Capsaicin-evoked cough responses in asthmatic patients: Evidence for airway neuronal dysfunction - 19/04/17
Abstract |
Background |
Cough in asthmatic patients is a common and troublesome symptom. It is generally assumed coughing occurs as a consequence of bronchial hyperresponsiveness and inflammation, but the possibility that airway nerves are dysfunctional has not been fully explored.
Objectives |
We sought to investigate capsaicin-evoked cough responses in a group of patients with well-characterized mild-to-moderate asthma compared with healthy volunteers and assess the influences of sex, atopy, lung physiology, inflammation, and asthma control on these responses.
Methods |
Capsaicin inhalational challenge was performed, and cough responses were analyzed by using nonlinear mixed-effects modeling to estimate the maximum cough response evoked by any concentration of capsaicin (Emax) and the capsaicin dose inducing half-maximal response (ED50).
Results |
Ninety-seven patients with stable asthma (median age, 23 years [interquartile range, 21-27 years]; 60% female) and 47 healthy volunteers (median age, 38 years [interquartile range, 29-47 years]; 64% female) were recruited. Asthmatic patients had higher Emax and lower ED50 values than healthy volunteers. Emax values were 27% higher in female subjects (P = .006) and 46% higher in patients with nonatopic asthma (P = .003) compared with healthy volunteers. Also, patients with atopic asthma had a 21% lower Emax value than nonatopic asthmatic patients (P = .04). The ED50 value was 65% lower in female patients (P = .0001) and 71% lower in all asthmatic patients (P = .0008). ED50 values were also influenced by asthma control and serum IgE levels, whereas Emax values were related to 24-hour cough frequency. Age, body mass index, FEV1, PC20, fraction of exhaled nitric oxide, blood eosinophil counts, and inhaled steroid treatment did not influence cough parameters.
Conclusion |
Patients with stable asthma exhibited exaggerated capsaicin-evoked cough responses consistent with neuronal dysfunction. Nonatopic asthmatic patients had the highest cough responses, suggesting this mechanism might be most important in type 2–low asthma phenotypes.
Le texte complet de cet article est disponible en PDF.Key words : Atopy, transient receptor potential vanilloid type 1, vagus, pharmacodynamic modeling
Abbreviations used : ACQ, ATS, C2, C5, ED50, Emax, Feno, LCQ, TRPV1
Plan
| Supported by the National Institute for Health Research, South Manchester Clinical Research Facility. Clinical Trial Registration: www.controlled-trials.com ISRCTN32052878 and ISRCTN23684347. |
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| Disclosure of potential conflict of interest: I. Satia receives research support from the North West Lung Centre Endowment Fund, University Hospital of South Manchester, SPR Research Prize (GlaxoSmithKline-sponsored event), and British Medical Association James Trust Award; receives payments for lectures from GlaxoSmithKline, Almirall, and AstraZeneca; and receives travel support from GlaxoSmithKline, Almirall, and Chiesi. M. Woodhead serves as a consultant for Pfizer. P. M. O'Byrne reports grants and personal fees from AstraZeneca, personal fees from Chiesi, grants from Novartis, personal fees from Boehringer Ingelheim, personal fees from GlaxoSmithKline, personal fees from MedImmune, personal fees from Merck, personal fees from Takeda, personal fees from Abbott, grants from Amgen, grants from Genentech, grants from Axican, and grants from Ono outside the submitted work. J. A. Smith reports grants and personal fees from Verona Pharma, grants from the British Lung Foundation, grants from Marie-Curie, a grant from the MRC MICA Research Grant with Almirall, grants from MRC AstraZeneca Mechanisms of Disease, grants from the Mayo Clinic Center for Translational Science Activities (CTSA), grants from the Mayo Clinic CR20 Award, grants and personal fees from GlaxoSmithKline, personal fees from Almirall, personal fees from Reckitt Benckiser, personal fees from Glenmark, grants and personal fees from Xention, personal fees from Patara Pharma, grants from Afferent, grants from the Medical Research Council, grants from the Moulton Charitable Trust, grants from NeRRe, and personal fees from Bayer outside the submitted work and has a patent A method for generating output data licensed to Vitalograph. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 139 - N° 3
P. 771 - mars 2017 Retour au numéro
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