Asthma and lower airway disease
Asthma morbidity among inner-city adolescents receiving guidelines-based therapy: Role of predictors in the setting of high adherence

https://doi.org/10.1016/j.jaci.2009.05.036Get rights and content

Background

With the expanding effort to provide guidelines-based therapy to adolescents with asthma, attention must be directed to evaluating which factors predict future asthma control when guidelines-based management is applied.

Objective

We evaluated the role of fraction of exhaled nitric oxide in parts per billion, markers of allergic sensitization, airway inflammation, and measures of asthma severity in determining future risk of asthma symptoms and exacerbations in adolescents and young adults participating in the Asthma Control Evaluation study.

Methods

Five hundred forty-six inner-city residents, ages 12 through 20 years, with persistent asthma were extensively evaluated at study entry for predictors of future symptoms and exacerbations over the subsequent 46 weeks, during which guidelines-based, optimal asthma management was offered. Baseline measurements included fraction of exhaled nitric oxide in parts per billion, total IgE, allergen-specific IgE, allergen skin test reactivity, asthma symptoms, lung function, peripheral blood eosinophils, and, for a subset, airway hyperresponsiveness and sputum eosinophils.

Results

The baseline characteristics we examined accounted for only a small portion of the variance for future maximum symptom days and exacerbations—11.4% and 12.6%, respectively. Future exacerbations were somewhat predicted by asthma symptoms, albuterol use, previous exacerbations, and lung function, whereas maximum symptom days were predicted, also to a modest extent, by symptoms, albuterol use, and previous exacerbations, but not lung function.

Conclusion

Our findings demonstrate that the usual predictors of future disease activity have little predictive power when applied to a highly adherent population with persistent asthma that is receiving guidelines-based care. Thus, new predictors need to be identified that will be able to measure the continued fluctuation of disease that persists in highly adherent, well-treated populations such as the one studied.

Section snippets

Study population and design

In brief, 546 participants, ages 12 to 20 years, with physician-diagnosed asthma were enrolled at 10 urban locations across the United States. Eligibility was limited to residents of census tracts in which at least 20% of households had incomes below the federal poverty threshold. In addition, individuals had to have evidence of moderate to severe persistent disease. Those receiving long-term control therapy were required to have symptoms of persistent disease or uncontrolled asthma, whereas

Participant characteristics at randomization

Of the 546 participants enrolled, 53% were male, and 64% were black. Table I describes additional demographic characteristics of the population as well as asthma-related symptoms, lung function, atopic status, and degree of allergic inflammation at randomization. The mean number of maximum symptom days over a 2-week period decreased significantly from 5.6 ± 4.6 at enrollment to 2.3 ± 2.9 after the 3-week run-in period at randomization (mean within-participant reduction, 3.4 days/2 weeks; P <

Discussion

Our study reveals that factors often used to predict future asthma risk in poorly controlled populations are of no clinical benefit in predicting future risk in a well treated, highly adherent population of inner-city adolescents and young adults with persistent asthma. We did find that future maximum symptom days and exacerbations could be predicted, but only to a minor extent, by using a combination of asthma-related symptoms and lung function measurements that included FEV1% predicted, FEV1

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    Supported in whole or in part with federal funds from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, under contracts NO1-AI-25496 and NO1-AI-25482 and from the National Center for Research Resources, National Institutes of Health, under grants RR00052, M01 RR00533, M01RR0071, 5UL1RR024992-02, and 5M01RR020359-04.

    Disclosure of potential conflict of interest: R. S. Gruchalla receives consulting fees from GlaxoSmithKline, research support from the National Institute of Allergy and Infectious Diseases/National Institutes of Health, Novartis, and ExxonMobil, and is a board member of the American Board of Allergy and Immunology. H. A. Sampson is a consultant for and 4% shareholder in Allertein Pharmaceuticals, LLC; is on the advisory board for Schering-Plough; receives grants from the Food Allergy Initiative and the National Institute of Allergy and Infectious Diseases/National Institutes of Health; is a consultant and scientific advisor for the Food Allergy Initiative; is 45% owner of Herbal Springs, LLC; and is a board member of the American Academy of Allergy, Asthma, and Immunology. E. Matsui receives research support from the National Institutes of Health. M. Brown is a speaker for GlaxoSmithKline and AstraZeneca and a consultant for Novartis. A. H. Liu is a speaker/consultant for GlaxoSmithKline, Merck, and AstraZeneca and receives research support from GlaxoSmithKline. G. R. Bloomberg receives research support from the National Institute of Allergy and Infectious Diseases/National Institutes of Health. J. F. Chmiel is a consultant for MyCysticFibrosis.com, receives honoraria from the France Foundation, and receives grant support from Cystic Fibrosis Foundation Therapeutics, Inc, and the National Institutes of Health. R. Kumar receives grant support from the National Heart, Lung, and Blood Institute/National Institutes of Health, is a member of the American Thoracic Society, and is vice president of the Illinois Society of Allergy and Immunology. C. A. Sorkness receives consulting fees and speaker honoraria from GlaxoSmithKline and receives research support from Pharmaxis and Schering-Plough. S. F. Steinbach receives research support from the National Institute of Allergy and Infectious Diseases/National Institutes of Health and is on the speakers bureau for Merck and GlaxoSmithKline. K. D. Stone receives research support from the National Institute of Allergy and Infectious Diseases/National Institutes of Health. S. J. Szefler is a consultant for GlaxoSmithKline, Genentech, and Merck and receives research support from the National Heart, Lung, and Blood Institute/National Institutes of Health, the National Institute of Allergy and Infectious Diseases/National Institutes of Health, Ross Pharmaceuticals, and GlaxoSmithKline. W. W. Busse is a consultant for Altair, GlaxoSmithKline, Merck, Wyeth, Pfizer, Centocor, Amgen, UCB, Johnson & Johnson, Novartis, AstraZeneca, Eisai, TEVA, CompleWare, KaloBios, and Boehringer Ingelheim Sandoz and receives research support from the National Heart, Lung, and Blood Institute/National Institutes of Health, the National Institute of Allergy and Infectious Diseases/National Institutes of Health, Novartis, Centocor, GlaxoSmithKline, MedImmune, and Ception. The rest of the authors have declared that they have no conflict of interest.

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