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Volume 124, Issue 5, Pages 921-927 (November 2009)


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Recent asthma exacerbations predict future exacerbations in children with severe or difficult-to-treat asthma

Tmirah Haselkorn, PhDaCorresponding Author Informationemail address, Robert S. Zeiger, MD, PhDb, Bradley E. Chipps, MDc, David R. Mink, MSd, Stanley J. Szefler, MDe, F. Estelle R. Simons, MDf, Marc Massanari, PharmDg, James E. Fish, MDa

Received 1 April 2009; received in revised form 22 August 2009; accepted 3 September 2009.

Background

Children with severe/difficult-to-treat asthma experience high morbidity including frequent severe exacerbations. More knowledge is required to identify predictors of these exacerbations to reduce their occurrence.

Objective

To investigate the risk of future severe exacerbations (FSEs) in children with severe/difficult-to-treat asthma and recent severe exacerbations (RSEs).

Methods

We analyzed the occurrence and association of RSE (defined as 1 or more corticosteroid bursts during the 3 months before each of 3 annual visits) and FSE (defined as 1 or more corticosteroid bursts 6 or 12 months later) in children age 6 to 11 years in The Epidemiology and Natural History of Asthma: Outcomes and Treatment Regimens 3-year observational study. Repeated measures logistic regression analysis assessed the risk of FSE adjusted for demographics and clinical variables.

Results

In a multivariable model, FSE at 6 months was most strongly predicted by RSE (odds ratio [OR], 3.08; 95% CI, 2.21-4.28) and having 3 to 4 allergic triggers (OR, 2.05; 95% CI, 1.31-3.20). Race (OR, 1.77; 95% CI, 1.25-2.51) and being very poorly controlled according to the impairment component of the National Heart, Lung, and Blood Institute guidelines (OR, 1.59; 95% CI, 1.14-2.23) also significantly predicted FSE.

Conclusion

Recent severe asthma exacerbations are an important independent predictor of FSE in children with severe/difficult-to-treat asthma and should be considered when establishing asthma management plans.

a Genentech, Inc, South San Francisco, Calif

b Kaiser-Permanente Medical Center, San Diego, Calif

c Capital Allergy and Respiratory Disease Center, Sacramento, Calif

d ICON Clinical Research, San Francisco, Calif

e National Jewish Health, Denver, Colo

f University of Manitoba, Winnipeg, Manitoba, Canada

g Novartis Pharmaceuticals Corp, East Hanover, NJ

Corresponding Author InformationReprint requests: Tmirah Haselkorn, PhD, Genentech, Inc, 1 DNA Way, MS 58B, South San Francisco, CA 94080.

 Support for third-party medical writing assistance was provided by Genentech USA, Inc, and Novartis Pharmaceuticals Corp.

 Disclosure of potential conflict of interest: T. Haselkorn is a consultant for Genentech. R. S. Zeiger is a consultant for Aerocrine, AstraZeneca, Dynavax, Genentech, GlaxoSmithKline, Merck, Novartis, and Schering-Plough and has received research support from AstraZeneca, Merck, GlaxoSmithKline, TEVA, Aerocrine, and the National Heart, Lung, and Blood Institute. B. E. Chipps is an advisor and/or speakers' bureau member for Alcon, Aventis, Genentech, AstraZeneca, Boehringer, GlaxoSmithKline, MedPoint, Novartis, Pfizer, Schering, Sepracor, and Merck and has received support for research and/or educational activities from Alcon, Aventis, Genentech, AstraZeneca, GlaxoSmithKline, MedPoint, Novartis, Schering, Sepracor, and Merck. D. R. Mink is an employee of ICON Clinical Research, which receives research funding from Genentech. S. J. Szefler is a consultant for GlaxoSmithKline, Genentech, and Merck and has received research support from the National Institutes of Health, the National Heart, Lung, and Blood Institute, the National Institute of Allergy and Infectious Diseases, Ross Pharmaceuticals, and GlaxoSmithKline. F. E. R. Simons has received research support from the Canadian Institutes of Health Research and has consulted for Genentech. M. Massanari is an employee of Novartis. J. E. Fish is an employee of Genentech.

PII: S0091-6749(09)01335-9

doi:10.1016/j.jaci.2009.09.006


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