Journal
IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA
Volume 36, Issue 4, Pages 749-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.iac.2016.06.009
Keywords
AA (arachidonic acid); AERD (aspirin-exacerbated respiratory disease); Asthma; COX (cyclooxygenase); Leukbtriene; 5-LO (5-lipoxygenase); NSAID (nonsteroidal inflammatory drug); Prostaglandin
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Aspirin-exacerbated respiratory disease (AERD) is a syndrome of severe asthma and rhinosinusitis with nasal polyposis with exacerbations of baseline eosinophil-driven and mast cell driven inflammation after nonsteroidal antiinflammatory drug ingestion. Although the underlying pathophysiology is poorly understood, dysregulation of the cyclooxygenase and 5-lipoxygenase pathways of arachidonic acid metabolism is thought to be key. Central features of AERD pathogenesis are overproduction of proinflammatory and bronchoconstrictor cysteinyl leukotrienes and prostaglandin (PG) D-2 and inhibition of bronchoprotective and antiinflammatory PGE(2). Imbalance in the ratio of these lipid mediators likely leads to the increased eosinophilic and mast cell inflammatory responses in the respiratory tract.
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