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Update on recent advances in the management of aspirin exacerbated respiratory disease.

Authors
Palikhe, NS; Kim, JH; Park, HS
Citation
Yonsei medical journal, 50(6):744-750, 2009
Journal Title
Yonsei medical journal
ISSN
0513-57961976-2437
Abstract
Aspirin intolerant asthma (AIA) is frequently characterized as an aspirin (ASA)-exacerbated respiratory disease (AERD). It is a clinical syndrome associated with chronic severe inflammation in the upper and lower airways resulting in chronic rhinitis, sinusitis, recurrent polyposis, and asthma. AERD generally develops secondary to abnormalities in inflammatory mediators and arachidonic acid biosynthesis expression. Upper and lower airway eosinophil infiltration is a key feature of AERD; however, the exact mechanisms of such chronic eosinophilic inflammation are not fully understood. Cysteinyl leukotriene over-production may be a key factor in the induction of eosinophilic activation. Genetic studies have suggested a role for variability of genes in disease susceptibility and response to medication. Potential genetic biomarkers contributing to the AERD phenotype include HLA-DPB1*301, LTC4S, ALOX5, CYSLT, PGE2, TBXA2R, TBX21, MS4A2, IL10 -1082A > G, ACE -262A > T, and CRTH2 -466T > C; the four-locus SNP set was composed of B2ADR 46A > G, CCR3 -520T > G, CysLTR1 -634C > T, and FCER1B -109T > C. Management of AERD is an important issue. Aspirin ingestion may result in significant morbidity and mortality, and patients must be advised regarding aspirin risk. Leukotriene receptor antagonists (LTRA) that inhibit leukotriene pathways have an established role in long-term AERD management and rhinosinusitis. Aspirin desensitization may be required for the relief of upper and lower airway symptoms in AERD patients. Future research should focus on identification of biomarkers for a comprehensive diagnostic approach.
MeSH terms
AnimalsAsthma, Aspirin-Induced/drug therapyAsthma, Aspirin-Induced/genetics*Asthma, Aspirin-Induced/immunology*Eosinophils/metabolismGenetic Predisposition to Disease/geneticsHumansLeukotriene Antagonists/therapeutic useLeukotrienes/metabolismModels, BiologicalPolymorphism, Genetic/geneticsPolymorphism, Genetic/physiology
DOI
10.3349/ymj.2009.50.6.744
PMID
20046412
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
AJOU Authors
김, 주희박, 해심
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