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Cameron et al 1 reported two cases of bronchiolitis obliterans organising pneumonia (BOOP) associated with the use of nitrofurantoin. These patients had a favourable outcome after treatment with corticosteroids. We wish to report a similar case.
An 82 year old woman presented in 1997 with a two year history of a cough productive of white sputum and gradually increasing breathlessness. She gave a history of 41 pack years of smoking but had stopped 23 years previously. Before referral she had received treatment with inhaled steroids and bronchodilators but without any effect on her symptoms. She had been taking nitrofurantoin 50 mg at night for prophylaxis against urinary tract infection for the previous four years. Her general health was otherwise good, there was no previous history of lung disease, and no exposure to noxious fumes or dusts.
She was breathless on minimal exertion and had fine inspiratory crackles at both lung bases extending up to the mid zones; there was no finger clubbing. Her oxygen saturation dropped from 95% breathing air at rest to 87% after climbing two short flights of stairs. Her lung function showed a restrictive ventilatory defect with forced expiratory volume in one second (FEV1) 0.94 l (57% predicted) and forced vital capacity (FVC) 1.33 l (65% predicted). Carbon monoxide transfer factor (Tlco) was reduced to 56% predicted. High resolution computer tomographic (CT) scans of the thorax showed marked mosaic perfusion affecting all areas with patchy ground glass opacification. There was associated mild interlobular thickening.
Nitrofurantoin related lung disease was suspected so the drug was stopped and an open lung biopsy was performed. Histological examination showed chronic interstitial pneumonia with interstitial chronic inflammatory cellular infiltration associated with the presence of occasional lymphoid follicles and aggregates of macrophages in several alveoli. In addition, there were some obstructive changes associated with the presence of buds of oedematous fibroblastic tissue within terminal and respiratory bronchioles and extending into adjacent alveoli, which are features of BOOP (fig 1).
Treatment with oral prednisolone was given for four months starting at 30 mg daily for six weeks then slowly tailing off. There was clinical improvement within one month of starting oral steroids with reduction in cough and breathlessness, and eight months after starting treatment she felt that she had returned to her previous best. Her FEV1 improved to 1.09 l (70% predicted), FVC to 1.72 l (88% predicted), and Tlco to 70% predicted. The chest radiograph showed improvement in the basal reticular shadowing; the CT scan was not repeated. She remains well three years after diagnosis.
This case further demonstrates the good response of BOOP associated with nitrofurantoin once the offending drug is withdrawn and treatment given with oral corticosteroids.
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