Published ahead of print on January 4, 2007, doi:10.1164/rccm.200511-1746OC
Am. J. Respir. Crit. Care Med., Volume 175, Number 8, April 2007, 783-790
A more recent version of this article appeared on April 15, 2007
Submitted on November 14, 2005
Accepted on January 4, 2007
Smoking Affects Response to Inhaled Corticosteroids or Leukotriene Receptor Antagonists in Asthma
Stephen C Lazarus1*, Vernon M Chinchilli2, Nancy J Rollings2, Homer A Boushey1, Reuben Cherniack3, Timothy J Craig2, Aaron Deykin4, Emily DiMango5, James E Fish6, Jean G Ford5, Elliot Israel4, James Kiley7, Monica Kraft3, Robert F Lemanske, Jr.8, Frank Leone6, Richard J Martin3, Gene R Pesola5, Stephen P Peters6, Christine A Sorkness8, and Stanley J Szefler3
1 The University of California at San Francisco, San Francisco, CA, USA,
2 Pennsylvania State University College of Medicine, Hershey, PA, USA,
3 National Jewish Medical and Research Center, Denver, CO, USA,
4 Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA,
5 Harlem Hospital Center and Columbia University, New York, NY, USA,
6 Thomas Jefferson University, Philadelphia, PA, USA,
7 National Heart, Lung, and Blood Institute, Bethesda, MD, USA,
8 The University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: lazma{at}ucsf.edu.
Rationale:
One-quarter to one-third of asthmatics smoke, which may affect response to therapy and contribute to poor asthma control.
Objectives:
To determine if the response to an inhaled corticosteroid or a leukotriene receptor antagonist is attenuated in asthmatics who smoke.
Methods:
In a multicenter, placebo-controlled double-blind, double-dummy, crossover trial, 44 non-smokers and 39 light smokers with mild asthma were assigned randomly to treatment twice daily with inhaled beclomethasone and once daily with oral montelukast.
Measurements and Main Results:
Primary outcome was change in pre-bronchodilator FEV1 in smokers versus non-smokers. Secondary outcomes included peak flow, Pc20 methacholine, symptoms, quality of life, and markers of airway inflammation. Despite similar FEV1, bronchodilator response, and sensitivity to methacholine
at baseline, asthmatics who smoked had significantly more symptoms, worse quality of life, and lower daily peak flow than non-smokers. Adherence to therapy did not differ significantly between smokers and non-smokers, or between treatment arms. Beclomethasone significantly reduced sputum
eosinophils and ECP in both smokers and non-smokers, but increased FEV1 (170ml, p=0.0003) only in non-smokers. Montelukast significantly increased AM peak flow in smokers (12.6l/min, p=0.002), but not non-smokers.
Conclusions:
In mild asthmatics who smoke, the response to inhaled corticosteroids is attenuated, suggesting that adjustments to standard therapy may be required to attain asthma control. The greater improvement seen in some outcomes in smokers treated with montelukast suggests that leukotrienes may be important in this setting. Larger prospective studies are required to determine whether leukotriene modifiers can be recommended for managing asthma in patients who smoke.
Key words: Anti-Asthmatic Agents, Smoking Adverse Effects, Corticosteroids, Leukotrienes
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