Abstract
Aspirin-exacerbated respiratory disease (AERD) is characterized by the induction of upper and lower respiratory symptoms after intake of COX-1 inhibitors. Cysteinyl leukotriene (cysLT) overproduction occurs even under stable disease condition, and urinary leukotriene E4 (uLTE4) levels further increase after an aspirin challenge test. We reported recently that platelets were significantly activated in AERD patients under stable disease condition (Mitsui et al. JACI 2016). Although cysLT overproduction after aspirin-induced reactions is the most important characteristic in AERD, the entire mechanism of cysLT overproduction in AERD has not been clarified in detail.
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