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Asthma is a chronic inflammatory disorder characterized by increased responsiveness of the airways to multiple stimuli. In susceptible individuals, the inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes usually are associated with widespread and varying airflow obstruction.

Although most acute attacks are reversible and improve spontaneously or within minutes to hours with treatment with symptom-free intervals in between, many asthmatic patients develop chronic airflow limitation. This impacts the diagnosis of, management of, and attempts to prevent acute exacerbations.

Asthma affects approximately 8% of the U.S. population, is the most common chronic disease of childhood (9% prevalence), affects 7% of the elderly, and has a similar prevalence in developed nations around the world.1,2,3 Approximately one half of cases of asthma develop before the age of 10 years old, and another one third develop before the age of 40 years old.


Asthma is characterized by an abnormal accumulation of eosinophils, lymphocytes, mast cells, macrophages, dendritic cells, and myofibroblasts in airways. The pathophysiologic hallmark of asthma is a reduction in airway diameter caused by smooth muscle contraction, vascular congestion, bronchial wall edema, and thick secretions. These changes are reflected in pulmonary function changes, increased work of breathing, and abnormal distribution of pulmonary blood flow (Table 69-1). Large and small airways contain plugs composed of mucus, serum proteins, inflammatory cells, and cellular debris. On a microscopic level, airways are infiltrated with eosinophils and mononuclear cells. Evidence of microvascular leakage, epithelial disruption, and vasodilation is frequently noted. The airway smooth muscle is hypertrophied and characterized by new vessel formation, an increased number of epithelial goblet cells, and deposition of interstitial collagen beneath the epithelium. Inflammation affects all bronchial pulmonary structures.

TABLE 69-1Physiologic Consequences of Airflow Obstruction

Asthma is a continuum from acute bronchospasm to airway inflammation to permanent airway remodeling. The structural changes associated with airway remodeling, such as sub–basement membrane thickening, subepithelial fibrosis, airway smooth muscle hypertrophy and hyperplasia, angiogenesis, and mucous gland hyperplasia and hypersecretion are associated with nonreversible loss of lung function.4 Acute allergic bronchoconstriction results from immunoglobulin E–dependent release of mediators from mast cells. These mediators include histamine, leukotrienes, tryptase, and prostaglandins that directly contract airway smooth muscle.4 Bronchospasm induced by aspirin and other nonsteroidal anti-inflammatory drugs also involves mediator release from airway cells.4

Inflammation plays a key role in the pathophysiology of asthma regardless of disease severity. Inhaled antigens activate immunoglobulin E, ...

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