For a study, researchers sought to offer a complete account of current knowledge on the pathophysiology of aspirin-exacerbated respiratory disease (AERD) and an update on its therapy. Increased amounts of 15-oxo-eicosatetraenoic acid (15-Oxo-ETE), a newly characterized arachidonic acid metabolite, had been found in nasal polyps of patients with AERD. In AERD, nasal polyps with activated basophils and interleukin-5 -receptor-positive IL-5R+ plasma cells had a higher risk of being severe. Alveolar monocyte-derived macrophages and their prolonged proinflammatory activation had been proposed as possible contributors to AERD. Even though they were not AERD-specific, 3 biological therapies were available to treat both nasal polyposis and asthma.
15-Oxo-ETE, a newly discovered downstream product of 15-lipoxygenase, was recently reported to be considerably higher in nasal polyps from AERD patients. The eicosanoid metabolite was most likely the result of a cross-talk between epithelium and mast cells. Nasal polyp basophils, IL-5R+ plasma cells, and alveolar macrophages had all been identified as key players in AERD inflammation. Aside from typical aspirin desensitization and therapy for AERD management, there were numerous biologics for the treatment of asthma, including 3 that had been licensed for nasal polyposis. The efficacy of these biological medicines in managing AERD symptoms varied.
