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Pathogenesis of nonsteroidal antiinflammatory drug-induced asthma.

Authors
Kim, SH; Park, HS
Citation
Current opinion in allergy and clinical immunology, 6(1):17-22, 2006
Journal Title
Current opinion in allergy and clinical immunology
ISSN
1528-40501473-6322
Abstract
PURPOSE OF REVIEW: To summarize recent findings related to the pathogenic mechanisms of aspirin-induced asthma with emphasis on molecular genetic mechanisms.



RECENT FINDINGS: The overproduction of cysteinyl leukotrienes with the increased expression of cysteinyl leukotriene receptor 1 (CYSLTR1) is a consistent finding in aspirin-induced asthma patients. Recent data have suggested a dysregulation of cyclooxygenase-2 and prostaglandin E2, increased levels of 15-hydroxyeicosatetranoic acid, and decreased lipoxin generation as characteristics of the condition. The HLA allele DPB10301 was documented as a strong genetic marker for susceptibility in an Asian population. Leukotriene C4 synthase has been established as a key genetic determinant of aspirin-induced asthma, but recent studies have demonstrated that several single nucleotide polymorphisms in the promoters of prostaglandin E2 receptor subtype 2, CYSLTR1 and CYSLTR2 and T-box expressed in T cells (TBX21) could increase risk for the condition. Although cyclooxygenase-2 and thromboxane A2 receptor polymorphisms were not associated with aspirin-induced asthma phenotype, they may exert functional effects.



SUMMARY: The identification of genetic markers for aspirin-induced asthma susceptibility along with in-vitro functional studies would help to elucidate the pathogenesis of the condition. Further studies of the interactions among genes and between genes and the environment will be essential.
MeSH terms
Anti-Inflammatory Agents, Non-Steroidal/adverse effects*Aspirin/adverse effects*Asthma/chemically induced*Asthma/geneticsFemaleHumansMale
DOI
10.1097/01.all.0000199794.79551.ec
PMID
16505607
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
Journal Papers > Research Organization > Regional Clinical Trial Center
AJOU Authors
김, 승현박, 해심
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