Aspirin Exacerbated Respiratory Disease: Epidemiology, Pathophysiology, and Management

Li, Kevin L.; Lee, Andrew Y.; Abuzeid, Waleed M.

doi:10.3390/medsci7030045

Cited by 32 publications

(43 citation statements)

References 98 publications

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“…The strong connection of salicylate intolerance and rhinosinusitis together with asthma, which can also be seen in Fig. 2 and Table 3, known as Samter's Triad, is a well-known triad of symptoms 29 , although this phenomenon in the SA populations has not yet been published. As there were significantly more patients with rhinosinusitis in group 2, the Samter's Triad might also explain why significantly more patients with salicylate intolerance were in this group.…”

Section: Discussionmentioning

confidence: 95%

Prevalence and characterization of severe asthma in Hungary

Csoma¹,

Gál²,

Gézsi³

et al. 2020

Sci Rep

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Background: Severe asthma (SA) database was established in Hungary to estimate the prevalence of SA and to define and analyze clinical phenotypes of the patients. Methods: SA questionnaires were sent out to 143 public pulmonary dispensaries specialized for diagnosing and caring pulmonary patients. Data of 520 SA patients were evaluated. Results: The prevalence of SA within the asthmatic population in Hungary was 0.89%. The mean age of patients were 56.4 ± 13.4 years, SA were more frequent in females (64%), the prevalence of allergy was 56.6%, 72.1% of patients had persistent airflow limitation (FEV1 < 80%), 37.9% severe airway obstruction (FEV1 ≤ 60%), 33.6% required systemic corticosteroid maintenance therapy, 21.5% had salicylate intolerance and 43.2% rhinosinusitis. A Bayesian dependency network was calculated which revealed several interdependencies between the characteristics. E.g. there was a strong association between salicylate intolerance and rhinosinusitis, more patients received regular systemic corticosteroid treatment who had salicylate intolerance and the proportion of salicylate intolerance was significantly higher in females. Conclusion: The prevalence of SA was determined in Hungary which was lower than in other studies. Using a Bayesian-based network analysis several interdependencies were revealed between patient characteristics.

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Section: Discussionmentioning

confidence: 95%

Prevalence and characterization of severe asthma in Hungary

Csoma¹,

Gál²,

Gézsi³

et al. 2020

Sci Rep

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“…However, there was no change in the expression of COX-1. Conversely, the 5-lipoxygenase (5-LO) pathway, which metabolizes AA into LTs, is markedly upregulated in these patients, resulting in an extremely high level of CysLTs, which activate mast cells and eosinophils [10,182]. Addition of nonsteroidal anti-inflammatory drugs, especially COX-1 inhibitors, forces AA metabolism towards LT synthesis and further decreases PGE 2 production, resulting in the uncontrolled release of LTC 4 , LTD 4 , LTE 4 , and PGD 2 by countering the suppressive effect of PGE 2 on 5-LO [183][184][185].…”

Section: Aspirin-exacerbated Respiratory Diseasementioning

confidence: 99%

The Biology of Prostaglandins and Their Role as a Target for Allergic Airway Disease Therapy

Lee

Kim

2020

IJMS

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Prostaglandins (PGs) are a family of lipid compounds that are derived from arachidonic acid via the cyclooxygenase pathway, and consist of PGD 2 , PGI 2 , PGE 2 , PGF 2 , and thromboxane B 2 . PGs signal through G-protein coupled receptors, and individual PGs affect allergic inflammation through different mechanisms according to the receptors with which they are associated. In this review article, we have focused on the metabolism of the cyclooxygenase pathway, and the distinct biological effect of each PG type on various cell types involved in allergic airway diseases, including asthma, allergic rhinitis, nasal polyposis, and aspirin-exacerbated respiratory disease.

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“…Note: Data from Li KL, Lee AY, and Abuzeid WM 50. Kuruvilla et al Dovepress submit your manuscript | www.dovepress.comDovePressJournal of Asthma and Allergy 2020:13…”

mentioning

confidence: 99%

<p>The Role of Mast Cells in Aspirin-Exacerbated Respiratory Disease (AERD) Pathogenesis: Implications for Future Therapeutics</p>

Kuruvilla

Vanijcharoenkarn

Levy

2020

JAA

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Mast cells (MC) have recently been demonstrated to play an integral role in the pathogenesis of aspirin-exacerbated respiratory disease (AERD). When activated, MCs release pre-formed granules of many pro-inflammatory mediators, including histamine, serotonin, and various chemokines and cytokines including tumor necrosis factor (TNF)-α, interferon ɣ (IFN ɣ), macrophage inhibitory factor, transforming growth factor, interleukin (IL) 1, 3-6, 9, 10, 13 and 16. These mediators promote inflammation in AERD by recruiting or activating a network of cells involved in acute and chronic inflammatory pathways, such as endothelial, epithelial, stromal, and other immune cells. Several studies have implicated multifactorial pathways for MC activation in AERD beyond classical IgE mediated mechanisms. The elucidation of these complex networks therefore represents important targets for innovative patient therapeutics. This review summarizes classic and alternative pathways of MC activation in AERD with a special focus in relation to new and emerging treatment strategies.

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Aspirin Exacerbated Respiratory Disease: Epidemiology, Pathophysiology, and Management

Cited by 32 publications

References 98 publications

Prevalence and characterization of severe asthma in Hungary

Prevalence and characterization of severe asthma in Hungary

The Biology of Prostaglandins and Their Role as a Target for Allergic Airway Disease Therapy

<p>The Role of Mast Cells in Aspirin-Exacerbated Respiratory Disease (AERD) Pathogenesis: Implications for Future Therapeutics</p>

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