There is a subset of patients with bronchial asthma who are susceptible to disease exacerbation upon receiving aspirin and other nonsteroidal anti-inflammatory drugs. This is a clinical syndrome, called aspirin-induced asthma (AIA), associated with alterations in arachidonate metabolism and cysteinyl-leukotriene overproduction. The natural history and clinical characteristics of this type of asthma were studied. Sixteen clinical centres in 10 European countries provided standardized information to the specially developed patient-oriented database regarding: medical history, physical examination, diagnosis, and treatment. Diagnosis of AIA was based on a typical history, confirmed by positive aspirin provocation tests, carried out in 91% of the patients. A total of 500 patients were enrolled in the study. AIA developed according to a pattern, characterized by a sequence of symptoms. First, persistent rhinitis, appearing at a mean age of 29.7+/-12.5 yrs, then asthma, aspirin intolerance and nasal polyposis appear. The clinical presentation in different European countries was remarkably similar. In females, who outnumbered males by 2.3:1, the onset of symptoms occurred significantly earlier and the disease was more progressive and severe than in males. Atopy, present in approximately a third of patients, led to earlier manifestation of rhinitis and asthma, but not of aspirin intolerance or nasal polyposis. A family history of aspirin intolerance, recorded in 6% of patients, had a less evident effect on the course of the disease than sex or atopy. Fifty one per cent of patients, in addition to inhaled steroids, required chronic systemic corticosteroid therapy at a mean dose of 8 mg prednisone x day(-1). Surprisingly, 15% of patients were unaware of intolerance to aspirin and learnt about it only after having provocation tests performed. All over Europe, aspirin-induced asthma develops in a similar characteristic way. Its course is influenced by sex and the presence of atopy. In half of the patients, asthma is severe, and steroid-dependent. The uniform natural history of aspirin-induced asthma might suggest a common underlying principle.