Aspirin-exacerbated respiratory
disease (AERD), so-called aspirinintolerant asthma, is a clinical syndrome
characterized by severe asthmatic attacks after ingestion of aspirin and/or
nonsteroidal antiinflammatory drugs (NSAIDs). AERD is known to be associated
with less atopic tendency, persistent eosinophilic infiltration in the airway
mucosa, and a more severe clinical course.
The
inhibitory action of aspirin and NSAID on cyclooxygenase activity may cause
diversion to the 5-lipoxygenase pathway, leading to the overproduction of
cysteinyl leukotrienes (LTs). A general consensus exists that increased levels
of cysteinyl LTs are key inflammatory mediators in AERD.
However, a study of Japanese
asthmatic patients demonstrated that prostaglandin D2 was overproduced during
aspirin-intolerant bronchoconstriction, and the urinary concentrations of LTE4
and metabolites of prostaglandin D2 correlatively increased during the reaction.
