Chronic, severe asthma and a high incidence (60–80%) of chronic rhinosinusitis with nasal polyps are two essential hallmarks of aspirin-aggravated respiratory disorders (AERDs), both of which are exacerbated by aspirin and other NSAIDs. Although the pathogenic processes of AERD are not fully known, numerous studies have revealed strong eosinophilic infiltrations of the upper and lower airway mucosa, as well as disruption of arachidonate metabolisms. For research, recent advances in the pathogenic processes of chronic rhinosinusitis with nasal polyps in aspirin-exacerbated respiratory disorders can be found.
Intense eosinophilic infiltration was linked to increased levels of cytokines and chemokines such IL-5 and eotaxin. Eosinophilic inflammation in nasal polyp tissue is aided by the reaction of local immunoglobulin E to staphylococcal enterotoxins. Other features include an increase in cysteinyl leukotriene synthesis and increased expression of cysteinyl leukotriene receptor-1, a decrease in prostaglandin E2 production, and a decrease in cyclooxygenase-2 and E-prostanoid receptor subtype-2 expression. Periostin is the most up-regulated gene in the nasal polyp tissue of AERD patients, according to recent gene expression profiling research.
Chronic rhinosinusitis with nasal polyps is a common concomitant illness in AERD patients, and it was linked to severe asthmatic symptoms. Invasive eosinophilic inflammation, mediated by increased production of eosinophil-related cytokines and chemokines, specific immunoglobulin E responses to staphylococcal enterotoxins, and altered arachidonic acid metabolism, are all significant pathologic findings in nasal polyp tissues. This might have an impact on present asthma therapies and techniques, resulting in a more severe and difficult-to-control AERD phenotype.