Volume 121, Issue 3 , Pages 607-613, March 2008
Natural history of asthma: Persistence versus progression—does the beginning predict the end?
Environmental exposures during the early years and airway obstruction that develops during this time, in conjunction with genetic susceptibility, are important factors in the development of persistent asthma in childhood. Established risk factors for childhood asthma include frequent wheezing during the first 3 years, a parental history of asthma, a history of eczema, allergic rhinitis, wheezing apart from colds, and peripheral blood eosinophilia, as well as allergic sensitization to aeroallergens and certain foods. Risk factors for the development of asthma in adulthood remain ill defined. Moreover, reasons for variability in the clinical course of asthma—persistence in some individuals and progression in others—remain an enigma. The distinction between disease persistence and disease progression suggests that these are different entities or phenotypes. There is currently no consensus on whether disease progression requires either airway inflammation or airway remodeling or the combination of the two. For patients with irreversible airway obstruction, inflammation might, in part, be necessary but perhaps not entirely sufficient to induce the irreversible component, some of which could be attributed to alterations in the structure of the bronchial wall. Intervening with intermittent or daily inhaled corticosteroids in high-risk infants and children does not prevent disease progression or impaired lung growth. These findings, however, might not apply to adults, and further study in adults is needed to determine the effect of inhaled corticosteroid therapy on disease progression.
Key words: Asthma, epidemiology, progression, persistence, remodeling, wheezing, childhood asthma, adult asthma, atopy, inhaled corticosteroids
Abbreviations used: API, Asthma Predictive Index, CAMP, Childhood Asthma Management Program, FVC, Forced vital capacity, RBM, Reticular basement membrane
Elizabeth Hillyer was supported by Merck & Co, Inc, Whitehouse Station, NJ.
Disclosure of potential conflict of interest: R. Covar has received research support from AstraZeneca and Ross Abbott Laboratories, Inc. E. V. Hillyer has received freelance writing work from Merck and Aerocrine. L. Bacharier has consulting arrangements with Schering-Plough and is on the speakers' bureau for AstraZeneca, Genentech, GlaxoSmithKline, and Merck. The rest of the authors have declared that they have no conflict of interest.
This article originated, in part, from a discussion at the National Respiratory Experts Forum, held June 15-17, 2006, in Chicago, IL. This was a scientific forum, sponsored by Merck, where specific topics and questions were explored for issues pertinent to the fields of asthma and respiratory medicine.
PII: S0091-6749(08)00134-6
doi:10.1016/j.jaci.2008.01.006
© 2008 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Volume 121, Issue 3 , Pages 607-613, March 2008
