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To the Editor A specific regulatory role of pros‐ taglandin E2 (PGE2) was postulated in aspirin‐ ‐induced asthma.1 Indeed, in this distinct asth‐ ma phenotype, several observations have accu‐ mulated pointing to depressed PGE2 production by peripheral blood cells, nasal polyps, and bron‐ chial fibroblasts; diminished EP2 receptor expres‐ sion on the inflammatory cells; and the associ‐ ation of EP2 gene polymorphism with aspirin hypersensitivity.2 We performed inhalation challenge with increas‐ ing doses of lysine aspirin2 in 14 patients with aspi‐ rin‐induced asthma and 11 asthmatics who tolerat‐ ed aspirin well. The mean age of the patients was 44.3 years, and the groups did not differ in their main clinical characteristics. In all subjects, exhaled breath condensates (EBC) were collected at base‐ line.3 The collection was repeated at the time of ap‐ pearance of the bronchial symptoms in subjects with aspirin‐induced asthma, and when the cu‐ mulative dose of 182 mg of aspirin was reached in aspirin‐tolerant asthmatics. In EBC samples, PGE2 and its main metabolite (tetranor‐PGEM) were measured using gas chromatography / mass spectrometry (GC/MS) and high‐performance liq‐ uid chromatography/tandem mass spectrometry (HPLC/MS/MS), respectively. The results were ex‐ pressed as raw concentration per 1 ml and as parts per million palmitic acid.3 Aspirin precipitated bronchial reactions in all subjects with aspirin‐induced asthma, but in no subjects from the aspirin‐tolerant group. At baseline, mean PGE2 values did not differ be‐ tween the groups, while tetranor‐PGEM was higher in subjects with aspirin‐induced asth‐ ma compared with the other group (P <0.001). Following aspirin challenge, the mean values remained unchanged (TabLE). The dose of aspi‐ rin had no effect on the response of PGE2 and its metabolite. There was a positive correla‐ tion between the levels of PGE2 and tetranor‐ ‐PGEM following aspirin challenge only in aspirin‐ ‐tolerant subjects (r = 0.93, P <0.001). Our results add to the observations on the changes in prostaglandin production in aspirin‐ ‐induced asthma2,4‐6 and indicate a rapid catabo‐ lism of PGE2 in the lungs – its rate is 4‐fold higher in aspirin‐induced than in aspirin‐tolerant asth‐ ma. The upregulation of the enzymes metabo‐ lizing PGE2 might be related to a specific proin‐ flammatory milieu operating in the bronchi of patients with aspirin‐induced asthma. LETTER TO THE EDITOR

Altered metabolism of prostaglandin E2 in asthma patients with aspirin hypersensitivity