Association between a TGFβ1 promoter polymorphism and the phenotype of aspirin-intolerant chronic urticaria in a Korean population

Park, H.‐J.; Ye, Y.‐M.; Hur, Gyu-Young; Kim, Seung Hyun

doi:10.1111/j.1365-2710.2008.00957.x

Cited by 22 publications

(8 citation statements)

References 38 publications

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“…The nonsynonymous variant on the diamine oxidase gene (DAO rs10156191, p.Thr16Met) was moderately but significantly associated with cross-intolerance to NSAIDs (OR, 1.59; 95% CI, 1.27-2.00; P = 6 9 10 À5 for the minor allele) (45). In contrast, HNMT was the only significant predictor of this pathway in NAR to aspirin (32,33,36). Results from these studies suggest that mutations in genes encoding histaminemetabolizing enzymes may increase the risk, or modify the clinical presentation, of NAR, in which histamine plays an important role.…”

Section: Genetic Predictors Of Nar: the Examples Of Nonspecific Reactmentioning

confidence: 84%

“…1). Among the 42 selected studies that reported genetic predictors in association with immediate-type hypersensitivity, 19 were related to BLs (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) (Table 1), 12 to aspirin (31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42) (Table 2), and eight to other NSAIDs (43-50) (Table 3). Three studies reported genetic predictors in association with biologicals, including hypersensitivity to asparaginase (51), EGF receptor inhibitors (52), and infliximab (53) ( Table 4).…”

Section: Literature Search Resultsmentioning

confidence: 99%

“…They highlighted the involvement of genes that can be grouped into four pathogenic groups: (i) the membrane-spanning 4A gene family (FCER1A (formerly, FceR1a), MS4A2 (formerly, FceR1b), and FCER1G (formerly, FceR1c); (ii) the histamine production pathway (HNMT) (34,35,38); (iii) the inflammatory cytokines (TGFB1, TNF, and IL18) (36,37,40); and (iv) the arachidonic acid pathway (ALOX5, LTC4S, TBXA2R, and PTGER4) (33,39,41,42) (Table 2 Fig. 3).…”

Section: Genetic Predictors Of Nar To Aspirinmentioning

confidence: 99%

See 2 more Smart Citations

Genetic variants associated with drugs-induced immediate hypersensitivity reactions: a PRISMA-compliant systematic review

Oussalah

Mayorga

Blanca

et al. 2016

Allergy

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Drug hypersensitivity includes allergic (AR) and nonallergic reactions (NARs) influenced by genetic predisposition. We performed a systematic review of genetic predictors of IgE-mediated AR and NAR with MEDLINE and PubMed search engine between January 1966 and December 2014. Among 3110 citations, the search selected 53 studies, 42 of which remained eligible. These eligible studies have evaluated genetic determinants of immediate reactions (IR) to beta-lactams (n = 19), NAR against aspirin (n = 12) and other nonsteroidal anti-inflammatory drugs (NSAIDs) (n = 8), and IR to biologics (n = 3). We reported two genomewide association studies and four case-control studies on candidate genes validated by replication. Genes involved in IR to beta-lactams belonged to HLA type 2 antigen processing, IgE production, atopy, and inflammation, including 4 genes validated by replications, HLA-DRA, ILR4, NOD2, and LGALS3. Genes involved in NAR to aspirin belonged to arachidonic acid pathway, membranespanning 4A gene family, histamine production pathway, and pro-inflammatory cytokines, while those involved in NAR to all NSAIDs belonged to arachidonic acid pathway and HLA antigen processing pathway. ALOX5 was a common predictor of studies on NAR to both aspirin and NSAIDs. Although these first conclusions could be drawn, this review highlights also the lack of reliable data and the need for replicating studies in contrasted populations, taking into account worldwide allele frequencies, gene-gene interactions, and contrasted situations of environmental exposure.Allergy 71 (2016) 443-462

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Section: Genetic Predictors Of Nar: the Examples Of Nonspecific Reactmentioning

confidence: 84%

Section: Literature Search Resultsmentioning

confidence: 99%

Section: Genetic Predictors Of Nar To Aspirinmentioning

confidence: 99%

See 1 more Smart Citation

Genetic variants associated with drugs-induced immediate hypersensitivity reactions: a PRISMA-compliant systematic review

Oussalah

Mayorga

Blanca

et al. 2016

Allergy

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“…The major allele frequency at TGFβ1 -509C>T was significantly higher in CU patients in an Iranian population 47. In contrast, the minor allele frequency of -509C>T was significantly higher in AICU patients in a Korean population, and this allele tended to be associated with a lower serum level of TGF-β1 48,49. The minor allele of this variant, TGFβ1 -509T, was identified as a risk factor in patients with AERD and asthma in two studies 49,50.…”

Section: The Candidate Gene Approach In Cumentioning

confidence: 92%

Molecular Genetic Mechanisms of Chronic Urticaria

Losol

Yoo

Park

2014

Allergy Asthma Immunol Res

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Chronic urticaria (CU) is a common allergic skin disease that requires long-term pharmacological treatment. Some patients with severe CU suffer a poor quality of life. Although the pathogenic mechanisms of CU are not clearly understood, several groups have suggested that genetic mechanisms are involved in various CU cohorts. To further understand the molecular genetic mechanisms of CU, we summarize recent genetic data in this review. Although a few HLA alleles were suggested to be candidate markers in different ethnic groups, further replication studies that apply the recent classification are needed. Genetic polymorphisms in histamine-related genes, including FcεRI and HNMT, were suggested to be involved in mast cell activation and histamine metabolism. Several genetic polymorphisms of leukotriene-related genes, such as ALOX5, LTC4S, and the PGE2 receptor gene PTGER4, were suggested to be involved in leukotriene overproduction, a pathogenic mechanism. Further investigations using candidate gene approaches and genome-wide association studies (GWAS) will provide new insights into the molecular genetic mechanisms of CU, which will provide new marker genes for differentiation of CU phenotypes and identification of potential therapeutic targets.

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“…An additional 15 articles were excluded. Five did not report case–control studies, 10–14 three were not asthma studies, 15–17 three were family‐based studies, 18–20 two did not report useable data, 21,22 one was a repeat publication 23 and one reported on TGF‐β2 polymorphisms rather than TGF‐β1 polymorphism 24 . Therefore, 14 eligible articles reporting on TGF‐β1 polymorphisms, 7,25–37 and meeting the inclusion criteria, were identified.…”

Section: Resultsmentioning

confidence: 99%

Polymorphisms in the transforming growth factor‐β1 gene and the risk of asthma: A meta‐analysis

Zhang¹,

Zhang

Huang

et al. 2010

Respirology

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Association between a TGFβ1 promoter polymorphism and the phenotype of aspirin-intolerant chronic urticaria in a Korean population

Abstract: These findings suggest that the -509C>T polymorphism in the TGFbeta1 promoter may contribute to the development of the AICU phenotype.

Cited by 22 publications

References 38 publications

Genetic variants associated with drugs-induced immediate hypersensitivity reactions: a PRISMA-compliant systematic review

Genetic variants associated with drugs-induced immediate hypersensitivity reactions: a PRISMA-compliant systematic review

Molecular Genetic Mechanisms of Chronic Urticaria

Polymorphisms in the transforming growth factor‐β1 gene and the risk of asthma: A meta‐analysis

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