Purpose of review
The key features of aspirin-exacerbated respiratory diseases (AERDs) include chronic, severe asthma and a high prevalence (60–80%) of chronic rhinosinusitis with nasal polyps, all of which are exacerbated by exposure to aspirin and other NSAIDs. Although the pathogenic mechanisms of AERD are not completely understood, repeated instances have shown intense eosinophilic infiltrations of upper and lower airway mucosa, and dysregulation of arachidonate metabolisms. Here, recent updates on the pathogenic mechanisms of chronic rhinosinusitis with nasal polyps in aspirin-exacerbated respiratory diseases are summarized.
Intense eosinophilic infiltration is closely related to the elevated production of cytokines and chemokines such as IL-5 and eotaxin. The response of local immunoglobulin E to staphylococcal enterotoxins contributes to eosinophilic inflammation in nasal polyp tissue. Other characteristics include the overproduction of cysteinyl leukotrienes and increased expression of cysteinyl leukotriene receptor-1, reduced production of prostaglandin E2, and the down-regulation of cyclooxygenase-2 and E-prostanoid receptor subtype-2. A recent gene expression profiling study has also suggested that periostin is the most up-regulated gene in the nasal polyp tissue of AERD patients.
Chronic rhinosinusitis with nasal polyps is a major comorbid condition of AERD patients that is closely associated with severe asthmatic symptoms. Significant pathologic findings in nasal polyp tissues include intense eosinophilic inflammation, which is caused by elevated production of eosinophil-related cytokines and chemokines, specific immunoglobulin E responses to staphylococcal enterotoxins, and altered arachidonic acid metabolism. This could affect the current treatments and methodologies that are used to control asthma, leading to a more severe and intractable AERD phenotype.