*Royal Free Hospital and School of Medicine, London N. W.3, and tBlackburn Royal Infirmary, Lancashire

Two cases of histologically proven pulmonary fibrosis resulting from amiodarone therapy but responding to conicosteroids are reported. Amiodarone is a powerful antiarrhythmic agent which is widely used in the management of refrac-tory arrhythmias!'-3!. Its adverse effects such as corneal microdeposits, photosensitivity and alter-ation in thyroid and liver function are well docu-mented!2-4!. Neurological disorders including peri-pheral neuropathy have been reported as rare side effects!4-5!. We describe two patients who developed pulmonary fibrosis while being treated with amiodarone. CASE 1 A 61-year-old man was admitted in November 1979 with an acute infero-postero-lateral myo-cardial infarction. Two months later he was re-admitted with ventricular tachycardia at a rate of 200 beats/min. After initial abolition of arrhyth-mias with lignocaine, he was treated with oral mexiletine and later, slow-release quinidine sul-phate, neither of which controlled the arrhythmia. Amiodarone 200 mg tds orally was therefore added to the slow-release quinidine sulphate 500 mg tds. Ambulatory monitoring confirmed suppression of the ventricular tachycardia and the dose of amio-darone was reduced to 400 mg a day after two months. Four months after commencing amiodarone, the patient developed dyspnoea, a dry cough, malaise and weight loss. The chest radiograph (Fig. la) revealed infiltration in both upper zones. ESR was 90 mm h~ ' and there was a diffuse increase in scrum gamma globulins, but no eosinophilia. The carbon monoxide transfer factor (T|_CO) was grossly Received for publication 12 July 1982; and in revised form 2