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Chairman's Remarks

Northwestern University, Feinberg School of Medicine, Chicago, Illinois

Most drugs in use for the treatment of asthma and chronic obstructive pulmonary disease (COPD) are traceable to compounds that have been used for centuries. Modern sympathomimetics were preceded by teas containing ephedra and then by adrenal extracts containing epinephrine. The anticholinergic drugs we use are descended from scopolamine- and atropine-containing preparations that were smoked. Phosphodiesterase inhibitors are evolved from a lineage that first exploited coffees and teas containing caffeine, theobromine, or theophylline. Likewise, corticosteroids were first used in the form of adrenal extracts in the late 1800s. In the middle of the twentieth century, the discovery of cortisone initiated the modern era of corticosteroid pharmacology. Unlike any of the classes of drugs mentioned above, corticosteroids are potent antiinflammatory drugs that inhibit tissue responses to injury and exposure. These tissue responses are designed to protect the lungs, but, because of their extent or localization, they inadvertently damage or obstruct the airways.

Corticosteroids are widely used in the therapeutic management of inflammatory diseases that affect many organ systems. Modern compounds and delivery systems focus these drugs quite well for use in the lungs and minimize systemic effects. As a class of medications, corticosteroids are peerless in their ability to prevent exacerbations of asthma, a fact that serves as an important rationale for their popularity. Many large studies have shown that inhaled corticosteroids prevent exacerbations and death in severe COPD; this is an area of continued investigation. The widespread use of oral corticosteroids to treat exacerbations of COPD reflects the broad perception that corticosteroids are beneficial in this disease.

Asthma and COPD are two of a small number of major diseases that have been increasing in prevalence in the past few decades. Although these diseases have some similarities, including airway obstruction, bronchoconstriction, chronicity (i.e., variability), and the host response as a source of pathogenesis, they differ in many important ways. Asthma is usually initiated by infinitesimally small amounts of exposure to otherwise innocuous protein antigens, while COPD is usually driven by exposure to large quantities of noxious smoke (primarily derived from cigarettes) that contains particulates and gases that can trigger a range of host responses designed for clearance and repair. In each case, and for reasons that are not entirely clear, disease develops in only a subset of individuals in response to these respective exposures.

This supplement reports the ideas and information presented at the Congress on Inhaled Corticosteroids for the Treatment of Asthma and COPD that was held in New York on July 11–13, 2003. An international panel of experts considered the beneficial effects of corticosteroids in the treatment of asthma and COPD and the mechanisms by which they improve quality of life, if not always lung function, in affected patients. We took a bedside-to-bench approach, starting with consideration of epidemiology, physiology, side effects, pathology, outcomes, and large therapeutic trials, then moving to basic science. Presentations on the cellular and molecular basis of corticosteroid action and disease pathogenesis were divided by cell type and advanced the theme of the meeting—the similarities and differences between asthma and COPD. The congress considered the molecular biology of corticosteroid action, with an eye toward recent discoveries that may serve as a wellspring for new therapeutic strategies, as well as improving our understanding of the molecular basis of the heterogeneity of patient responses to medication.

I would like to thank the congress faculty and participants who so generously made special efforts to apply their expertise to the goals of the meeting. I would also like to thank my colleagues on the program/organizing committee, Drs. Peter Barnes, James Donohue, Malcolm Johnson, and Donald Mahler. They made this not only a successful project, as I hope this supplement will prove, but also a thoroughly enjoyable experience. On behalf of the organizers, I would like to thank the staff of HealthMatters Communications for their cheerful and skillful efforts in organizing the meeting and this supplement. Finally, I would like to offer special thanks to GlaxoSmithKline, which generously provided financial support for the meeting on which this supplement is based through an independent educational grant.

	ACKNOWLEDGMENTS

 
R.P.S. received $2,500 from GlaxoSmithKline in 2002 and $2,500 in 2003, and received $3,000 from Aventis Pharmaceuticals in 2002 and $4,000 in 2003, and received $10,000 a year in 2001, 2002, and 2003 from Dynavax, and his laboratory received $60,000 from GlaxoSmithKline in 2002 and $48,000 in 2003.

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