Aspirin‐induced asthma and HLA‐DRB1 and HLA‐DPB1 genotypes

Dekker, James; Nizankowska, E; Schmitz-Schumann, M; Pile, K; Bochenek, Grażyna; Dyczek, Andrzej; Cookson, W. O. C. M.; Szczeklik, Andrzej

doi:10.1111/j.1365-2222.1997.tb00747.x

Cited by 102 publications

(13 citation statements)

References 18 publications

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“…HLA-DPB1*0301, member of MHC class II family, has been reported as a susceptibility allele to AIA in several populations. [9][10][11] Interestingly, HLA-DPB1*0301 may predict leukotrien inhibitor requirement in patients with AERD. 12 By contrast, limited data exist on the association of other HLA genes with AERD.…”

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confidence: 99%

HLA-DRB and HLA-DQ Genetic Variability in Patients with Aspirin-Exacerbated Respiratory Disease

Esmaeilzadeh

Nabavi

Amirzargar

et al. 2015

Am J Rhinol�Allergy

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confidence: 99%

HLA-DRB and HLA-DQ Genetic Variability in Patients with Aspirin-Exacerbated Respiratory Disease

Esmaeilzadeh

Nabavi

Amirzargar

et al. 2015

Am J Rhinol�Allergy

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“…Clinical data from in vivo provocation testing of adult asthmatics have failed to show consistent significant differences in leukotriene urinary excretion between ASA-sensitive and nonsensitive individuals [27]. Genetic analyses in different groups of patients also involve abnormalities in the TBX21 gene and interferon-γ production [28], in the DR/DP haplotypes associated with antigen presentation [29,30], and even a viral etiology has been postulated in adults [31]. No genetic association studies have been published so far in children, and the mechanisms of ASA-associated angioedema and urticaria, the most prevalent form of NSAID hypersensitivity in this age group, are still speculative.…”

Section: Resultsmentioning

confidence: 99%

Nonsteroidal Anti-Inflammatory Drug Hypersensitivity in Preschool Children

Kidon

Kang

Chin

et al. 2007

All Asth Clin Immun

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Although extensively studied in adults, nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity in children, especially in young children, remains poorly defined. Pediatricians, prescribing antipyretics for children, rarely encounter significant problems, but the few epidemiologic studies performed show conflicting results. Although it is clear that some patients with acetylsalicylic acid (ASA)-sensitive asthma have their clinical onset of disease in childhood and bronchoconstriction after ASA challenge is seen in 0 to 22% of asthmatic children so challenged, ibuprofen at antipyretic doses may cause acute respiratory problems only in a very small number of mild to moderate asthmatics. The recently elucidated mechanism of action of acetaminophen may explain some occurrences of adverse reactions in patients with cross-reactive NSAID hypersensitivity on the basis of its inhibitory activity on the newly described enzyme, cyclooxygenase (COX)-3. This nonspecific sensitivity to inhibition of COX is most likely genetically determined and shows a remarkable association with atopic disease even in the very young age group and possibly an increased predilection in specific ethnic groups. This review summarizes state-of-the-art published data on NSAID hypersensitivity in preschool children.

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“…Many genetic studies have focused on CysLTs-related and eosinophil activating genes (major pathogenic mechanisms) according to single nucleotide polymorphisms (SNPs) and genome-wide association studies (GWASs) (Pavón-Romero et al, 2017). (Table 1) HLA DPB1*0301 has been regarded as a strong genetic marker and replicated in the 2 ethnic groups Polish and Korean populations (Dekker et al, 1997;Choi et al, 2004a). Patients suffering from this allele manifested the typical clinical characteristics of NERD, and had lower FEV1 levels and a higher prevalence of CRS and/or NPs (Choi et al, 2004a).…”

Section: Genetic Mechanismsmentioning

confidence: 98%

NSAID-Exacerbated Respiratory Disease (NERD): From Pathogenesis to Improved Care

2020

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Nonsteroidal antiinflammatory drug (NSAID)-exacerbated respiratory disease (NERD) is characterized by moderate-to-severe asthma and a higher prevalence of chronic rhinosinusitis/nasal polyps, but is a highly heterogeneous disorder with various clinical manifestations. Two major pathogenic mechanisms are: (1) overproduction of cysteinyl leukotrienes with dysregulation of arachidonic acid metabolism and (2) increased type 2 eosinophilic inflammation affected by genetic mechanisms. Aspirin challenge is the gold standard to diagnose NERD, whereas reliable in vitro biomarkers have yet not been identified. Therapeutic approaches have been done on the basis of disease severity with the avoidance of culprit and cross-reacting NSAIDs, and when indicated, aspirin desensitization is an effective treatment option. Biologic approaches targeting Type 2 cytokines are emerging as potential therapeutic options. Here, we summarize the up-to-date evidence of pathophysiologic mechanisms and diagnosis/management approaches to the patients with NERD with its phenotypic classification.

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Aspirin‐induced asthma and HLA‐DRB1 and HLA‐DPB1 genotypes

Abstract: The presence of an HLA association suggests that immune recognition of an unknown antigen may be part of the aetiology of AIA.

Cited by 102 publications

References 18 publications

HLA-DRB and HLA-DQ Genetic Variability in Patients with Aspirin-Exacerbated Respiratory Disease

HLA-DRB and HLA-DQ Genetic Variability in Patients with Aspirin-Exacerbated Respiratory Disease

Nonsteroidal Anti-Inflammatory Drug Hypersensitivity in Preschool Children

NSAID-Exacerbated Respiratory Disease (NERD): From Pathogenesis to Improved Care

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