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Dirkje S. Postma, MD; Michael D. Lebowitz, PhD

Arch Intern Med. 1995;155(13):1393-1399.

Abstract
Background
Some patients with chronic obstructive pulmonary disease may share the clinical characteristics of those with asthma; their disease is sometimes called "asthmatic bronchitis." Whether there is a difference between asthmatics who do and do not develop chronic bronchitis is not yet clear. We investigated whether asthma and chronic bronchitis may share some "allergic" phenotypes and whether asthmatic individuals who develop chronic bronchitis subsequently have steeper declines in lung function.

Methods
Known risk factors for decline in lung function were analyzed in a representative community population of adults followed up longitudinally since 1972 in Tucson, Ariz, in groups with persistent, newly developed, and past diagnoses of asthma and chronic bronchitis. We evaluated contributions of initial level of forced expiratory volume in 1 second (FEV₁), reversibility with isoproterenol hydrochloride nebulized aerosol bronchodilator treatment, percentage of blood eosinophils to determine eosinophilia, and IgE level.

Results
The concurrence of chronic bronchitis and asthma is associated with a steeper decline in FEV₁ than is asthma as the sole diagnosis. Asthmatics (those with persistent asthma with and without chronic bronchitis) had the greatest prevalence of increased reversibility with isoproterenol therapy and with eosinophilia. The prevalence of eosinophilia was also high in those with newly diagnosed chronic bronchitis without asthma; however, this was not the case in those with persistent chronic bronchitis without asthma. Larger bronchodilator responses were related to steeper declines in FEV₁, both in persistent asthma and in chronic bronchitis.

Conclusions
Bronchodilator response and eosinophilia are generally believed to be hallmarks of asthma. We show that these characteristics may be present in chronic bronchitis as well. The presence of a large (>25%) bronchodilator response is associated with a steeper decline in FEV₁.

(Arch Intern Med. 1995;155:1393-1399)

Author Affiliations
From the Departments of Pulmonology and Medicine, State University of Groningen (the Netherlands) (Dr Postma), and the Respiratory Sciences Center and Department of Medicine, University of Arizona College of Medicine, Tucson (Dr Lebowitz).

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