Aspirin Exacerbated Respiratory Disease
1Department of Immunogenetics and Allergy, National Institute of Respiratory Diseases, Mexico City, DF, Mexico
2Division of Infection, Inflammation and Immunity, School of Medicine, University of Southampton, Southampton, UK
3Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, Republic of Korea
Aspirin Exacerbated Respiratory Disease
Description
Aspirin exacerbated respiratory disease (AERD) is characterized by chronic inflammation of the upper and lower respiratory tract and affects both nonatopic and atopic subjects. This clinical syndrome is a combination of chronic rhinosinusitis progressing to chronic hyperplastic sinusitis, moderate-to-severe asthma, nasal polyposis, and aspirin intolerance. The mechanisms of aspirin sensitivity remain unclear, but most studies conclude that aspirin causes the inhibition of cyclooxygenase-1 (COX-1), shunting arachidonic acid metabolism towards an overproduction of cysteinyl-leukotrienes (cys-LTs) while there is a rapid decrease in the synthesis of COX-1 products including prostaglandin E2. Moreover, an extensive infiltration of eosinophils and mast cells takes place into the airways of aspirin-sensitive patients. Genetic studies have shown that a single-nucleotide polymorphism (SNP) 444 nucleotides upstream of the translational start site (–444A/C) in the promoter region of the LTC4S gene correlates with aspirin sensitivity in severe steroid-dependent AERD in both European and Japanese patients. However, this SNP is only weakly associated with asthma and not at all with AERD in other populations. The HLA DPB1*0301 has been found associated with AERD in Korean population.
Authors are invited to submit either original research manuscripts or review articles which may help to understand the mechanism of AERD. Potential topics include, but are not limited to:
- Mechanism(s) involved in cyclooxygenase inhibition by aspirin
- Identification of the cellular site of COX inhibition and the relative involvement of COX-1 and COX-2 isozymes
- Advances in the identification of genes which influence AERD
- Immunological changes associated with AERD
- The role of respiratory viruses in the development of AERD
- Identification of new biomarkers for early diagnosis
- Defining the mechanism(s) of desensitization with aspirin in the improvement of chronic disease and severity
- New therapies for AERD
Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/ja/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: