[Asthma induced by aspirin and arachidonic acid metabolites. II. The role of leukotrienes (part four)].
Although the mechanism of aspirin-induced asthma is unknown, it has be suggested that adverse nasal and bronchial reactions are caused by an increased production of lipoxygenase products. We have measured 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 overproduction 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 pursued further, it must also accommodate the clinical effect of aspirin densitization.
Div Allergy and Immunology, Scripps Clinic & Research Foundation, La Jolla, CA 92037.
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Salazar Villa
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Zambrano Villa
D016718:Arachidonic Acid / Q000378:metabolism; D001241:Aspirin / Q000009:adverse effects*; D001249:Asthma / Q000139:chemically induced*; D006801:Humans; D015289:Leukotrienes / Q000378:metabolism
D015289:Leukotrienes; D016718:Arachidonic Acid; D001241:Aspirin
Asma inducida por aspirina y metabolitos del ácido araquidónico. II. La participación de los leucotrienos (cuarta parte).