Table of Contents
Journal of Allergy
Volume 2012, Article ID 794890, 6 pages
Review Article

Genetic Mechanisms in Aspirin-Exacerbated Respiratory Disease

Department of Allergy and Clinical Immunology, Ajou University School of Medicine, San-5, Woncheondong, Youngtonggu, Suwon 442-721, Republic of Korea

Received 12 April 2011; Accepted 14 June 2011

Academic Editor: Luis M. Teran

Copyright © 2012 Nami Shrestha Palikhe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aspirin-exacerbated respiratory disease (AERD) refers to the development of bronchoconstriction in asthmatics following the exposure to aspirin or other nonsteroidal anti-inflammatory drugs. The key pathogenic mechanisms associated with AERD are the overproduction of cysteinyl leukotrienes (CysLTs) and increased CysLTR1 expression in the airway mucosa and decreased lipoxin and PGE2 synthesis. Genetic studies have suggested a role for variability of genes in disease susceptibility and the response to medication. Potential genetic biomarkers contributing to the AERD phenotype include HLA-DPB1, LTC4S, ALOX5, CYSLT, PGE2, TBXA2R, TBX21, MS4A2, IL10, ACE, IL13, KIF3A, SLC22A2, CEP68, PTGER, and CRTH2 and a four-locus SNP set composed of B2ADR, CCR3, CysLTR1, and FCER1B. Future areas of investigation need to focus on comprehensive approaches to identifying biomarkers for early diagnosis.