[Demonstration of specific platelet function anomaly in asthma induced by aspirin: diagnostic consequences]

Aspirin-sensitive asthma is a common and severe disorder characterized by asthmatic attacks after oral ingestion of cyclooxygenase inhibiting drugs. Yet its pathophysiology remains unknown, and no specific in vitro abnormality, neither humoral nor cellular, has been detected in these patients. We have recently described a new model of platelet activation--IgE-dependent platelet activation--expressed by the release of cytocidal mediators and oxygen metabolites. We have now investigated whether cyclooxygenase inhibitors induce a similar response in platelets from aspirin-sensitive asthmatics in vitro. Aspirin or indomethacin strikingly activated platelets from 12 aspirin-sensitive asthmatics to the same extent as IgE-dependent stimuli, but had no effect on platelets from 18 controls (p less than 0.0001). Sodium salicylate, which does not inhibit cyclooxygenase, did not trigger platelets from aspirin-sensitive asthmatics. Preincubation with sodium salicylate or prostaglandin endoperoxides (PGH2), selectively prevented further platelet activation by aspirin or indomethacin (90% inhibition), suggesting that this abnormal platelet activation is the consequence of cyclooxygenase inhibition. This represents the first identification of a specific abnormal cellular response in aspirin-sensitive asthma, provides the basis for an in vitro diagnostic test of the disease, and for new insights on its pathogenesis and its prevention.