title: Upper airways in aspirin-exacerbated respiratory disease.
abstract: OBJECTIVE
  This review updates the status of chronic rhinosinusitis with nasal polyps (CRSwNP) in aspirin-exacerbated respiratory disease (AERD) in the contexts of epidemiology, diagnosis, pathogenesis, and treatment.
  
  
  RESULTS
  Recent studies have shown that prostaglandin E₂ (PGE₂) deficiency induces an AERD phenotype in PGE₂ synthase-1 knock-out mice and also PGE₂ resistance in granulocytes of AERD patients. The numbers of platelet-adherent leukocytes increase in AERD patients, enhancing production of cysteinyl leukotrienes (CysLTs) via transcellular metabolism of arachidonate. INF-γ released from eosinophils of the sinus tissue of AERD patients promotes eosinophil maturation, increases leukotriene-associated gene expression, and releases CysLTs. The serum periostin level has been suggested to be a useful biomarker predicting the AERD/CRSwNP phenotype. Aspirin desensitization was reported to decrease the levels of CD4⁺ T cell-derived cytokines, including INF-γ and IL-10, in line with the newly defined role of INF-γ in AERD.
  
  
  CONCLUSIONS
  Recent findings further support the notion that arachidonic acid metabolism is dysregulated in AERD patients. This is reflected by resistance to PGE₂, overproduction of CysLTs by enhanced numbers of platelet-adherent leukocytes, and cellular stimulation by INF-γ released from eosinophils. Aspirin desensitization may be a useful treatment option in AERD patients exhibiting recalcitrant CRSwNP.
authors.affiliation: aDepartment of Pulmonology and Allergy, Hallym University Dongtan Sacred Heart Hospital, Hwaseong bDepartment of Allergy and Clinical Immunology, Ajou University Hospital, Suwon, Korea.
authors.forename: Jeong-Hee
authors.initials: JH
authors.lastname: Choi
authors.forename: Ji-Hye
authors.initials: JH
authors.lastname: Kim
authors.forename: Hae-Sim
authors.initials: HS
authors.lastname: Park
mesh_terms: D000818:Animals; D055963:Asthma, Aspirin-Induced / Q000175:diagnosis* / Q000276:immunology / Q000628:therapy*; D015415:Biomarkers / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood; D002908:Chronic Disease; D003888:Desensitization, Immunologic; D015232:Dinoprostone / Q000378:metabolism; D020022:Genetic Predisposition to Disease; D006801:Humans; D019746:Intramolecular Oxidoreductases / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D000071876:Prostaglandin-E Synthases; D012220:Rhinitis / Q000175:diagnosis* / Q000276:immunology / Q000628:therapy*; D012852:Sinusitis / Q000175:diagnosis* / Q000276:immunology / Q000628:therapy*
chemical_list: D015415:Biomarkers; D015815:Cell Adhesion Molecules; C512835:POSTN protein, human; D019746:Intramolecular Oxidoreductases; D000071876:Prostaglandin-E Synthases; D015232:Dinoprostone