Nitrofurantoin
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Lung toxicity: case report A 79-year-old woman developed lung toxicity in the form chronic, rarely productive cough (sputum without discolouration), progressive exertional dyspnea, feeling of chest heaviness and mild chest pain during chronic prophylactic administration of nitrofurantoin for recurrent urinary tract infections [duration of treatment to reactions onsets not stated]. The woman, who was a lifelong non-smoker, had been receiving treatment [details not stated] for type 2 diabetes, peripheral artery disease, arterial hypertension, chronic renal failure, hyperlipidaemia, glaucoma, anxiety depressive disorder, gastroesophageal reflux, disease of the oesophagus and incipient senile dementia. In March 2019, she was examined by a urologist for interstitial nephritis. At that time, a normal lung parenchyma was observed and chronic prophylactic administration of nitrofurantoin [dosage and route not stated] was initiated for recurrent urinary tract infections. She subsequently presented with a chronic, rarely productive cough (sputum without discolouration), progressive exertional dyspnea, feeling of chest heaviness and mild chest pain. The problem lasted for about half a year and gradually progressed. The cardiac aetiology of the problem was repeatedly ruled out by the attending internist. On examination, her oxygen saturation was 96% without oxygen therapy. Bilaterally basally fine crepitations were noted by auscultation. Initial functional examination of the lungs in August 2019 revealed the following: vital capacity of the lungs (VC) 2.35L, forced expiratory volume in one second (FEV1) 1.70 L/S, diffusing capacity for carbon monoxide (DLCO) 3.09 mL/min/mmHg and the carbon monoxide transfer coefficient (KCO) 0.76 mL/min/mmHg/L. The initial chest skiagram in August 2019 showed reticulations in the lungs and even confluent infiltrations predominantly in the middle lung fields bilaterally. Further laboratory examinations revealed a normal CRP, a normal leukocyte count and a normal differential count of individual leukocyte classes, as well as a negative basic panel of autoantibodies (antinuclear antibody, extractable nuclear antibody, antineutrophil cytoplasmic antibody, anti-single-stranded DNA antibody, anti-double-stranded DNA antibody and rheumatoid factor). Cultivation from sputum and serology for chlamydia and mycoplasma was microbiologically negative. A highresolution computed tomography (HRCT) of the lung in August 2019 demonstrated ground-glass opacities and reticulations with predominance in the middle and the lower lobes. The upper lobes remained unaffected. In terms of differential diagnosis, druginduced lung involvement, organising pneumonia, nonspecific interstitial pneumonia and chronic eosinophilic pneumonia were considered. Due to the normal finding on the lung parenchyma in March 2019 (i.e. detected before the initiation of nitrofurantoin) and the newly developed problem of the lung following the initiation of nitrofurantoin, a working diagnosis of nitrofurantoininduced lung involvement was
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