Association of IL13 genetic polymorphisms with atopic dermatitis

Lee, Eun; Kim, Jeong Hyun; Lee, So Yeon; Kang, Mi Jin; Park, Yoon Mee; Park, Min Jee; Rhee, Eun Sang; Ahn, Kangmo; Kim, Kyung Won; Shin, Youn Ho; Suh, Dong In; Hong, Soo Jong

doi:10.1016/j.anai.2020.04.023

Cited by 12 publications

(15 citation statements)

References 29 publications

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“…A number of genetic factors, such as germline mutations, polymorphisms, and gene replications are considered to predispose to more severe hypersensitivity reactions, atopic disorders and MCA. Examples are IL-4 and IL-13 gene polymorphisms leading to an excess production of IgE and thus predisposing to more extensive IgE-dependent allergies; or certain filaggrin gene (FLG) mutations predisposing to the development of atopic dermatitis [52][53][54][55][56].…”

Section: Impact Of Genetic Predisposition In Mca and Mcasmentioning

confidence: 99%

“…Patients with HAT have been reported to variably present with complaints indicating multi-organ disease and MCA. More recent data suggest that HAT is a valid genetic biomarker that associates with more severe mediator-related symptoms and thus MCA in anaphylaxis, IgE-dependent allergies and mastocytosis [46][47][48]55,56,60,61].…”

Section: Impact Of Genetic Predisposition In Mca and Mcasmentioning

confidence: 99%

“…Especially in patients who have HAT as well as a co-existing allergy and/or a co-existing clonal MC disorder (mastocytosis), the risk for development of MCAS may be greater [46][47][48]56,60,61]. Based on these studies, HAT can be regarded as a novel emerging genetic biomarker and modifying risk factor for MCA and MCAS in various patient cohorts, including SM and IgE-dependent allergies.…”

Section: Impact Of Genetic Predisposition In Mca and Mcasmentioning

confidence: 99%

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Diagnosis, Classification and Management of Mast Cell Activation Syndromes (MCAS) in the Era of Personalized Medicine

Valent

Akin

Nedoszytko

et al. 2020

IJMS

120

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Mast cell activation (MCA) is seen in a variety of clinical contexts and pathologies, including IgE-dependent allergic inflammation, other immunologic and inflammatory reactions, primary mast cell (MC) disorders, and hereditary alpha tryptasemia (HAT). MCA-related symptoms range from mild to severe to life-threatening. The severity of MCA-related symptoms depends on a number of factors, including genetic predisposition, the number and releasability of MCs, organs affected, and the type and consequences of comorbid conditions. In severe systemic reactions, MCA is demonstrable by a substantial increase of basal serum tryptase levels above the individual’s baseline. When, in addition, the symptoms are recurrent, involve more than one organ system, and are responsive to therapy with MC-stabilizing or mediator-targeting drugs, the consensus criteria for the diagnosis of MCA syndrome (MCAS) are met. Based on the etiology of MCA, patients can further be classified as having i) primary MCAS where KIT-mutated, clonal, MCs are detected; ii) secondary MCAS where an underlying IgE-dependent allergy or other reactive MCA-triggering pathology is found; or iii) idiopathic MCAS, where neither a triggering reactive state nor KIT-mutated MCs are identified. Most severe MCA events occur in combined forms of MCAS, where KIT-mutated MCs, IgE-dependent allergies and sometimes HAT are detected. These patients may suffer from life-threatening anaphylaxis and are candidates for combined treatment with various types of drugs, including IgE-blocking antibodies, anti-mediator-type drugs and MC-targeting therapy. In conclusion, detailed knowledge about the etiology, underlying pathologies and co-morbidities is important to establish the diagnosis and develop an optimal management plan for MCAS, following the principles of personalized medicine.

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Section: Impact Of Genetic Predisposition In Mca and Mcasmentioning

confidence: 99%

Section: Impact Of Genetic Predisposition In Mca and Mcasmentioning

confidence: 99%

Section: Impact Of Genetic Predisposition In Mca and Mcasmentioning

confidence: 99%

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Diagnosis, Classification and Management of Mast Cell Activation Syndromes (MCAS) in the Era of Personalized Medicine

Valent

Akin

Nedoszytko

et al. 2020

IJMS

120

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“…( 8) Previous studies have identified that polymorphisms in the IL-13 promoters are associated with the development of AD,(9, 10) and among them, many studies have focused on rs20541, especially in terms of its relationship with AD, in the existing Asian population. (11)(12)(13) Following on from the above considerations, we hypothesized that antibiotic exposure influences the AD phenotype and this relationship can be modified by IL-13 polymorphism. In this study, we explored the association of the occurrence and phenotype of AD with antibiotic exposure within 6 months of age, considering the dose administered and IL-13 (rs20541) polymorphism.…”

Section: Months(3)mentioning

confidence: 99%

“…(1) The prevalence rate of childhood AD ranges from 15% to 20% (2) and varies widely from one country to another globally. In Korea, primary surveys of children and adolescents demonstrated increasing trends in the prevalence of AD symptoms within the last 12…”

Section: Introductionmentioning

confidence: 99%

Effect of early-life antibiotic exposure and IL-13 polymorphism on atopic dermatitis phenotype

Park

Lee

et al. 2021

Preprint

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Background: Although atopic dermatitis (AD) is associated with certain gene variants, the rapidly increasing incidence of AD suggests that environmental factors contribute to disease development. In this study, we investigated the association of AD incidence and phenotype with antibiotic exposure within 6 months of age, considering the dose administered and genetic risk. Methods: This study included 1,637 children from the COCOA birth cohort. Pediatric allergists assessed the presence of AD at each visit and obtained information about antibiotic exposure for more than 3 days. IL-13 (rs20541) polymorphism was genotyped by the TaqMan method. We stratified the AD phenotypes into 4 groups and used multinomial logistic regression models for analysis. Results: Antibiotic exposure within 6 months of age was found to increase the risk of AD within 3 years of life (aOR=1.40, 95%, CI 1.09–1.81) in dose-dependent manner. Antibiotic exposure more than twice increased the risk of the early-persistent AD phenotype (aOR=2.50, 95% CI 1.35–4.63). There was a weak interaction between genetic polymorphisms and environmental factors on the development of AD (p for interaction=0.06). Children with the IL-13 (rs20541) GA+ AA genotype have a higher risk of the early-persistent AD phenotype when exposed to antibiotics more than twice than those with the IL-13 (rs20541) GG genotype and without exposure to antibiotics (aOR=4.73, 2.01–11.14). Conclusion: Antibiotic exposure within 6 months was related to the incidence of early-persistent AD and a dose-dependent increase in the incidence of AD in childhood, whose effect was modified by the IL-13 (rs20541) genotype.

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Genetic association of beta-lactams-induced hypersensitivity reactions: A systematic review of genome-wide evidence and meta-analysis of candidate genes

Lumkul,

Wongyikul,

Kulalert

et al. 2023

World Allergy Organization Journal

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Association of IL13 genetic polymorphisms with atopic dermatitis

Cited by 12 publications

References 29 publications

Diagnosis, Classification and Management of Mast Cell Activation Syndromes (MCAS) in the Era of Personalized Medicine

Diagnosis, Classification and Management of Mast Cell Activation Syndromes (MCAS) in the Era of Personalized Medicine

Effect of early-life antibiotic exposure and IL-13 polymorphism on atopic dermatitis phenotype

Genetic association of beta-lactams-induced hypersensitivity reactions: A systematic review of genome-wide evidence and meta-analysis of candidate genes

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