Aspirin-Exacerbated Respiratory Disease--New Prime Suspects.

@article{Laidlaw2016AspirinExacerbatedRD,
  title={Aspirin-Exacerbated Respiratory Disease--New Prime Suspects.},
  author={Tanya M. Laidlaw and Joshua A. Boyce},
  journal={The New England journal of medicine},
  year={2016},
  volume={374 5},
  pages={
          484-8
        }
}
NSAIDs that inhibit cyclooxygenase-1 can provoke severe asthma and rhinosinusitis with nasal polyps and eosinophil infiltration. Cysteinyl leukotriene generation by the leukotriene C4 synthase pathway may cause the bronchoconstriction, vascular leak, and mucous secretion. 
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103 Citations
Highly Influential Citations
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Background Citations
31
Methods Citations
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103 Citations

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Citation Type

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The objective of this review is to provide otolaryngologists with an overview of the pathophysiology, diagnosis, and treatment of this under‐recognized condition.
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Surfactant protein D alleviates eosinophil‐mediated airway inflammation and remodeling in patients with aspirin‐exacerbated respiratory disease
Surfactant protein D (SPD) is a member of the collectin family that lines the airway epithelial cells with host defense. However, the role of SPD in the pathogenesis of aspirin‐exacerbated…
Mechanisms of Benefit with Aspirin Therapy in Aspirin-Exacerbated Respiratory Disease.
Potential Biomarkers for NSAID-Exacerbated Respiratory Disease
TLDR
The known potential biomarkers of NERD that are distinct from those of aspirin-tolerant asthma are summarized and an overview of the different N ERD subgroups is provided.
Aspirin exacerbated respiratory disease: Current topics and trends.
Aspirin or Nonsteroidal Anti-inflammatory Drug-Exacerbated Chronic Rhinosinusitis.
Aspirin-exacerbated respiratory disease: Mediators and mechanisms of a clinical disease.
  • K. Cahill, J. Boyce
  • Medicine, Biology
    The Journal of allergy and clinical immunology
  • 2017
Which Factors Associated With Activated Eosinophils Contribute to the Pathogenesis of Aspirin-Exacerbated Respiratory Disease?
TLDR
Recent findings about key mechanisms of eosinophil activation in the airway inflammation of AERD are highlighted and current biologics (targeting type 2 immune responses) were suggested to control eOSinophilic inflammation for AerD patients.
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References

SHOWING 1-10 OF 31 REFERENCES
Aspirin-Exacerbated Respiratory Disease Involves a Cysteinyl Leukotriene–Driven IL-33–Mediated Mast Cell Activation Pathway
TLDR
It is demonstrated that patients with AERD have markedly increased epithelial expression of the alarmin-like cytokine IL-33 in nasal polyps, as compared with polyps from aspirin-tolerant control subjects, and this component of a cysLT-driven innate type 2 immune response that drives pathogenic MC activation and contributes substantially to AERd pathogenesis.
Prostaglandin E2 deficiency causes a phenotype of aspirin sensitivity that depends on platelets and cysteinyl leukotrienes
TLDR
It is demonstrated that mice selectively lacking the capacity to up-regulate the generation of prostaglandin E2 with inflammation develop an AERD-like phenotype that depends critically on platelets and thromboxane receptors, which drive transcellular synthesis of cysLTs, which, in turn, activate mast cells with aspirin challenge.
The pivotal role of 5-lipoxygenase products in the reaction of aspirin-sensitive asthmatics to aspirin.
TLDR
The effects of an inhibitor of 5-lipoxygenase, zileuton, was examined in a group of eight asthmatic patients with known sensitivity to ASA accompanied by LTE4 hyperexcretion to confirm ASA sensitivity and an increase in urinary LTE4 after ASA ingestion.
Overexpression of leukotriene C4 synthase in bronchial biopsies from patients with aspirin-intolerant asthma.
TLDR
Aspirin may remove PGE2-dependent suppression in all subjects, but only in AIA patients does increased bronchial expression of LTC4 synthase allow marked overproduction of cys-LTs leading to bronchoconstriction.
Aspirin-sensitive rhinosinusitis is associated with reduced E-prostanoid 2 receptor expression on nasal mucosal inflammatory cells.
Benefits from adding the 5-lipoxygenase inhibitor zileuton to conventional therapy in aspirin-intolerant asthmatics.
TLDR
It is suggested that addition of a leukotriene pathway inhibitor such as zileuton may bring about greater control of asthma than what is achieved by treatment with medium to high doses of glucocorticosteroids alone.
Cysteinyl leukotriene overproduction in aspirin-exacerbated respiratory disease is driven by platelet-adherent leukocytes.
TLDR
A disturbance in platelet-leukocyte interactions may be partly responsible for the respiratory tissue inflammation and the overproduction of cysLTs that characterize AERD.
Inhaled PGE2 prevents aspirin-induced bronchoconstriction and urinary LTE4 excretion in aspirin-sensitive asthma.
TLDR
It is suggested that PGE2 is highly effective in preventing aspirin-induced asthma and this effect is mediated by inhibition of sulfidopeptide leukotriene production.
Reduced expression of COXs and production of prostaglandin E(2) in patients with nasal polyps with or without aspirin-intolerant asthma.
Prostaglandin D₂: a dominant mediator of aspirin-exacerbated respiratory disease.
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