An abnormality of arachidonic acid metabolism is not a generalized phenomenon in patients with aspirin-induced asthma.

Aspirin (ASA)-induced asthma is a distinct clinical syndrome in which bronchoconstrictive response to nonsteroidal anti-inflammatory drugs can be predicted on the basis of their in vitro activity as inhibitors of cyclooxygenase. In ten ASA-sensitive asthmatics and ten matched healthy controls we measured 12-hydroxy-eicosatetraenoic acid (12-HETE) production by platelets and 5-hydroxy-eicosatetraenoic acid (5-HETE) and leukotriene B4 (LTB4) production by polymorphonuclear leucocytes. The blood cells were obtained before administration of the threshold doses of ASA and during the ASA-induced reactions. Initial levels of eicosanoids determined did not differ between the two groups. In both groups, after ASA challenge, 12-HETE rose to similar levels while 5-HETE and LTB4 remained unchanged. These data do not support the concept that an abnormality in the regulation of arachidonic acid oxidative pathways in ASA-sensitive asthmatics is a generalized phenomenon which embraces the platelets and leucocytes; rather it is inhibition of cyclo-oxygenase within the tissues of the respiratory tract that triggers asthmatic attacks in the sensitive patients.