title: Aspirin-exacerbated respiratory disease: an update.
abstract: The pathophysiology of aspirin-exacerbated respiratory disease (AERD) is not fully understood and diagnostic methods and so far, treatments for AERD have not been standardized. We summarize recent research into the pathological mechanisms of AERD, diagnostic methods, and treatments for AERD patients.
  
  
  
  In AERD pathophysiology, not only the reduced expression of E prostanoid 2 but also the dysfunction of its pathway could be involved. Moreover, eosinophils of AERD patients could be directly activated by aspirin to produce prostaglandin D2. Platelet activations are well known to be involved in AERD; however, plasma markers do not change during aspirin challenge tests. Additionally, novel genetic polymorphisms, such as P2RY12 and dipeptidyl peptidase 10 gene, and epigenetic predispositions of AERD were found. In AERD diagnosis, bronchial and nasal aspirin challenges have been applied in addition to oral challenge. Serum periostin has been suggested as a potential biomarker for AERD. Apart from standard pharmacological treatment and aspirin desensitization, biologics, including omalizumab and mepolizumab, as well as CRTH2 antagonists have been suggested as promising therapies for AERD treatment.
  
  
  
  AERD is usually associated with severe asthma phenotypes. AERD pathophysiology mainly involves the dysregulation of eicosanoid metabolisms, activations of effector cells, which could be influenced by genetic/epigenetic factors. Understanding the pathophysiology of AERD is key to improve the diagnostic methods and proper management of AERD patients.
authors.affiliation: aDepartment of Allergy and Clinical Immunology, Ajou University School of Medicine bDepartment of Biomedical Sciences, Ajou University School of Medicine, Suwon, South Korea cFaculty of Medicine, University of Medicine and Pharmacy, Ho Chi Minh City, Vietnam.
authors.forename: Duy
authors.initials: D
authors.lastname: Le Pham
authors.forename: Ji-Ho
authors.initials: JH
authors.lastname: Lee
authors.forename: Hae-Sim
authors.initials: HS
authors.lastname: Park
mesh_terms: D001241:Aspirin / Q000009:adverse effects*; D055963:Asthma, Aspirin-Induced / Q000235:genetics / Q000276:immunology; D015415:Biomarkers / Q000378:metabolism; D003888:Desensitization, Immunologic; D006801:Humans; D010641:Phenotype; D011110:Polymorphism, Genetic
chemical_list: D015415:Biomarkers; D001241:Aspirin