Case report Severe pneumocystis jiroveci pneumonia in a patient on temozolomide therapy: A case report and review of literature Babar Ahmad Khan, MD, Sania Khan, MD, Benjamin White, MD, Ambika Eranki, MD MPH * SUNY/Upstate Medical University, USA article info Article history: Received 2 May 2017 Received in revised form 31 July 2017 Accepted 11 August 2017 Keywords: Pneumocystis jiroveci Temozolomide CNS lymphoma abstract A 66 year old man was diagnosed with CNS diffuse large B-cell lymphoma, and underwent treatment with Temozolomide, Dexamethasone, Rituximab, and radiation therapy, and prolonged steroid taper with Dexamethasone. Approximately one month after this, he presented with severe acute hypoxemic respiratory failure, and was admitted to the Medical Intensive Care Unit. Imaging showed diffuse ground glass opacities. Patient underwent diagnostic bronchoalveolar lavage which was positive for Pneumo- cystis jiroveci. He did not respond well to appropriate therapy and was transitioned to comfort care per his family's wishes, and expired. Pneumocystis jiroveci should always be included in the differential diagnosis of pneumonia in patients treated with Temozolomide, especially when this agent is used in combination with long term, high dose corticosteroids and radiation therapy. © 2017 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). 1. Case report A 66-year-old man presented to emergency department for worsening headaches and bilateral lower extremity weakness for two weeks, leading to a fall on the day of presentation. A week prior, he was found to have a mass in the corpus callosum extending into bilateral parietal lobes. He reported insidious onset of diffuse headaches, progressively getting worse, recurrent falls, dizziness and lower extremity weakness. He was started on leve- tiracetam and oral dexamethasone 4 mg four times a day. Patient's past medical history was remarkable for Factor V Leiden mutation and had been on Coumadin previously. Upon initial admission, patient was afebrile, and hemodynamically stable. Neurologic exam was remarkable for markedly decreased strength in lower ex- tremities, and patellar hyper-reflexia. Laboratory work-up revealed hemoglobin 15.1 g/dL, leukocyte count of 12.9  10 9 /L with 13% lymphocytes (reference 13%e52%) and 78% neutrophils (important to note; patient was on oral dexamethasone). CT head showed 5.8  1.8 cm hyper-dense mass involving splenium of the corpus callosum with extension into the corona radiata of bilateral parietal lobes, and surrounding vasogenic edema causing mass effect on the adjacent lateral ventricles. Patient underwent right parieto- occipital stereotactic brain biopsy, and the results were consistent with Diffuse Large B-Cell Lymphoma (DLBCL). CALGB 50202 protocol-based chemotherapy, was initiated and patient received Methotrexate 8 mg/m2 IV on day 1 and 15, Leucovorin, Temozo- lomide 150 mg/m2/day PO on days 7e11 and Rituximab 375 mg/ m2 IV days (3,10,17,24). Patient tolerated the chemotherapy well and was discharged home on a tapering dose of dexamethasone after a month long stay in the hospital. The patient continued to follow up with physical therapy and made a remarkable recovery, was able to ambulate without any support. However a month later he had syncope at home, wit- nessed by family. He was brought to our emergency department and was diagnosed with sepsis secondary to complicated urinary tract infection and pneumonia. Broad spectrum antibiotic therapy with piperacillin/tazobactam, vancomycin and azithromycin was started. On arrival to the emergency department, he was found to be in respiratory distress and was profoundly hypoxic (Pulse ox- imetry 83%), hence he was started on face-mask 50% oxygen and later switched to high flow oxygen. CT head with contrast did not show any interval change. CT thorax with contrast ruled out pul- monary emboli, however significant new ground glass opacities were noted throughout the lung fields along with pneumo- mediastinum (Fig. 1). Thoracic surgeon did not recommend any intervention at that time; it was believed to be due to possible pleural bleb rupture. Patient continued to have worsening of his oxygenation and was transitioned to non-invasive positive pressure * Corresponding author. Department of Internal Medicine, Division of Infectious Diseases, SUNY/Upstate Medical University, 725 Irving Ave, Ste 311, Syracuse, NY, 13210, USA. E-mail address: erankia@upstate.edu (A. Eranki). Contents lists available at ScienceDirect Respiratory Medicine Case Reports journal homepage: www.elsevier.com/locate/rmcr http://dx.doi.org/10.1016/j.rmcr.2017.08.012 2213-0071/© 2017 The Authors. Published byElsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). Respiratory Medicine Case Reports 22 (2017) 179e182