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The pharmacogenetics of asthma: a candidate gene approach

The Pharmacogenomics Journal volume 1, pages 27–37 (2001)Cite this article

Asthma is a common respiratory syndrome characterized by partially reversible airflow obstruction, airway hyperresponsiveness, and airway inflammation. The syndrome is caused by a complex interaction between genetic and environmental factors that results in a spectrum of biologic and clinical features. Among the spectrum of features is a highly variable response to asthma therapeutics. There are currently three major classes of asthma therapeutics available: (1) beta2-agonists (β-agonist); (2) glucocorticoids (GC); and (3) inhibitors of the cysteinyl-leukotriene pathway (cLI). Asthmatic patients vary greatly in their response to all three classes of drugs and it is estimated that up to 60–80% of this variability may have a pharmacogenetic basis. Over the past 10 years, several polymorphic loci have been discovered in genes that play a role in the action of these drugs. Data suggest that these polymorphisms directly or indirectly alter an asthmatic’s response to therapy and can be used to predict the response to certain asthma drugs, thereby maximizing efficacy and avoiding adverse effects. It is likely that many, as yet undiscovered, polymorphisms exist given the large number of gene products involved in the pharmacodynamic and pharmacokinetic pathways of all three classes of asthma drugs. In this review we discuss the established asthma pharmacogenetic loci and describe a candidate gene approach that is being used to uncover additional polymorphisms with pharmacogenetic potential.

Asthma is a clinical syndrome with three defining characteristics: (1) recurrent episodes of airway obstruction that resolve either spontaneously or as a result of therapy; (2) increased airway hyperresponsiveness, which is an increased bronchoconstrictor response to stimuli that would have little or no effect in nonasthmatic subjects; and (3) chronic airway inflammation, often with abundant eosinophils.1,2,3 Asthma severity is usually measured by the presence or absence of symptoms, the frequency of exacerbations, and the degree of airflow resistance as measured by the forced expiratory volume in one second (FEV1). As a clinical problem, asthma is both prevalent and associated with substantial morbidity. There are approximately 17 million asthmatic patients in the United States (6% of the adult population), and asthma is the number one cause of hospitalizations and emergency room visits for children. The health care costs approximate 8 billion dollars per year of which 35–40% are due to medication costs. Moreover, the problem has been getting worse with a worldwide increase in prevalence of 30% over the two past decades.4 Strategies to more effectively treat this syndrome would be of great benefit.

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Acknowledgements

Supported by UO1 HL65899 from the National Heart, Lung, and Blood Institutes of the National Institutes of Health.

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Authors and Affiliations

  1. Department of Medicine, Channing Laboratory, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA

    E S Silverman, R M Baron, S T Weiss & J M Drazen

  2. Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA

    S B Liggett

  3. Departments of Medicine and Pediatrics, National Jewish Medical and Research Center, University of Colorado Health Sciences Center, Denver, CO, USA

    E W Gelfand & L J Rosenwasser

  4. Whitehead Institute for Genome Research, Massachusetts Institute of Technology, Boston, MA, USA

    S Bolk

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Silverman, E., Liggett, S., Gelfand, E. et al. The pharmacogenetics of asthma: a candidate gene approach. Pharmacogenomics J 1, 27–37 (2001). https://doi.org/10.1038/sj.tpj.6500005

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