Aspirin-exacerbated respiratory disease (AERD) is
characterized by the triad of asthma, nasal polyposis, and hypersensitivity to
aspirin and other cyclooxygenase (COX)-1 inhibitors. Aspirin intolerance is one
of the risk factors for severe asthma, particularly in patients with persistent
airflow limitation (PAFL).
The overproduction of
cysteinyl leukotriene (cysLT) is the biochemical hallmark of AERD. Urinary
leukotriene levels are 3-4 fold higher in AERD patients than in ATA patients,
which further increase after aspirin-induced reaction in AERD patients.
Decreased levels of prostaglandin E2 (PGE2) were also a characteristic
feature of AERD patients. Impaired E prostanoid 2 (EP2) expression and
resistance to PGE2 were detected in nasal polyp fibroblasts from AERD patients.
However, the mechanism underlying the development of AERD has not been
clarified in detail.
In addition to their role in hemostasis,
platelets have the capacity to mediate immune responses during inflammation and
to facilitate granulocyte recruitment into airways. Platelet activation has
been detected in several allergic diseases, including asthma. Platelets play an
important role in asthma, which contributes to airway hyper reactivity (AHR),
bronchoconstriction, airway inflammation and airway remodeling. Recently,
Laidlaw and Boyce have demonstrated that platelet activity is strongly
associated with the pathophysiology of AERD.
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