Aspirin intolerance (AI) is characterized by polypous rhinosinusitis, bronchial asthma and adverse reactions to aspirin. The common intolerance to all cyclo-oxygenase inhibitors allows us to focus study of the pathogenesis of AI on the metabolism of arachidonic acid (AA). We studied the metabolism of AA in nine aspirin intolerant asthmatics (AIA) and eight healthy volunteers (controls) by measuring prostaglandin E2 (PGE2) and peptido-leukotrienes (pLT = LTC4/D4/E4) in nasal tissue and peripheral blood cells (PBCs) using a specific immunoassay. In all patients with AI the tests were performed before and after bronchial provocation with lysine-ASA. In the control group the tests were done before and after 500 mg ASA p.o. The release of pLT in nasal polyps of AIA was found to be significantly higher than in normal mucosa of AIAs and controls. In every tissue a significant increase of pLT after aspirin challenge was observed. Nasal polyps of AIA show a significantly lower release of PGE2 than normal mucosa of AIAs and controls. Peripheral blood cells of AIA show a significantly higher release of pLT and a significantly lower release of PGE2 than PBCs of controls. Therefore clinical manifestations of AI may be based on an alteration of AA metabolism in AIA.