Unraveling the Genetic Basis of Aspirin Hypersensitivity in Asthma Beyond Arachidonate Pathways.
10.4168/aair.2013.5.5.258
- Author:
Se Min PARK
1
;
Jong Sook PARK
;
Hae Sim PARK
;
Choon Sik PARK
Author Information
1. Genome Research Center for Allergy and Respiratory Disease, Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Korea. mdcspark@unitel.co.kr
- Publication Type:Review
- Keywords:
Aspirin;
hypersensitivity;
asthma;
single nucleotide polymorphism;
genome-wide association study;
methylation
- MeSH:
Aspirin;
Asthma;
Genome-Wide Association Study;
Humans;
Hypersensitivity;
Methylation;
Polymorphism, Single Nucleotide
- From:Allergy, Asthma & Immunology Research
2013;5(5):258-276
- CountryRepublic of Korea
- Language:English
-
Abstract:
Although aspirin-exacerbated respiratory disease (AERD) has attracted a great deal of attention because of its association with severe asthma, it remains widely under-diagnosed in the asthmatic population. Oral aspirin challenge is the best method of diagnosing AERD, but this is a time-consuming procedure with serious complications in some cases. Thus, development of non-invasive methods for easy diagnosis is necessary to prevent unexpected complications of aspirin use in susceptible patients. For the past decade, many studies have attempted to elucidate the genetic variants responsible for risk of AERD. Several approaches have been applied in these genetic studies. To date, a limited number of biologically plausible candidate genes in the arachidonate and immune and inflammatory pathways have been studied. Recently, a genome-wide association study was performed. In this review, the results of these studies are summarized, and their limitations discussed. In addition to the genetic variants, changes in methylation patterns on CpG sites have recently been identified in a target tissue of aspirin hypersensitivity. Finally, perspectives on application of new genomic technologies are introduced; these will aid our understanding of the genetic pathogenesis of aspirin hypersensitivity in asthma.
