Chronic hyperplastic eosinophilic sinusitis as a predictor of aspirin-exacerbated respiratory disease

Mascia, Kimberly; Borish, Larry; Patrie, James T.; Hunt, J.F.; Phillips, C. Douglas; Steinke, John W.

doi:10.1016/s1081-1206(10)61323-3

Cited by 82 publications

(68 citation statements)

References 27 publications

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“…1,25 Computed tomographies of subjects with AERD showed pansinusitis and are typically some of the worst seen in chronic sinus disease, with complete or near-complete opacification of the sinuses. 26 In reflecting the progressive nature of this inflammatory process, surgery is unlikely to be curative. Even when followed by optimal medical therapy, patients with AERD typically required multiple revision surgeries in their lifetime.…”

Section: Chronic Sinusitis With Npsmentioning

confidence: 99%

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Aspirin-Exacerbated Respiratory Disease: Prevalence, Diagnosis, Treatment, and Considerations for the Future

Kennedy

Stoner

Borish

2016

Am J Rhinol�Allergy

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Section: Chronic Sinusitis With Npsmentioning

confidence: 99%

“…AERD is also linked to increased airway remodeling, which results in increased residual volume and diminished diffusing capacity. 26,34 …”

Section: Asthmamentioning

confidence: 99%

Aspirin-Exacerbated Respiratory Disease: Prevalence, Diagnosis, Treatment, and Considerations for the Future

Kennedy

Stoner

Borish

2016

Am J Rhinol�Allergy

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“…A spirin-exacerbated respiratory disease (AERD) affects 5-10% of all adults with asthma (1-3), ∼30% with severe asthma (4), and ∼40% with refractory chronic hyperplastic sinusitis (5). It involves severe eosinophilic respiratory tract inflammation and is defined by bronchoconstriction following the ingestion of nonselective COX inhibitors (6).…”

mentioning

confidence: 99%

Prostaglandin E₂deficiency causes a phenotype of aspirin sensitivity that depends on platelets and cysteinyl leukotrienes

Liu

Laidlaw

Katz

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

108

105

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Aspirin-exacerbated respiratory disease (AERD) is characterized by asthma, tissue eosinophilia, overproduction of cysteinyl leukotrienes (cysLTs), and respiratory reactions to nonselective cyclooxygenase (COX) inhibitors. Ex vivo studies suggest that functional abnormalities of the COX-2/microsomal prostaglandin (PG)E 2 synthase-1 system may underlie AERD. We demonstrate that microsomal PGE 2 synthase-1 null mice develop a remarkably AERD-like phenotype in a model of eosinophilic pulmonary inflammation. Lysine aspirin (Lys-ASA)-challenged PGE 2 synthase-1 null mice exhibit sustained increases in airway resistance, along with lung mast cell (MC) activation and cysLT overproduction. A stable PGE 2 analog and a selective E prostanoid (EP) 2 receptor agonist blocked the responses to Lys-ASA by ∼90%; EP 3 and EP 4 agonists were also active. The increases in airway resistance and MC products were blocked by antagonists of the type 1 cysLT receptor or 5-lipoxygenase, implying that bronchoconstriction and MC activation were both cysLT dependent. Lys-ASA-induced cysLT generation and MC activation depended on platelet-adherent granulocytes and T-prostanoid (TP) receptors. Thus, lesions that impair the inducible generation of PGE 2 remove control of platelet/granulocyte interactions and TP-receptor-dependent cysLT production, permitting MC activation in response to COX-1 inhibition. The findings suggest applications of antiplatelet drugs or TP receptor antagonists for the treatment of AERD.A spirin-exacerbated respiratory disease (AERD) affects 5-10% of all adults with asthma (1-3), ∼30% with severe asthma (4), and ∼40% with refractory chronic hyperplastic sinusitis (5). It involves severe eosinophilic respiratory tract inflammation and is defined by bronchoconstriction following the ingestion of nonselective COX inhibitors (6). Cysteinyl leukotrienes (cysLTs) (LTC 4 , LTD 4 , and LTE 4 ) drive these reactions, as well as some of the chronic features of AERD (7,8). CysLTs derive from arachidonic acid metabolized by 5-lipoxygenase (5-LO) to LTA 4 , conjugated to reduced glutathione by leukotriene C 4 synthase (LTC 4 S) to LTC 4 in mast cells (MCs), eosinophils, basophils, macrophages, and granulocyte-platelet complexes (9). After export, LTC 4 is converted sequentially to LTD 4 and LTE 4 . CysLTs induce bronchoconstriction (10, 11), tissue eosinophilia (12), and remodeling (13) through G-protein-coupled receptors (GPCRs) expressed by structural and hematopoietic cells (14-16). Individuals with AERD display higher urinary levels of LTE 4 than do aspirin-tolerant asthmatic (ATA) control subjects (17). Reactions to aspirin or other nonselective COX inhibitors are accompanied by marked further increases in urinary levels of LTE 4 and can be blocked by pretreatment with the 5-LO inhibitor zileuton or with antagonists of the type 1 receptor for cysLTs (CysLT 1 R) (18,19). The dependency on COX products to maintain homeostasis over 5-LO activity is a unique feature of AERD. Remarkably, subjects with AERD can tolerate selective ant...

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“…It affects 10% of the population with asthma; however, its prevalence increases to 21% when provocation tests are used [1]. AERD is a disease characterized by restructuring of the airway [2] and the presence of extensive hyperplastic eosinophilic sinusitis with the formation of nasal polyps [3]. The most important clinical characteristic is bronchoconstriction after the administration of aspirin (ASA) or other nonsteroidal anti-inflammatory drugs (NSAIDs) [2,4].…”

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Single Nucleotide Polymorphisms in TNF are Associated with Susceptibility to Aspirin-exacerbated Respiratory Disease but not to Cytokine Levels: a Study in Mexican Mestizo Population

et al. 2017

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Aim:To evaluate the association of three single nucleotide polymorphisms in TNF and one in LTA in Mexican patients with aspirin-exacerbated respiratory disease (AERD) and the correlation of those single nucleotide polymorphisms with serum levels of TNF-α. Patients & methods: Case-control study including 133 patients with AERD, 135 patients with asthma (aspirin-tolerant asthmatics) and 182 healthy subjects. Results: GA genotype of rs1800629 in TNF was found to be associated with the risk of developing AERD (p < 0.05; odds ratio = 2.36) and by dominant model (p < 0.05; odds ratio = 2.51). Furthermore, there was a difference in the serum levels between the aspirin-tolerant asthmatics group and the other groups (p < 0.001). Conclusion: The GA genotype of rs1800629 is associated with genetic susceptibility to AERD, but it does not correlate to protein serum levels. Aspirin-exacerbated respiratory disease (AERD) is a clinical disease characterized by hypersensitivity to aspirin, asthma and chronic rhinosinusitis with nasal polyps. It affects 10% of the population with asthma; however, its prevalence increases to 21% when provocation tests are used [1]. AERD is a disease characterized by restructuring of the airway [2] and the presence of extensive hyperplastic eosinophilic sinusitis with the formation of nasal polyps [3]. The most important clinical characteristic is bronchoconstriction after the administration of aspirin (ASA) or other nonsteroidal anti-inflammatory drugs (NSAIDs) [2,4]. The physiopathology involves a block in the cyclooxygenase pathway that promotes a diversion of arachidonic acid metabolism toward the lipoxygenase pathway, inducing the synthesis of leukotrienes such as LTC4, LTD4 and LTE4 [5,6], proteins that induce inflammatory cell chemotaxis, and the release of cytokines such as TNF-α [7] and lymphotoxin. TNF-α is a critical molecule in the regulation of inflammation because it induces a cascade of other inflammatory cytokines, chemokines and growth factors [8]. The results of various in vivo and in vitro studies indicate that the increase in their production is involved in the severity of the inflammation, due to their participation in restructuring the airway and in the pro-oxidative response [9]. In relation to single nucleotide polymorphisms (SNPs), it has been reported that rs1800629 (G→A change in position -308) increases transcriptional activity [10,11], in addition to being associated with different pulmonary pathological diseases such as chronic obstructive pulmonary disease and asthma [9,12,13]. However, no SNPs have been reported in TNF or LTA that are associated with AERD.

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Chronic hyperplastic eosinophilic sinusitis as a predictor of aspirin-exacerbated respiratory disease

Cited by 82 publications

References 27 publications

Aspirin-Exacerbated Respiratory Disease: Prevalence, Diagnosis, Treatment, and Considerations for the Future

Aspirin-Exacerbated Respiratory Disease: Prevalence, Diagnosis, Treatment, and Considerations for the Future

Prostaglandin E₂deficiency causes a phenotype of aspirin sensitivity that depends on platelets and cysteinyl leukotrienes

Single Nucleotide Polymorphisms in TNF are Associated with Susceptibility to Aspirin-exacerbated Respiratory Disease but not to Cytokine Levels: a Study in Mexican Mestizo Population

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Chronic hyperplastic eosinophilic sinusitis as a predictor of aspirin-exacerbated respiratory disease

Cited by 82 publications

References 27 publications

Aspirin-Exacerbated Respiratory Disease: Prevalence, Diagnosis, Treatment, and Considerations for the Future

Aspirin-Exacerbated Respiratory Disease: Prevalence, Diagnosis, Treatment, and Considerations for the Future

Prostaglandin E2deficiency causes a phenotype of aspirin sensitivity that depends on platelets and cysteinyl leukotrienes

Single Nucleotide Polymorphisms in TNF are Associated with Susceptibility to Aspirin-exacerbated Respiratory Disease but not to Cytokine Levels: a Study in Mexican Mestizo Population

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Prostaglandin E₂deficiency causes a phenotype of aspirin sensitivity that depends on platelets and cysteinyl leukotrienes