PT -期刊文章盟Menzies-Gow Andrew AU -Mansur, Adel H. AU - Brightling, Christopher E. TI - Clinical utility of fractional exhaled nitric oxide (FeNO) in severe asthma management AID - 10.1183/13993003.01633-2019 DP - 2020 Jan 01 TA - European Respiratory Journal PG - 1901633 4099 - //www.qdcxjkg.com/content/early/2020/01/03/13993003.01633-2019.short 4100 - //www.qdcxjkg.com/content/early/2020/01/03/13993003.01633-2019.full AB - Asthma is a chronic inflammatory disease of the airways, affecting over 350 million people worldwide and placing a significant burden on healthcare providers and wider society. Approximately 5–10% of asthma patients are diagnosed with severe asthma and typically are associated with increased risk of hospitalisation from exacerbations, increased morbidity, mortality and higher asthma-associated healthcare costs. Nitric oxide (NO) is an important regulator of immune responses and is a product of inflammation in the airways that is over-produced in asthma. Fractional exhaled NO (FeNO) is predominantly used as a predictor of response to inhaled corticosteroids (ICSs), to monitor adherence and as a diagnostic tool in ICS-naïve patients. In the UK, the National Institute for Health and Care Excellence (NICE) guidelines recommend the use of FeNO for the initial diagnosis of patients with suspected asthma. In the US, the American Thoracic Society (ATS) guidelines recommend FeNO as part of the initial diagnosis of asthma and for monitoring of airway inflammation. FeNO has also been shown to be a predictive factor for asthma exacerbations, with higher levels being associated with a greater number of exacerbations. In addition, higher levels of FeNO have been shown to be associated with a decline in lung function. FeNO testing is a cost-effective procedure and has been shown to improve patient management when combined with standard assessment methods. Recent evidence suggests that FeNO may also be useful as a surrogate biomarker for the assessment and management of severe asthma and to predict responsiveness to some biological therapies.FootnotesThis manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article.Conflict of interest: Dr. Menzies-Gow reports attending advisory boards for AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Novartis, Sanofi and Teva. He has received speaker fees from AstraZeneca, Boehringer Ingelheim, Novartis, Teva and Vectura, and participated in research for which his host institution has been remunerated by AstraZeneca. He has attended international conferences sponsored by Boehringer Ingelheim and Teva, and has consultancy agreements with AstraZeneca, Sanofi and Vectura.Conflict of interest: Dr. Mansur reports an educational grant for service support from AstraZeneca; and fees for talks and advisory group contribution and conference attendance from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Napp Pharmaceuticals, Novartis, Sanofi , and other outside the submitted work.Conflict of interest: Dr. Brightling reports non-financial support from Sanofi Genzyme Inc., UK, during the conduct of the study; grants from Air-PROM, Medical Research Council UK, and National Institute for Health Research UK; grants and personal fees from 4DPharma, AstraZeneca/Medimmune, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Gossamer, Mologic, Novartis, Roche/Genentech, and Sanofi/Regeneron; personal fees from Gilead, Pfizer, PreP, Teva, Theravance , and Vectura, outside the submitted work.