Another reason to dislike medication.

In August, 2006, a 57-year-old woman came to the emergency department of our hospital: she had nonproductive cough, shortness of breath, and fatigue. These symptoms had been present for 6 weeks, during which time the cough had become steadily more frequent. The patient did not smoke; nor was she exposed to substances that might provoke cough. She had no history of allergy, and no fever. She had gastro-oesophageal refl ux disease and depression, for which she took pantoprazole and venlafaxine, respectively. However, her adherence to drug regimens was sporadic: she “disliked” pills. On examination, the patient was dyspnoeic: her respiratory rate was 24 breaths per min, and her arterial oxygen saturation was only 89% on room air. Her pulse rate was 96 beats per min. We heard inspiratory crackles in both lung bases, and intermittent widespread wheezes. The white-cell count was high, at 14×109 cells per L; chest radiography showed bilateral interstitial markings. We diagnosed pneumonia, and prescribed levofl oxacin 500 mg once daily. We suspected that the patient also had chronic bronchoconstriction, caused by asthma or gastrooesophageal refl ux: so we prescribed a salbutamol inhaler, and pantoprazole, as well as giving oxygen. However, cultures from blood and sputum were negative; moreover, after 7 days of treatment, the patient was no better. High-resolution CT showed reticulonodular interstitial infi ltrates, throughout both lungs, with a “tree-in-bud” pattern typical of bronchiolo-alveolitis (fi gure). CT also showed marked dilatation of the oesophagus. On further discussion, the patient said that she had had diffi culty swallowing, especially solid food, for 12 years. Videofl uoroscopy, while the patient spoke and swallowed, showed no aspiration. However, oesophageal manometry revealed severe hypomotility; oesophagogastroduodenoscopy showed a tortuous, moderately dilated oesophagus, in the middle of which a pantoprazole pill was perched. We also saw a small epiphrenic diverticulum. Histopathological analysis of biopsy samples from the oesophagus showed no evidence of systemic sclerosis. We diagnosed a primary oesophageal motility disorder. Given the fi ndings on CT, and the evident risk of aspiration, we diagnosed diff use bronchiolar disease, secondary to gastro-oesophageal refl ux. We advised the patient to avoid eating large, fatty meals; drinking large volumes of water with meals; eating less than 3 h before going to bed; and lying down or stooping less than 3 h after a meal. We also advised her to sleep with more than one pillow. Her health improved rapidly—she was discharged a week later. When last seen, in July, 2007, the patient was well. Diff use bronchiolar disease, also known as diff use aspiration bronchiolitis, is chronic infl ammation of the bronchioles, in response to aspirated particles. Infl ammation causes widespread nodules and reticular infi ltrates, which are hyperlucent on chest radiography. Our patient had oesophageal dysmotility and an epiphrenic diverticulum, both of which are associated with aspiration; moreover, fi ndings on CT were typical of diff use bronchiolar disease: and her breathing improved with simple antirefl ux measures. Diff use bronchiolar disease is probably underdiagnosed: in Japan, the disease was found in 31 of 4880 patients, at autopsy; notably, however, most of the patients had died in a geriatrics unit. Diff use bronchiolar disease is thought to respond to treatments that reduce aspiration, but not to steroids.