ReviewYonsei medical journal2006
Genetic markers for differentiating aspirin-hypersensitivity.
Review in Yonsei medical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 42 citations in OpenAlex.
- Trial
- Trial
- Genetic Susceptibility ofBiomedicines · 2023Article
- Complementary Participation of Genetics and Epigenetics in Development of NSAID-exacerbated Respiratory Disease.Allergy, asthma & immunology research · 2019Review
- Gene Polymorphism of Aspirin-Induced Urticaria in Children With Kawasaki Disease.Frontiers in pediatrics · 2019Article
- Genetic and Epigenetic Components of Aspirin-Exacerbated Respiratory Disease.Immunology and allergy clinics of North America · 2016Review
- Correlation analysis of gene polymorphisms and β-lactam allergy.Journal of Zhejiang University. Science. B · 2015Article
- Genome-Wide Association Study Identifies Novel Pharmacogenomic Loci For Therapeutic Response to Montelukast in Asthma.PloS one · 2015Article
- Prostaglandin E2 receptors in asthma and in chronic rhinosinusitis/nasal polyps with and without aspirin hypersensitivity.Respiratory research · 2014Review
- Molecular genetic mechanisms of chronic urticaria.Allergy, asthma & immunology research · 2014Review
- Mite-induced inflammation: More than allergy.Allergy & rhinology (Providence, R.I.) · 2012Article
- Hypersensitivity Reactions to Nonsteroidal Anti-Inflammatory Drugs: An Update.Pharmaceuticals (Basel, Switzerland) · 2010Review
- Association of beta 2-adrenergic receptor polymorphism with the phenotype of aspirin-intolerant acute urticaria.Yonsei medical journal · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aspirin-induced asthma (AIA) and aspirin-induced urticaria/ angioedema (AIU) are two major aspirin-related allergies. We summarize recent findings related to their molecular genetic mechanisms in order to identify genetic susceptibility markers for differentiating AIU and AIA. The overproduction of cysteinyl leukotriene has been suggested as a mechanism in both AIU and AIA. Increased expression of CYSLTR1 with CYLSTR1 and CYSLTR2 polymorphisms are new findings in AIA, while the ALOX5 promoter polymorphism has been noted in AIU. An HLA study suggested that DPB1*0301 is a strong genetic marker for AIA, and that HLA DRB1*1302 and DQB1*0609 are markers for AIU susceptibility. Several single nucleotide polymorphisms (SNPs) in the promoters of EP2, TBX21, COX-2, Fc epsilon RIbeta, and TBXA2R were associated with AIA, while an Fc epsilon RIalpha promoter polymorphism was associated with AIU. The functional studies of the key genes involved in AIA and AIU are summarized. The identification and functional study of genetic markers for AIA and AIU susceptibility would further elucidate the pathogenic mechanisms and facilitate the development of early diagnostic markers to establish therapeutic targets.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.