Asthma is a chronic disease characterized by inflammation of the airways and reversible bronchoconstriction resulting in wheezing, coughing, shortness of breath, and exercise intolerance. It affects 26 million people worldwide at some time in their lives. Among that number, 10.6 million have had an episode of asthma within the past year. The prevalence of asthma is increasing, particularly in young people. It is the number one serious chronic illness among children and is the primary cause of school-related absence.
Between 1982 and 1994, the prevalence of asthma increased by 61.2% in the overall population and by 72.3% in the pediatric population. The impact of uncontrolled asthma on the healthcare system is significant. Each year, asthma claims the lives of 5,000 Americans and costs the healthcare system more than $12.4 billion. These trends in prevalence, mortality and economic impact signal the need for earlier and more aggressive diagnosis and treatment of this chronic and potentially life-threatening disease.
In 1997, the National Heart, Lung, and Blood Institute released an updated set of guidelines for the diagnosis and management of asthma. In their treatment guidelines, asthma is described as a chronic inflammatory disorder in which mast cells, eosinophils, T-lymphocytes, and other cellular elements contribute to ongoing inflammation. These inflammatory cells secrete mediators that affect airway function either directly or through neural mechanisms.
Inflammatory mediators can cause airway injury through increased smooth muscle responsiveness, mucus hypersecretion, altered vascular permeability, aberrations in control of autonomic neural tone, and alterations in mucociliary function. These mediators also cause proliferation of epithelial cells and myofibroblasts that deposit collagen beneath the basement membrane. This can cause subendothelial thickening, leading to possibly irreversible airway changes.
Asthma is also associated with an exaggerated bronchoconstrictor response to various stimuli, which is mediated through the beta2 receptors on the airway. This hyperresponsiveness is correlated with airway inflammation which may be controlled with anti-inflammatory therapy, but not completely eradicated by it. Changes in the airway associated with the activation of inflammatory mediators include acute bronchoconstriction, airway edema, chronic mucus plug formation, and airway “remodeling” (i.e., irreversible thickening of the basement membrane). These changes lead to bronchial obstruction, resulting in limited airflow. Thus, inflammation contributes to airway hyperresponsiveness, respiratory symptoms, limited airflow, and a chronic disease process.
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