normal range, 0.01-0.47 mg/dL); total protein, 5.7 g/dL; albumin, 3.4 g/dL, aspartate aminotransferase/alanine aminotransferase, 27/28 U/L; lactate dehydrogenase, 853 IU/ L; and blood urea nitrogen/creatinine 13.4/0.99 mg/dL. His arterial blood gas analysis on room air revealed pH, 7.447; PaO 2 , 31.2 mm Hg; PaCO 2 , 79.0 mm Hg; and HCO 3 , 21.2 mEq/ L with oxygen saturation of 96.6%. A chest X-ray showed diffuse ground glass opacities and reticular nodules on both lung fields ( Figure 1) . A chest computed tomography (CT) scan revealed patchy ground glass opacity and septal thickening in the middle and lower zones of both lungs (Figure 2A) . A pulmonary function test showed a forced vital capacity (FVC) of 3.85 L (83.6% of predicted value), forced expiratory volume in 1 second (FEV1) of 2.81 L (79.4% of predicted value), FEV1/ FVC of 78.36%, and a carbon monoxide diffusing capacity of Figure 1 . Chest X-ray shows bilateral reticulonodular infiltration in both lungs at admission (A) and slight regression of peribronchial patchy opacities in both lungs at 2 weeks after discontinuing imatinib and commencing steroid treatment (B). www.e-trd.org 50.2%. He underwent a bronchoscopy with bronchoalveolar lavage (BAL) and transbronchial lung biopsy (TBLB). The differential counts in the BAL fluid revealed macrophages, 15%; lymphocytes, 75%; neutrophils, 5%; and eosinophils, 2%. A microbiologic study including the culture of bacteria, fungus with Pneumocystis jirovecii, and Mycobacterium in bronchial specimens was all negative. The polymerase chain reaction assays of mycoplasma pneumonia, nine respiratory viruses such as influenza virus A and B, respiratory syncytial virus, metapneumo virus, rhino virus, parainfluenza virus, adeno virus, corona virus, bocavirus, and cytomegalovirus were all negative. Histological findings for the TBLB at the lingular segment demonstrated fibroblastic plug formations in the alveoli with infiltrations of chronic inflammatory cells and type II pneumocyte proliferation, mild fibrous thickening in the interstitium, which suggested organizing pattern of interstitial pneumonia ( Figure 3 ). No evidence suggested infectious pneumonia; thus, we strongly suspected drug-induced interstitial pneumonitis caused by imatinib. We stopped the imatinib and started 1 mg/kg prednisolone daily. After 2 weeks of treatment, the dyspnea and abnormal X-ray findings improved, and he was discharged with 30 mg prednisolone ( Figure 1B ). After 1 month of treatment, he restarted 300 mg imatinib to control the underlying disease concomitant with 20 mg prednisolone. No recurrence of respiratory symptoms was observed on a chest CT after 12 weeks of imatinib rechallenge ( Figure 2B ).
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