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Original Research: ASTHMA |

Maximal Response Plateau to Adenosine 5′-Monophosphate in Asthma: Relationship With the Response to Methacholine, Exhaled Nitric Oxide, and Exhaled Breath Condensate pH

Luis Prieto, PhD; Saioa Esnal, MD; Victoria Lopez, MD; Desire Barato, MD; Rocio Rojas, RN; Julio Marín, PhD
Author and Funding Information

*From the Asociacion Valenciana de Investigaciones Clinicas (Drs. Prieto, Lopez, and Barato, and Ms. Rojas), Valencia, Spain; Servicio de Alergologia (Dr. Esnal), Hospital Santiago Apostol, Vitoria, Spain; and Universidad de Valencia (Dr. Marín), Valencia, Spain.

Correspondence to: Luis Prieto, PhD, Seccion de Alergologia, Hospital Universitario Dr Peset, Gaspar Aguilar 90, 46017 Valencia, Spain; e-mail: prieto_jes@gva.es


The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

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):1521-1526. doi:10.1378/chest.08-2392
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Background:  No information is available on the plateau in response to adenosine 5′-monophosphate(AMP). The aims of the present study were (1) to determine whether plateau can be detected with AMP and the relation with the plateau in response to methacholine, and (2) to identify the relation between the plateau and indirect markers of airway inflammation, such as exhaled nitric oxide (ENO) and exhaled breath condensate (EBC) pH.

Methods:  Airway responsiveness to high concentrations of methacholine and AMP, ENO levels, and EBC pH values were obtained in 31 subjects with well-controlled asthma. Concentration-response curves were characterized by their concentration of agonist that produces a decrease in FEV1 of 20% and, if possible, by the level of plateau.

Results:  Although the prevalence of plateau with methacholine (48%) and AMP (58%) was similar, the two challenges did not identify plateau in exactly the same individuals. In 14 subjects who showed plateau with both bronchoconstrictor agents, the mean plateau level for methacholine was 26.0% (95% confidence interval [CI], 21.3 to 30.8), compared with 16.5% (95% CI, 12.2 to 20.8; p < 0.0001) for AMP. Both ENO and EBC pH values were similar in subjects with plateau and in those without plateau.

Conclusions:  In well-controlled asthmatics, the plateau in response to AMP can be identified at a milder degree of obstruction than the plateau in response to methacholine, but the two agonists are not identifying the same airway abnormalities. Furthermore, if ENO and EBC pH are markers of inflammation, the determination of the presence or level of plateau is not a reliable method to identify airway inflammation in asthma.

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