This observation suggests that, as expected, the disturbed COX regulation in AERD nasal polyp fibroblasts results in a similarly deficient production of all prostanoids tested so far (PGE2 and PGD2), supporting the hypothesis that the downregulation of prostanoid metabolism reported in AERD is primarily localised in the airway epithelium, while inflammatory cells (mast cells and eosinophils) escape this anomaly. Here, HPGDS is linked to nasal cavity polyp.