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  • Episodic or chronic symptoms of wheezing, dyspnea, or cough.

  • Symptoms frequently worse at night or in the early morning.

  • Prolonged expiration and diffuse wheezes on physical examination.

  • Limitation of airflow on pulmonary function testing or positive bronchoprovocation challenge.

  • Reversibility of airflow obstruction, either spontaneously or following bronchodilator therapy.


Asthma is a common disease, affecting approximately 8–10% of the population. It is slightly more common in male children (younger than 14 years) and in female adults. There is a genetic predisposition to asthma. Prevalence, hospitalizations, and fatal asthma have all increased in the United States over the past 20 years. Each year, approximately 10 million office visits, 1.8 million emergency department visits, and more than 3500 deaths in the United States are attributed to asthma. Hospitalization rates have been highest among blacks and children, and death rates are consistently highest among blacks aged 15–24 years.


Asthma is a chronic disorder of the airways characterized by variable airway obstruction, airway hyperresponsiveness, and airway inflammation. No single histopathologic feature is pathognomonic but common findings include airway inflammatory cell infiltration with eosinophils, neutrophils, and lymphocytes (especially T cells); goblet cell hyperplasia, sometimes plugging of small airways with mucus; collagen deposition beneath the basement membrane; hypertrophy of bronchial smooth muscle; airway edema; mast cell activation; and denudation of airway epithelium. IgE plays a central role in the pathogenesis of allergic asthma. Interleukin-5 is important in promoting eosinophilic inflammation.

The strongest identifiable predisposing factor for the development of asthma is atopy, but obesity is increasingly recognized as a risk factor. Exposure of sensitive patients to inhaled allergens increases airway inflammation, airway hyper-responsiveness, and symptoms. Symptoms may develop immediately (immediate asthmatic response) or 4–6 hours after allergen exposure (late asthmatic response). Common allergens include house dust mites (often found in pillows, mattresses, upholstered furniture, carpets, and drapes), cockroaches, cat dander, and seasonal pollens. Substantially reducing exposure reduces pathologic findings and clinical symptoms.

Nonspecific precipitants of asthma include exercise, upper respiratory tract infections, rhinosinusitis, postnasal drip, aspiration, gastroesophageal reflux, changes in the weather, and stress. Exposure to products of combustion (eg, from tobacco, crack cocaine, methamphetamines, and other agents) increases asthma symptoms and the need for medications and reduces lung function. Air pollution (increased air levels of respirable particles, ozone, SO2, and NO2) precipitate asthma symptoms and increase emergency department visits and hospitalizations. Selected individuals may experience asthma symptoms after exposure to aspirin (aspirin-exacerbated respiratory disease), nonsteroidal anti-inflammatory drugs, or tartrazine dyes. Other medications may precipitate asthma symptoms (see Table 9–24). Occupational asthma is triggered by various agents in the workplace and may occur weeks to years after initial exposure and sensitization. Women may experience catamenial asthma at predictable times during the menstrual cycle. Exercise-induced bronchoconstriction begins during exercise or within 3 minutes after its end, peaks within 10–15 minutes, ...

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