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Severe dyspnoea in a patient with chronic myelogenous leukaemia on a tyrosine kinase inhibitor
  1. Celalettin Ustun1,
  2. Nicole Randall1,
  3. Eitan Podgaetz2,
  4. Khalid Amin3,
  5. H Erhan Dincer4
  1. 1Division of Hematology, Oncology and Transplantation, Department of Medicine, University of Minnesota, Minneapolis, Minnesota, USA
  2. 2Division of Cardiothoracic Surgery, Department of Surgery, University of Minnesota, Minneapolis, Minnesota, USA
  3. 3Department of Pathology and Laboratory Medicine, University of Minnesota, Minneapolis, Minnesota, USA
  4. 4Department of Pulmonary, Critical Care and Sleep Medicine, University of Minnesota, Minneapolis, Minnesota, USA
  1. Correspondence to Dr Celalettin Ustun, Division of Hematology, Oncology and Transplantation, Department of Medicine, University of Minnesota, 14-100 PWB, 516 Delaware Street SE, Minneapolis, MN 55455, USA; custun{at}umn.edu

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NR (Haematology fellow): A 78-year-old male patient with chronic myelogenous leukaemia (CML) diagnosed initially in 2011 presented to the haematology clinic with fatigue and dyspnoea at rest and with exertion. His medical history included benign prostatic hyperplasia and a prior diagnosis of acute myelogenous leukaemia (AML) with translocation 8;21 (good risk AML) diagnosed in 2009, which was in complete remission after standard cytarabine and daunorubicin induction chemotherapy and cytarabine consolidation chemotherapy, requiring no treatment since January 2010. He had also been a smoker, with a 40 pack-year smoking history, who quit 40 years ago. His chest X-ray and CT from 2012 prior to nilotinib therapy demonstrated no focal airspace disease, no evidence of small airways disease and no pleural effusion (figure 1). In July 2013 prior to this current presentation, he had developed a pleural effusion while receiving dasatinib as a second-line agent because of suboptimal response to imatinib. Pleural fluid analysis at that time demonstrated an exudative effusion with 81% of lymphocyte predominance (395 white blood cells, WBCs) and negative staining and cultures for bacterial, fungal and acid fast bacilli. It was consistent with dasatinib-induced pleural effusion. Dasatinib was switched to nilotinib, and pleural effusion resolved until October 2014 when he presented again with fatigue and dyspnoea to the clinic.

Figure 1

There are no focal airspace opacities, no evidence of pleural effusion or thickening. The cardiac silhouette is not enlarged. The pulmonary vessels are slightly distinct.

On examination, the patient's heart rate was 82 bpm, blood pressure 115/70 mm Hg, respiratory rate 24 breaths/min, SpO2 94% and temperature 97.3°F. The patient was in mild respiratory distress, actively working to take deep breaths. Respiratory examination was remarkable for poor air entry at the lung bases bilaterally with dullness to percussion to the mid-lung fields posteriorly, right side greater than left. There was no egophony …

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