Methotrexate
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Methotrexate Infections: case report
A 63-year-old man developed influenza-A H1N1, invasive pulmonary aspergillosis, aspergillus ventriculitis and hospital acquired Klebsiella pneumoniae associated pneumonia following treatment with methotrexate for rheumatoid arthritis [route, dosage and duration of treatment to reaction onset not stated]. The man presented with a 1 week history of pyrexia and dyspnoea. He had a history of seropositive rheumatoid arthritis, for which he had been receiving treatment with methotrexate. Following admission, he was tachypnoeic, normotensive with heart rate of 91 bpm and he required 4L of oxygen in order to maintain oxygen saturation above 94%. Laboratory tests showed elevated CRP and lymphopenia with reduced no of lymphocytes. A chest X-ray indicated bilateral airspace opacification. The man’s methotrexate was stopped and considering a possible diagnosis of community acquired pneumonia, he was started on benzylpenicillin and clarithromycin. Due to ongoing pyrexia, antibiotics were changed to piperacillin/tazobactam 3 days later. A viral throat swab showed influenza A H1N1, for which treatment was started with zanamivir. On day 7 of admission, a CT thorax was performed which showed bilateral patchy consolidation with associated thin walled cavities and the chest X-ray also showed worsening changes. Laboratory testing showed worsening inflammatory markers including neutrophils, lymphocytes and elevated CRP. Despite treatment, pyrexia persisted and thus he was commenced on a 14 day course of linezolid and meropenem. A repeat CT thorax showed progression of consolidation in the left lung, a cavity in the left upper lobe with an interior mass consistent with aspergilloma and the changes were indicative of influenza. Thus, bronchoalveolar lavage (BAL) was performed on day 21 and simultaneously empirical antifungal treatment was started with voriconazole. The PCR testing was positive for Influenza A virus H1N1pdm09 and BAL culture showed no any fungal or bacterial growth. Therefore, voriconazole was stopped after a 10 day course. His serum galactomannan level was also negative. Following treatment, initial improvement was noted. However, he experienced generalised slowing of speech and executive function although he was oriented to time and place. Subsequently, he also developed unsteady gait and urinary incontinence. On day 22 of admission, a CT head and MRI of the head showed significant hydrocephalus with a non-dilated 4th ventricle. There were no any obstructing masses and papilloedema was also absent. He underwent lumbar puncture and 15mL of CSF was removed. Clinical testing of the CSF showed a total white cell count of 83 cells/µL, glucose of 0.4 mmol/L and total protein content of 4 g/L. Further testing for Cryptococcus antigen, toxoplasma serology and lyme serology showed negative results. The urine culture was also negative for acid-fast bacilli. Further treatment was started with ceftriaxone. On day 35, a contrast MRI showed stable hydrocephalus, but there was a lesion in the
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