2022
DOI: 10.1111/resp.14263
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Bronchiectasis enters the inflammation era

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Cited by 7 publications
(6 citation statements)
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“…Neutrophils are the most abundant airway inflammatory cell in bronchiectasis, but the importance of eosinophils recently was recognized. 32 In a post hoc analysis of bronchiectasis trial data from 86 participants, inhaled fluticasone reduced bronchiectasis exacerbations in those with BEC of ≥ 150 cells/μL. 33 A large European multicenter cohort of 1,007 patients with bronchiectasis reported that approximately one-fifth of patients exhibited sputum eosinophil counts of > 3%.…”
Section: Discussionmentioning
confidence: 99%
“…Neutrophils are the most abundant airway inflammatory cell in bronchiectasis, but the importance of eosinophils recently was recognized. 32 In a post hoc analysis of bronchiectasis trial data from 86 participants, inhaled fluticasone reduced bronchiectasis exacerbations in those with BEC of ≥ 150 cells/μL. 33 A large European multicenter cohort of 1,007 patients with bronchiectasis reported that approximately one-fifth of patients exhibited sputum eosinophil counts of > 3%.…”
Section: Discussionmentioning
confidence: 99%
“…Molecular endotyping, assessing disease through underlying pathobiological mechanisms and/or treatment response, should be combined with phenotyping for a holistic view. Classic examples of this include inflammatory patterns such as neutrophilic/neutrophil extracellular traps versus eosinophilic/type 2 airway inflammation ( 26 , 28 , 48 , 49 ). Each clinical phenotype may be driven by multiple endotypes and vice versa, and a therapeutic target identified through a phenotype or endotype is termed a treatable trait.…”
Section: Redefining Bronchiectasis By Advanced Endophenotypingmentioning
confidence: 99%
“…Noteworthy, 21 of 35 (60%) in the SEA + BE cohort had severe bronchiectasis according to BSI. Statistically significant differences between SEA and SEA + BE patients were observed in the proportion of patients with CMH (51.3% in SEA vs. 82.9% in SEA + BE, p = 0.0064), microbial colonization (10.3% in SEA vs. 34.3% in SEA + BE, p = 0.0219), asthma exacerbations/year [5 (3.5-7) in SEA vs. 7 (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16) in SEA + BE, p = 0.0012], ACT score [15 (10-18) in SEA vs. 13 (8)(9)(10)(11)(12)(13)(14)(15)(16) in SEA + BE, p = 0.0175], FEV 1 /FVC% [64% (55.9-76) in SEA vs. 57% (54-65) in SEA + BE, p = 0.0202] and in the proportion of patients on OCS (69.2% in SEA vs. 100% in SEA + BE, p = 0.0078).…”
Section: Baseline Patient Demographics and Clinical Characteristicsmentioning
confidence: 99%
“…Eosinophilic inflammation promotes tissue damage and airway remodelling, contributing to the pathogenesis of bronchiectasis (BE), especially in patients with severe eosinophilic asthma (SEA) [ 9 , 10 , 11 ]. Indeed, the prevalence of BE is significantly higher in patients with SEA (approximately 24–40%) than in those with mild asthma (3%) and their presence is associated with more frequent exacerbations and hospitalisations, higher OCS consumption and poor quality of life [ 12 , 13 , 14 ].…”
Section: Introductionmentioning
confidence: 99%
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