SummaryEleven patients with asthma and aspirin hypersensitivity have been challenged with eight non-steroidal antiinflammatory drugs. Each drug was given by mouth in at least three different doses and the patients' symptoms and peak expiratory flow (PEF) rates were observed over a three-hour period. Indomethacin 5 mg caused bronchoconstriction in all patients. Therapeutic doses of mefenamic or flufenamic acid caused bronchoconstriction in most patients. Phenylbutazone 200-400 mg induced a moderate fall in PEF. There were no reactions to therapeutic doses of salicylamide, paracetamol, benzydamine, and chloroquine. Microsomal prostaglandin synthetase activity was inhibited by aspirin,indomethacin, mefenamic acid, flufenamic acid, and phenylbutazone. The other four drugs had no inhibitory effect.We suggest that precipitation of attacks in asthmatic patients hypersensitive to certain anti-inflammatory drugs is related to the drug's ability to inhibit prostaglandin biosynthesis.

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Patients with AD differ in the ability to clear S. aureus from the skin during anti-inflammatory treatment, which appears to be related to the abnormalities in immunological parameters. Local antibiotic therapy should be considered only in patients with persistent S. aureus colonization.

Studies carried out in 68 patients with idiosyncratic reactions to noramidopyrine and/or aminophenazone led to distinction of two different groups. In the first group: 1) noramidopyrine, aminophenazone, phenylbutazone and sulfinpyrazone as well as several other inhibitors of cyclooxygenase, including aspirin, precipitated bronchoconstriction; 2) skin tests with pyrazolone drugs were virtually negative; 3) all patients had chronic asthma. In the second group: 1) noramidopyrine and aminophenazone induced anaphylactic shock and/or urticaria; 2) skin tests with these drugs were highly positive; 3) phenylbutazone, sulfinpyrazone and several other cyclooxygenase inhibitors, including aspirin, could be taken with impunity; 4) chronic bronchial asthma was present in only one-fourth of the patients. We suggest that the pathogenic mechanisms responsible for the idiosyncratic reactions involve inhibition of cyclooxygenase in the first group, and allergic reactions in the second group. Distinction of these two groups is of clinical importance since in individual patients it gives insight into the safe administration of pyrazolone and aspirin-like drugs.

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