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Clinical Commentary |

Rescue Treatment in Asthma: More Than As-Needed Bronchodilation

Alberto Papi, MD; Gaetano Caramori, MD, PhD; Ian M. Adcock, PhD; Peter J. Barnes, MD, FCCP
Author and Funding Information

*From Centro di Ricerca su Asma e BPCO (Drs. Papi and Caramori), Università di Ferrara, Ferrara, Italy; and Airway Disease Section (Drs. Adcock and Barnes), National Heart and Lung Institute, Imperial College London, London, UK.

Correspondence to: Alberto Papi, MD, Centro di Ricerca su Asma e BPCO, Università di Ferrara, Via Savonarola 9, 44100 Ferrara, Italy; e-mail: alberto.papi@unife.it


Dr. Papi received research funding from and has been on scientific advisory boards for AstraZeneca, Chiesi, GlaxoSmithKline, and UCB; Dr. Caramori has received lecture fees from GSK and Chiesi Farmaceutici; Dr. Adcock received research funding from and has been on scientific advisory boards for GlaxoSmithKline, Chiesi, and AstraZeneca; and Dr. Barnes received research funding from and has been on scientific advisory boards for AstraZeneca, Chiesi, Cipla, GlaxoSmithKline, and UCB.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;135(6):1628-1633. doi:10.1378/chest.08-2536
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International guidelines recommend the use of rapid-onset inhaled β2-agonists alone for symptom relief in all asthmatic patients. However, recent clinical trials have shown that the “as-required,” or PRN, use of inhaled combinations of a corticosteroid and a rapid-onset β2-agonist provides clinical advantages over the traditional PRN inhaled rapid-onset β2-agonists alone in patients with different degrees of asthma severity.

Asthma symptoms are associated not only with bronchoconstriction but also with increased airway inflammation. Inhaled β2-agonists have a rapid onset of bronchodilator action that is mainly mediated by a relaxing effect on airway smooth muscle. Inhaled corticosteroids also have rapid clinical effects that can suppress lower airway inflammation, and there is a rapid synergistic potentiation of the antiinflammatory effect of corticosteroids and of the bronchodilatory action of β2-agonists when the two drugs are given simultaneously. On the basis of this emerging evidence, we propose that the current rescue use of rapid-onset inhaled β2-agonists alone should now be replaced by an inhaled rapid-acting β2-agonist combined with a corticosteroid as preferred PRN strategy. We conclude with a call for clinical trials aimed to test the superiority of this approach in all degrees of asthma severity in a real-world setting in addition to any of the regular treatments recommended by international guidelines. In the future it might even be possible to control asthma entirely with PRN combination inhalers without maintenance therapy, at least in patients with less severe disease.


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