A 42-year-old man presented to our hospital with the sudden onset of right chest pain and dyspnea on 19 March 1992 and was admitted when a right pneumothorax was demonstrated on chest radiograph. At 32 years of age, he developed bronchial asthma that was responsive to bronchodilator therapy for several years but then gradually became refractory to this treatment despite initiation of oral steroid treatment in 1990. In July, and then again in August 1991, he presented with spontaneous right pneumothoraces that occurred during periods free of asthmatic exacerbations, and that subsequently improved with conservative treatment. On the most recent admission, routine laboratory tests were within normal limits and serum immunoglobulin analysis revealed a markedly increased IgE level (1647 IU ml I; normal ~300). An arterial blood gas determination revealed a pH of 7.42, a PaCO, of 37.8 mmHg, and a PaO, of 74.7 mmHg, findings consistent with mild hypoxaemia. Cardiac examination (ECG, echocardiography) was unremarkable. Pulmonary function tests performed before the present admission (18 January 1992) revealed a reduced vital capacity (VC; 2.6 1, 72% of predicted), forced vital capacity (FVC; 2.1 1, 59% of predicted), l-s forced expiratory volume (FEV,; 1.4 1, 47% of predicted), and FEV,/FVC (66%). However, diffusing capacity for carbon monoxide (DLCO) was normal (19.7 ml min ‘, 93% of predicted).