2021
DOI: 10.1016/j.jaci.2021.08.015
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Eicosanoid dysregulation and type 2 inflammation in AERD

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Cited by 23 publications
(16 citation statements)
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“…AERD is also characterized by severe and persistent type 2 airway inflammation with extensive eosinophilic infiltration. 27 Compared with ATA, AERD shows extensive eosinophilic infiltration in the upper and lower airways. 28 In our study, increased sputum eosinophil count effectively distinguished the AERD group from the ATA group, but was comparable between the severe and nonsevere AERD groups.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…AERD is also characterized by severe and persistent type 2 airway inflammation with extensive eosinophilic infiltration. 27 Compared with ATA, AERD shows extensive eosinophilic infiltration in the upper and lower airways. 28 In our study, increased sputum eosinophil count effectively distinguished the AERD group from the ATA group, but was comparable between the severe and nonsevere AERD groups.…”
Section: Discussionmentioning
confidence: 99%
“…AERD is also characterized by severe and persistent type 2 airway inflammation with extensive eosinophilic infiltration 27 . Compared with ATA, AERD shows extensive eosinophilic infiltration in the upper and lower airways 28 .…”
Section: Discussionmentioning
confidence: 99%
“…24 AERD's pathophysiology is due to eicosanoid dysregulation through overproduction of inflammatory cysteinyl leukotrienes and PGD 2 and defective inhibitory regulation through PGE 2 (R) and COX-2. 25 Diagnostic confirmation of AERD without a history of NSAID/aspirin intolerance remains challenging given the absence of a sensitive biomarker to date. 26 Although this patient had pre-existing mild persistent asthma and developed asymptomatic polyposis before starting nivolumab, a cyclical pattern of aggravation with nivolumab and improvement with benralizumab suggests a probable association.…”
Section: Discussionmentioning
confidence: 99%
“…A varied sequence of onset of symptoms in AERD is typical, with COX-1 inhibitor intolerance often the last feature of the triad to develop 24. AERD’s pathophysiology is due to eicosanoid dysregulation through overproduction of inflammatory cysteinyl leukotrienes and PGD 2 and defective inhibitory regulation through PGE 2 (R) and COX-2 25. Diagnostic confirmation of AERD without a history of NSAID/aspirin intolerance remains challenging given the absence of a sensitive biomarker to date 26…”
Section: Discussionmentioning
confidence: 99%
“…CRSwNP (and AERD) is predominantly characterized by type 2 inflammation, [17][18][19] and several RCTs have evaluated whether biologics targeting soluble IgE (omalizumab), soluble IL-5 (mepolizumab, reslizumab), the IL-5 receptor alpha (benralizumab), or the IL-4 receptor alpha (dupilumab) are safe and effective in this patient population. Although large studies evaluating the efficacy of these drugs specifically in patients with AERD are lacking, post hoc analyses of the subset of participants with AERD have been performed using data gathered from the clinical trials in CRSwNP.…”
Section: Benefits and Efficacy Of Available Respiratory Biologics For...mentioning
confidence: 99%