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.