Fibrinolysis, blood coagulation, and platelet function during aspirin-induced bronchoconstriction in aspirin-intolerant asthmatics.

Nineteen asthmatic patients, 11 with and eight without aspirin (ASA) intolerance were studied in order to test possible platelet and coagulation system involvement in the pathogenesis of aspirin-induced bronchoconstriction (AIB). Aspirin-intolerant asthmatics were challenged with a previously established ASA threshold dose and, in nine of them, a positive asthmatic reaction occurred (mean fall in FEV1 39.4%). Seven out of nine patients with a positive reaction had a significant decrease in euglobulin lysis time (P less than .01) during AIB. A positive reaction after ASA was accompanied by an increase in the plasma recalcification time in five of these patients. There were no concomitant statistically significant changes in the platelet count, circulating platelet aggregates, and platelet factor 4 activity. In a control group of ASA-tolerant asthmatics, aspirin at a 200-mg dose did not evoke any respiratory reaction and, during two hours after ASA, no significant variation was found in any of the laboratory parameters studied. We conclude that activation of fibrinolysis accompanying AIB results from intrinsic pharmacologic properties of aspirin, and may contribute to the pathogenesis of aspirin intolerance through a more generalized activation of plasma proteolytic activity.