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[Asthma induced by aspirin and arachidonic acid metabolites. Role of leukotrienes (third part)].

Although the mechanism of aspirin-induced asthma is unknown, it has been suggested that adverse nasal and bronchial reactions are caused by an increased production of lipoxigenase products. In examining the hypothesis of inhibition on cycloxigenase, we support evidence in favor of this theory. We have measure the release of urinary LTE4, TXB2 and 11-dehydro-TXB2 of aspirin-induced asthmatics and controls by radioimmunoassay and HPLC methods during aspirin challenge and after desensitization. The over production demonstration of urinary LTE4 during aspirin challenge and the decrease after desensitization in inversal direct proportion manner with TXB2 suggest a "shunting" of the arachidonic acid metabolites of the target cells. Whichever theory is to be pursed further, it must also accommodate the clinical effect of aspirin desensitization.