Aspirin-exacerbated respiratory illness (AERD) includes bronchial asthma, nasal polyps, and aspirin hypersensitivity linked to dysregulated eicosanoid metabolism. Understanding AERD heterogeneity is crucial for bettering prognosis and therapy. On this challenge, Szatkowski et al (p 616) present new insights into metabolic variations in AERD, a extreme type of bronchial asthma characterised by irritation and poor response to therapy, in contrast with aspirin-tolerant bronchial asthma (ATA). The researchers analyzed blood plasma and urine samples from sufferers with AERD and ATA, measuring ranges of particular metabolites derived from the 15-lipoxygenase (15-LOX) and 5-lipoxygenase (5-LOX) pathways.
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