Cyclophosphamide/prednisolone Reactions 1680, p104 - 2 Dec 2017 Pleuritis caused by Mycobacterium kyorinense infection: case report A 48-year-old man developed pleuritis caused by Mycobacterium kyorinense infection during treatment with cyclophosphamide and prednisolone [routes and time to reaction onset not stated]. The man presented to the emergency department with complaints of cough and dyspnoea for five days. Ten years prior, he had been diagnosed with follicular lymphoma and received chemotherapy for its treatment. He underwent unrelated allogenic bone marrow transplantion, and a complete response was achieved three years later. The transplant was complicated by disseminated Herpes zoster and invasive Aspergillosis. He had been receiving therapy with cyclophosphamide 20 mg/day and prednisolone 20 mg/day for three years for chronic graft versus host disease with chronic bilateral pleural effusion and skin lesions. On admission, temperature 37.8°C, BP 185/127mm Hg and oxygen saturation 93% at room air were noted. Weak breath sounds were revealed by auscultation. Pitting oedema was observed on his lower limbs. Increased accumulation of right pleural effusion was observed from a chest x-ray, as compared with a chest x-ray obtained one month prior. A chest CT scan revealed no pulmonary lesion. Laboratory tests revealed elevated WBC count and C-reactive protein level, reduced lymphocyte count, high creatinine and blood urea nitrogen concentration. Right pleural fluid analysis revealed elevated WBC count with predominant neutrophils, elevated protein, adenosine deaminase and lactate dehydrogenase levels and decreased glucose levels. Three consecutive samples of pleural fluid were positive for acid-fast staining. The fluid cultures yielded mycobacteria. Thickened, oedematous and hyperaemic pleura with multiple areas of necrosis, adhesion and fibrotic septa were revealed by a thoracoscopy. Granulomas surrounded by neutrophil infiltration and fibrous changes were revealed by the histopathology of parietal pleural biopsy specimen. Cultures of the biopsy specimen yielded mycobacteria. However, PCR for M. avium, M. tuberculosis and M. intracellulare were negative. A tentative diagnosis of tuberculous pleuritis was made. The man received empirical treatment with rifampicin, ethambutol, pyrazinamide and isoniazid. However, no improvement was observed. Phylogenetic analyses 16S rRNA and hsp65 of the isolates of first effusion sample were consistent with the gene sequence of M. kyorinense. A diagnosis of pleuritis due to M. kyorinense infection was made. The therapy was changed to a combination of clarithromycin and moxifloxacin due to the susceptibility of the strain. He recovered after six months of therapy. Author comment: "We hypothesize that the impairment of cellular immunity by immunosuppressant agents was one of the contributing factors that resulted in primary pleural infection in the present case." Ikeue T, et al. Pleuritis caused by Mycobacterium kyorinense without pulmonary involvement. Internal Medicine 56: 2785-2790, No. 20, 15 Oct 2017. Available from: URL: - Japan 803285265 0114-9954/17/1680-0001/$14.95 Adis © 2017 Springer International Publishing AG. All rights reserved Reactions 2 Dec 2017 No. 1680 Reactions Weekly Springer Journals


Reactions Weekly , Volume 1680 (1) – Dec 2, 2017
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Springer International Publishing
Copyright © 2017 by Springer International Publishing AG, part of Springer Nature
Medicine & Public Health; Drug Safety and Pharmacovigilance; Pharmacology/Toxicology
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