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Fifty-eight patients with chronic asthma in whom airflow obstruction was relieved by bronchodilator aerosols but not by oral corticosteroids were compared with 58 other chronic asthmatics who responded equally well to both treatments. The two groups were matched for age and sex. The only significant clinical differences between the two groups were that in the "corticosteroid-resistant" patients there was a more frequent family history of asthma and a longer duration of symptoms. Resistant patients also had a relatively lower peak expiratory flow rate in the morning than later in the day and a greater degree of bronchial reactivity to methacholine. Such features, however, may not be specific criteria of corticosteroid resistance since they were also observed in untreated asthmatics who subsequently responded well to corticosteroids. The failure of prednisolone to inhibit a monocyte-mediated bronchial reaction may explain why some chronic asthmatics do not respond to corticosteroids. Patients with corticosteroid-resistant asthma should be recognised at an early stage so that regular treatment with oral corticosteroids may be withdrawn. Failure to do this results in needless exposure to the risk of developing serious side effects.

In a series of 65 patients with asthma with pulmonary eosinophilia 54 were adequately investigated for allergic aspergillosis and this was present in 32 (59%). Asthma with pulmonary eosinophilia was found to carry a relatively poor prognosis in terms of permanent symptoms, impairment of pulmonary function and residual radiographic abnormality. The prognosis was least favourable when allergic aspergillosis was associated with long-standing asthma. On the other hand there was a group of patients with asthma with pulmonary eosinophilia who had relatively little permanent disability. These were mainly women with asthma of recent onset, and in these evidence of allergy to Aspergillus fumigatus was less apparent. Those patients who received long-term daily corticosteroid therapy were less likely to develop further radiographic opacities than those given intermittent corticosteroid therapy. To prevent recurrent pulmonary infiltrates it is probably necessary to give prednisolone in a daily dosage of at least 10 mg for an indefinite period.

Three patients with chronic asthma developed pulmonary eosinophilia while oral prednisolone was being withdrawn after the introduction of treatment with beclomethasone dipropionate aerosol. These observations suggest that the development of pulmonary eosinophilia in patients with chronic asthma can be prevented by the systemic administration of corticosteroids, but not by a corticosteroid aerosol given by inhalation. It is considered that radiological examination of the chest should be carried out at frequent intervals during and for a few months after the substitution of corticosteroid aerosol therapy for oral corticosteroid therapy in order to ensure that those patients who are liable to develop pulmonary eosinophilia will be identified at an early stage. These precautions are even more essential when there is a previous history of pulmonary eosinophilia.

Double-blind studies of the bronchodilator effects of rimiterol, terbutaline and a combination of rimiterol and terbutaline were performed in patients with chronic asthma. An objective assessment in 21 patients showed no significant differences between the mean improvements in FEV1 during the first 30 minutes after drug administration. At 45 minutes and thereafter terbutaline produced a significantly greater degree of bronchodilatation than rimiterol or the combination of rimiterol and terbutaline. In a subjective study of 27 patients it was found that they were able to detect the more prolonged duration of bronchodilator activity of terbutaline but not the more rapid speed of onset of action of rimiterol.