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Interstitial Pneumonitis in a Patient with Chronic Myeloid Leukemia Kronik Miyeloid Lösemi Hastasinda Geli^en înterstisyel Pnömoni

Figure 1: Gbest X-ray sbowed bilateral interstitial infiltrates (A). Tboracic GT revealed patcby parencbymal consolidations in botb apical lungs, bilateral superior segments of tbe lower lobes, and tbe posterior regions of botb lungs (B).

Ahmet Emre Eçkazan^, Ay§e Salihoglu^, Serdar Erturan^, Teoman SoysaP ^Istanbul University Cerrahpa^a Faculty of Medicine, Department of Internal Medicine, Division of Hematology, Istanbul, Turkey ^Istanbul University Cerrahpa^a Faculty of Medicine, Department of Chest Disease, Istanbul, Turkey

Address for Correspondence: Teoman SOYSAL, M.D., Istanbul University Cerrahpaça Faculty of Medicine, Department of Internal Medicine, Division of Hematology, Istanbul, Turkey Phone: +90 212 589 79 34 E-mail: [email protected] Received/Gelis tarihi : August 24, 2012 Accepted/Kabul tarihi : December 14, 2012

DOI: 10.4274/Tjh.2012.0115

A 43-year-old otherwise bealtby male patient was admitted to our bematology clinic witb leukocytosis in April 2008. Pbiladelpbia-positive cbronic pbase cbronic myeloid leukemia (GML) was tbe diagnosis. Imatinib mesylate (IM) at 400 mg/day was initiated in May 2008. He tolerated tbe tberapy quite well; only a mild skin rasb developed, wbicb was easily controlled witb antibistamines. He was admitted witb dry cougb and sbortness of breatb, unresponsive to moxifloxacin tberapy, in February 2010, after 20 montbs of IM treatment. He bad a 15-pack-year bistory of smoking, wbicb be bad quit 2 years ago. He was afebrile and tbere were crackles on auscultation in botb lungs. His cbest X-ray sbowed bilateral interstitial infiltrates (Image lA), and tboracic computed tomograpby (GT) revealed patcby parencbymal consolidations in botb apical lungs, bilateral superior segments of tbe lower lobes, and tbe posterior regions of botb lungs (Image IB). Pulmonary function tests sbowed a restrictive ventilatory defect. No elevations of tbe acute pbase reactants were detected, and tbe IgE blood level was witbin tbe normal limits. Eiberoptic broncboscopy revealed normal airways, and broncboalveolar lavage sbowed no abnormalities witb tbe transbroncbial flne needle biopsy sbowing nonspecific interstitial inflammation. Tbe diagnosis was nonspecific interstitial pneumonitis and tbe possible cause was tbougbt to be IM. Imatinib was discontinued and metbylprednisolone (80 mg/day) was initiated. Under tbe corticosteroid tberapy, bis symptoms and radiological findings were resolved. Imatinib is indicated in tbe first-line treatment of GML. It is generally well tolerated, but mild adverse events including edema, nausea, diarrbea, abdominal pain, muscle cramps, and skin rasb can be seen. Pulmonary complications sucb as dyspnea and cougb are usually due to tbe pulmonary edema and pleural effusion tbat are seen in approximately 7%-14% of tbe patients receiving IM [1,2]. Interstitial pneumonitis during imatinib tberapy is a rare entity [3]. Wbile receiving IM and between days 10 and 337 of treatment, interstitial pneumonitis cases are documented [1]. Tbe patbogenesis of tbe interstitial pulmonary disease during IM includes tbe direct toxic effects of tbe inflammatory and immune system cells resulting in parencbymal lung injury and fibrosis [4]. Our patient bad tolerated IM well until montb 20 of treatment, wben a serious pulmonary complication occurred. Interstitial pneumonitis can be reversible wben diagnosed early and treated quickly; tbus, pulmonary symptoms in patients receiving IM sbould be closely monitored and possible pulmonary toxicity sbould always be kept in mind. Informed consent was obtained. 435

TurkJ Hematol 2013,30:435-436

, et al: Interstitial Pneumonitis in a CML Patient

Key words: CML, imatinib, interstitial pneumonitis Conflict of Interest Statement The authors of this paper have no conflicts of interest, including speciflc financial interests, relationships, and/ or affiliations relevant to the subject matter or materials included. References 1. Yokoyama T, Miyazawa K, Kurakawa E, Nagate A, Shimamoto T, Iwaya K, Akata S, Aoshima M, Serizawa H, Ohyashiki K. Interstitial pneumonia induced by imatinib mesylate: pathologic study demonstrates alveolar destruction and fibrosis with eosinophilic infiltration. Leukemia 2004;18:645-646.

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2. Raj da J, Phatak PD. Reversible drug-induced interstitial pneumonitis following imatinib mesylate therapy Am J Hematol 2005;79:80-81. 3. Isshiki I, Yamaguchi K, Okamoto S. Interstitial pneumonitis during imatinib therapy Br J Haematol 2004;125:420. 4. Robibaro B, Kropfmueller A, Prokop M, Haber P, Gisslinger H. Imatinib, cytokines and interstitial lung disease in a patient with primary myelofibrosis. Ann Hematol 2010;89:829-831.

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Interstitial pneumonitis in a patient with chronic myeloid leukemia.

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