ArticlePloS one2014
The SNP rs3128965 of HLA-DPB1 as a genetic marker of the AERD phenotype.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Investigation of the Relationship between Aspirin-Sensitivity and Poor Response to Medical Management in NSAIDs-exacerbated Respiratory Disease Patients with Sinonasal Polyposis.Medical journal of the Islamic Republic of Iran · 2023Article
- Article
- Genome-Wide Association Study of Korean Asthmatics: A Comparison With UK Asthmatics.Allergy, asthma & immunology research · 2021Article
- Article
- NSAID-Exacerbated Respiratory Disease (NERD): From Pathogenesis to Improved Care.Frontiers in pharmacology · 2020Review
- Lessons Learned From GWAS of Asthma.Allergy, asthma & immunology research · 2019Review
- Article
- Integrative information theoretic network analysis for genome-wide association study of aspirin exacerbated respiratory disease in Korean population.BMC medical genomics · 2017Article
- Potential Biomarkers for NSAID-Exacerbated Respiratory Disease.Mediators of inflammation · 2017Review
- Genetic and Epigenetic Components of Aspirin-Exacerbated Respiratory Disease.Immunology and allergy clinics of North America · 2016Review
- Aspirin-exacerbated respiratory disease: pathophysiological insights and clinical advances.Journal of asthma and allergy · 2016Review
- Aspirin-Exacerbated Diseases: Advances in Asthma with Nasal Polyposis, Urticaria, Angioedema, and Anaphylaxis.Current allergy and asthma reports · 2015Review
- Hypersensitivity to Aspirin and other NSAIDs: Diagnostic Approach in Patients with Chronic Rhinosinusitis.Current allergy and asthma reports · 2015Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTwo common clinical syndromes of acetylsalicylic acid (aspirin) hypersensitivity, aspirin-exacerbated respiratory disease (AERD) and aspirin-exacerbated cutaneous disease (AECD), were subjected to a genome-wide association study to identify strong genetic markers for aspirin hypersensitivity in a Korean population.
methodsA comparison of SNP genotype frequencies on an Affymetrix Genome-Wide Human SNP array of 179 AERD patients and 1989 healthy normal control subjects (NC) revealed SNPs on chromosome 6 that were associated with AERD, but not AECD. To validate the association, we enrolled a second cohort comprising AERD (n = 264), NC (n = 238) and disease-control (aspirin tolerant asthma; ATA, n = 387) groups.
resultsThe minor genotype frequency (AG or AA) of a particular SNP, rs3128965, in the HLA-DPB1 region was higher in the AERD group compared to the ATA or NC group (P = 0.001, P = 0.002, in a co-dominant analysis model, respectively). Comparison of rs3128965 alleles with the clinical features of asthmatics revealed that patients harboring the A allele had increased bronchial hyperresponsiveness to inhaled aspirin and methacholine, and higher 15-HETE levels, than those without the A allele (P = 0.039, 0.037, and 0.004, respectively).
conclusionsThis implies the potential of rs3128965 as a genetic marker for diagnosis and prediction of the AERD phenotype.
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