Is sputum eosinophilia a good or poor predictor of benefit from inhaled corticosteroid therapy in asthma?

Pizzichini, M.M.M.

doi:10.1183/09031936.02.00068102

Cited by 8 publications

(8 citation statements)

References 27 publications

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“…This is also supported by the clinical improvement in asthma with fluticasone. In addition, this study confirms the excellent clinical response to corticosteroids in patients with the eosinophilic inflammatory phenotype 5 24. Perhaps more importantly, as previously suggested, it shows that benefits could also be observed in patients without obvious airway eosinophilia 25 26…”

supporting

confidence: 87%

Effects of steroid therapy on inflammatory cell subtypes in asthma

Boulet

2010

Thorax

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supporting

confidence: 87%

Effects of steroid therapy on inflammatory cell subtypes in asthma

Boulet

2010

Thorax

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“…Alternatively, the raised sputum neutrophil count in smokers with asthma might be poorly responsive to corticosteroid therapy [109]. However, there is conflicting data on the effects of corticosteroids on neutrophilic inflammation in asthma [110]. Inhibition by corticosteroids of T-lymphocyte proliferation of peripheral blood mononuclear cells is impaired in patients with corticosteroid-resistant asthma compared with patients with corticosteroid-sensitive asthma [111].…”

Section: Mechanisms Of Corticosteroid Resistance In Smokers With Asthmamentioning

confidence: 99%

Asthma and cigarette smoking

Thomson

Chaudhuri²,

Livingston³

2004

European Respiratory Journal

467

269

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In most developed countries y25% of adults with asthma are current cigarette smokers. Asthma and active cigarette smoking interact to cause more severe symptoms, accelerated decline in lung function, and impaired short-term therapeutic response to corticosteroids.Cigarette smoking may modify inflammation that is associated with asthma, although there is limited published data on airway pathology in smokers with asthma. To date, the evidence points towards a combination of both heightened and suppressed inflammatory responses in smokers compared with nonsmokers with asthma.The mechanisms of corticosteroid resistance in asthmatic smokers are unexplained, but could be as a result of alterations in airway inflammatory cell phenotypes (e.g. increased neutrophils or reduced eosinophils), changes in the glucocorticoid receptor-a to -b ratio (e.g. overexpression of glucocorticoid receptor b), and increased activation of pro-inflammatory transcription factors (e.g. nuclear factor-kB) or reduced histone deacetylase activity.In conclusion, every effort should be made to encourage asthmatics who smoke to stop, although the effects of smoking cessation upon reversing the adverse effects of tobacco smoke on asthma control, therapeutic response to corticosteroids and airway pathology have yet to be fully elucidated. Alternative or additional therapies to inhaled corticosteroids are needed for asthmatic patients who are unable to quit smoking.

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“…Increasing emphasis is being given to categorising patients in relation to inflammatory phenotype using induced sputum analysis. This may provide insights into both the natural history1 and the potential for treatment response 2. Four subtypes have been identified—eosinophilic, neutrophilic, paucigranulocytic or mixed cellularity—depending on the presence or absence of sputum eosinophils and/or neutrophils 3.…”

Section: Introductionmentioning

confidence: 99%

Effects of steroid therapy on inflammatory cell subtypes in asthma

Cowan

Palmay

et al. 2009

Thorax

276

220

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Rationale Airway inflammation in asthma is heterogeneous with different phenotypes. The inflammatory cell phenotype is modified by corticosteroids and smoking. Steroid therapy is beneficial in eosinophilic asthma (EA), but evidence is conflicting regarding non-eosinophilic asthma (NEA). Objectives To assess the inflammatory cell phenotypes in asthma after eliminating potentially confounding effects; to compare steroid response in EA versus NEA; and to investigate changes in sputum cells with inhaled corticosteroid (ICS). Methods Subjects undertook ICS withdrawal until loss of control or 28 days. Those with airway hyperresponsiveness (AHR) took inhaled fluticasone 1000 mg daily for 28+ days. Cut-off points were $/<2% for sputum eosinophils and $/<61% for neutrophils. Results After steroid withdrawal (n¼94), 67% of subjects were eosinophilic, 31% paucigranulocytic and 2% mixed; there were no neutrophilic subjects. With ICS (n¼88), 39% were eosinophilic, 46% paucigranulocytic, 3% mixed and 5% neutrophilic. Sputum neutrophils increased from 19.3% to 27.7% (p¼0.024). The treatment response was greater in EA for symptoms (p<0.001), quality of life (p¼0.012), AHR (p¼0.036) and exhaled nitric oxide (p¼0.007). Lesser but significant changes occurred in NEA (ie, paucigranulocytic asthma). Exhaled nitric oxide was the best predictor of steroid response in NEA for AHR (area under the curve 0.810), with an optimum cut-off point of 33 ppb. Conclusions After eliminating the effects of ICS and smoking, a neutrophilic phenotype could be identified in patients with moderate stable asthma. ICS use led to phenotype misclassification. Steroid responsiveness was greater in EA, but the absence of eosinophilia did not indicate the absence of a steroid response. In NEA this was best predicted by baseline exhaled nitric oxide.

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Is sputum eosinophilia a good or poor predictor of benefit from inhaled corticosteroid therapy in asthma?

Cited by 8 publications

References 27 publications

Effects of steroid therapy on inflammatory cell subtypes in asthma

Effects of steroid therapy on inflammatory cell subtypes in asthma

Asthma and cigarette smoking

Effects of steroid therapy on inflammatory cell subtypes in asthma

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