Introduction
Background
Asthma is an airway disorder that causes respiratory hypersensitivity, inflammation, and intermittent obstruction. Asthma commonly causes constriction of the smooth muscles in the airway, wheezing, and dyspnea.
Asthma is a common chronic disease worldwide and affects 22 million persons in the United States. Asthma is the most common chronic disease in childhood, affecting an estimated 6 million children, and it is a common cause of hospitalization for children in the United States.
Despite recent advances in the understanding of the pathophysiology, assessment, and treatment of asthma, the condition continues to have significant medical and economic impacts worldwide. In 1991, the National Asthma Education and Prevention Program Expert Panel from the US National Institutes of Health issued its first report on the guidelines for the diagnosis and management of asthma. They defined asthma as follows:
Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial responsiveness to a variety of stimuli. Reversibility of airflow limitation may be incomplete in some patients with asthma.
The most recent 2007 Expert Panel Report 3 simplified the definition to the following:
The Expert Panel Report 2 was issued in 1997 and further refined effective asthma management and assessment based on the following components1 :Asthma is a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation. The interaction of these features of asthma determines the clinical manifestations and severity of asthma and the response to treatment.
- Objective measures of lung function
- Environmental control measures
- Comprehensive pharmacologic therapy
- Patient education
The most recent and updated Expert Panel Report 3 was recently published in 2007 and emphasizes new areas of severity, control, impairment, and risk that are key to maintaining asthma control.2 A major difference is the emphasis on asthma control. The revised paradigm for asthma management now recommends that asthma management and assessment decisions should be initially based on categorization of asthma severity and, subsequently, on assessment of asthma control.
Exercise-induced asthma (EIA), or exercise-induced bronchospasm (EIB), is an asthma variant defined as a condition in which exercise or vigorous physical activity triggers acute bronchospasm in persons with heightened airway reactivity. It is observed primarily in persons who have asthma (exercise-induced bronchospasm in asthmatic persons) but can also be found in patients with normal resting spirometry findings with atopy, allergic rhinitis, or cystic fibrosis and even in healthy persons, many of whom are elite athletes (exercise-induced bronchospasm in athletes). Exercise-induced bronchospasm is often a neglected diagnosis, and the underlying asthma may be silent in as many as 50% of patients, except during exercise.3,4
Currently, 2 comprehensive guidelines (published in 2007) are available for asthma diagnosis, assessment, and asthma treatment. Additionally, both publications have summary guidelines that were developed for clinicians. These 2 extensive publications are as follows:
- National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health, 2007 Revision.2
- National Heart, Lung, and Blood Institute. Global strategy for asthma management and prevention. National Institutes of Health, 2008 Revision.5
Additionally, the following summary guidelines may be a helpful resource:
- Key clinical activities for quality asthma care: recommendations of the National Asthma Education and Prevention Program.6
- Education for a partnership in asthma care. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma.7
- Managing asthma long term-special situations. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma.8
- Managing exacerbations of asthma. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma.9
- Measures of asthma assessment and monitoring. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma.10
- Medications. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma.11
- Managing asthma long term in children 0-4 years of age and 5-11 years of age. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma.12
- Managing asthma long term in youths >=12 years of age and adults. In: National Asthma Education and Prevention Program (NAEPP). Expert panel report 3: guidelines for the diagnosis and management of asthma.13
Pathophysiology
The pathophysiology of asthma is complex and involves the following components:
- Airway inflammation
- Intermittent airflow obstruction
- Bronchial hyperresponsiveness
The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity. Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present.14
Asthma causes and symptoms. Antigen presentation by the dendritic cell with the lymphocyte and cytokine response leading to airway inflammation and asthma symptoms.
Some of the principal cells identified in airway inflammation include mast cells, eosinophils, epithelial cells, macrophages, and activated T lymphocytes. T lymphocytes play an important role in the regulation of airway inflammation through the release of numerous cytokines. Other constituent airway cells, such as fibroblasts, endothelial cells, and epithelial cells, contribute to the chronicity of the disease. Other factors, such as adhesion molecules (eg, selectins, integrins), are critical in directing the inflammatory changes in the airway. Finally, cell-derived mediators influence smooth muscle tone and produce structural changes and remodeling of the airway.15,16
The presence of airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma.
Airflow obstruction can be caused by a variety of changes, including acute bronchoconstriction, airway edema, chronic mucous plug formation, and airway remodeling. Acute bronchoconstriction is the consequence of immunoglobulin E–dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response. Airway edema occurs 6-24 hours following an allergen challenge and is referred to as the late asthmatic response. Chronic mucous plug formation consists of an exudate of serum proteins and cell debris that may take weeks to resolve. Airway remodeling is associated with structural changes due to long-standing inflammation and may profoundly affect the extent of reversibility of airway obstruction.17
The 2007 Expert Panel Report 3 noted several key new differences in the pathophysiology of asthma, as follows:- The critical role of inflammation has been further substantiated, but evidence is emerging for considerable variability in the pattern of inflammation, thus indicating phenotypic differences that may influence treatment responses.
- Of the environmental factors, allergic reactions remain important. Evidence also suggests a key and expanding role for viral respiratory infections in these processes.
- The onset of asthma for most patients begins early in life, with the pattern of disease persistence determined by early, recognizable risk factors including atopic disease, recurrent wheezing, and a parental history of asthma.
- Current asthma treatment with anti-inflammatory therapy does not appear to prevent progression of the underlying disease severity.
The pathogenesis of exercise-induced bronchospasm is controversial. The disease may be mediated by water loss from the airway, heat loss from the airway, or a combination of both. The upper airway is designed to keep inspired air at 100% humidity and body temperature at 37°C (98.6°F). The nose is unable to condition the increased amount of air required for exercise, particularly in athletes who breathe through their mouths. The abnormal heat and water fluxes in the bronchial tree result in bronchoconstriction, occurring within minutes of completing exercise. Results from bronchoalveolar lavage studies have not demonstrated an increase in inflammatory mediators. These patients generally develop a refractory period, during which a second exercise challenge does not cause a significant degree of bronchoconstriction.
Frequency
United States
Asthma affects 5-10% of the population or an estimated 22 million persons, including 6 million children. The overall prevalence rate of exercise-induced bronchospasm is 3-10% of the general population if persons who do not have asthma or allergy are excluded, but the rate increases to 12-15% of the general population if patients with underlying asthma are included. The rate of exercise-induced symptoms in persons with asthma has been reported to vary from 40-90%.18
International
Asthma is common in industrialized nations such as Canada, England, Australia, Germany, and New Zealand, where much of the asthma data have been collected. The prevalence rate of severe asthma in industrialized countries ranges from 2-10% and is estimated to affect 300 million persons worldwide. Trends suggest an increase in both the prevalence and morbidity of asthma, especially in children younger than 6 years. Factors that have been implicated include urbanization, air pollution, passive smoking, and change in exposure to environmental allergens.
Mortality/Morbidity
- The estimate of lost work and school time from asthma is approximately 100 million days of restricted activity. More than 1.8 million emergency department evaluations for asthma occur annually. The figures from the 1997 National Institutes of Health report1 an estimated 500,000 hospitalizations and 5,000 deaths from asthma annually. International asthma mortality is reported as high as 0.86 deaths per 100,000 persons in some countries. US asthma mortality rates in 2002 were reported at 1.5 deaths per 100,000 persons. Mortality is primarily related to lung function, with an 8-fold increase in patients in the lowest quartile, but mortality has also been linked with asthma management failure, especially in young persons. Other factors that impact mortality include age older than 40 years, cigarette smoking more than 20-pack years, blood eosinophilia, forced expiratory volume in one second (FEV1) of 40-69% predicted, and greater reversibility.19
- Exercise-induced bronchospasm has not been reported to cause death. Morbidity is associated with exercise limitation. This is observed most dramatically in elite athletes with high levels of exercise who may be limited by airway hyperreactivity. Exercise-induced bronchospasm in asthmatic persons generally does not cause significant morbidity.
Race
- Asthma occurs in persons of all races worldwide. In the United States, asthma prevalence, especially morbidity and mortality, is higher in blacks than in whites.
- Although genetic factors are of major importance in determining a predisposition to the development of asthma, environmental factors play a greater role than racial factors in asthma onset. A national concern is that some of the increased morbidity is due to differences in asthma treatment afforded certain minority groups.
Sex
- Asthma predominantly occurs in boys in childhood, with a male-to-female ratio of 2:1 until puberty, when the male-to-female ratio becomes 1:1.
- Asthma prevalence is greater in females after puberty, and the majority of adult-onset cases diagnosed in persons older than 40 years occur in females.
- Boys are more likely than girls to experience a decrease in symptoms by late adolescence.
Age
- Asthma prevalence is increased in very young persons and very old persons because of airway responsiveness and lower levels of lung function.20 Two thirds of all asthma cases are diagnosed before the patient is aged 18 years. Approximately half of all children diagnosed with asthma have a decrease or disappearance of symptoms by early adulthood.21
- The assessment and diagnosis of exercise-induced bronchospasm is made more often in children and young adults than in older adults and is related to high levels of physical activity. Exercise-induced bronchospasm can be observed in persons of any age based on the level of underlying airway reactivity and the level of physical exertion.
Clinical
History
A detailed assessment of the medical history should address (1) whether symptoms are attributable to asthma, (2) whether findings support the likelihood of asthma (eg, family history), (3) asthma severity, and (4) the identification of possible precipitating factors.
- Asthma symptoms may include the following:
- Cough, worse particularly at night22
- Wheezing
- Shortness of breath
- Chest tightness
- Sputum production
- Decreased exercise tolerance
- Asthma symptom patterns can vary as follows:
- Perennial versus seasonal
- Continual versus episodic
- Duration, severity, and frequency
- Diurnal variations (nocturnal and early-morning awakenings)
- Precipitating or aggravating factors for asthma, also discussed in Causes, may include the following:
- Environmental allergen exposure (dust mites, pet dander, pollens)
- Occupation
- Medications
- Exercise
- Viral upper respiratory tract infections
- Strong emotional expression
- Menstrual cycles
- Airborne dusts or chemicals
- Asthma development variables include the following:
- Age at onset
- History of injury early in life due to infection or passive smoke exposure
- Progress of disease
- Current response to asthma management
- Comorbid conditions (sinusitis, rhinitis, gastroesophageal reflux)
- Family history may reveal the following conditions:
- Social history may reveal the following conditions:
- Home characteristics
- Smoking
- Workplace or school characteristics
- Educational level
- Employment
- Social support
- Determine the profile of a typical asthma exacerbation.
- The impact asthma has on the patient and family may have involved the following:
- Emergency department visits, hospitalizations, ICU admissions, intubations
- Missed days from work or school or activity limitation
- Assess the patient's disease perception based on the following elements:
- Knowledge of asthma and treatment
- Use of medications
- Coping mechanisms
- Family support
- Economic resources
The clinical history findings for exercise-induced bronchospasm are typical of asthma but are only associated with exercise. Typical symptoms include cough, wheezing, shortness of breath, and chest pain or tightness. Some individuals also may report sore throat or GI upset.
- Asthma symptoms are usually associated with exercise but may be related to exposure to cold air or other triggers, such as seasonal allergens, pollutants (eg, sulfur, nitrous oxide, ozone), or upper respiratory tract infections.
- Initially, airway dilation is noted during exercise. If exercise continues beyond approximately 10 minutes, bronchoconstriction supervenes, resulting in asthma symptoms. If the exercise period is shorter, symptoms may develop up to 5-10 minutes after completion of exercise. A higher intensity level of exercise results in a more intense attack. Running produces more symptoms than walking.
- Patients may note asthma symptoms are related to seasonal changes or the ambient temperature and humidity in the environment in which a patient exercises. Cold, dry air generally provokes more obstruction than warm, humid air. Consequently, many athletes have good exercise tolerance in sports such as swimming. Athletes who are more physically fit may not notice the typical asthma symptoms and may only report a reduced or more limited level of endurance.
- Several modifiers in the history should prompt an evaluation for causes other than exercise-induced bronchospasm. While patients may report typical obstructive symptoms, a history of a choking sensation with exercise, inspiratory wheezing, or stridor should prompt an evaluation for evidence of vocal cord dysfunction.
Physical
- General asthma physical findings
- Evidence of respiratory distress manifests as increased respiratory rate, increased heart rate, diaphoresis, and use of accessory muscles of respiration.
- Marked weight loss or severe wasting may indicate severe emphysema.
- Pulsus paradoxus: This is an exaggerated fall in systolic blood pressure during inspiration and may occur during an acute asthma exacerbation.
- Depressed sensorium: This finding suggests a more severe asthma exacerbation with impending respiratory failure.
- Chest examination
- End-expiratory wheezing or a prolonged expiratory phase is found most commonly, although inspiratory wheezing can be heard.
- Diminished breath sounds and chest hyperinflation (especially in children) may be observed during acute asthma exacerbations.
- The presence of inspiratory wheezing or stridor may prompt an evaluation for an upper airway obstruction such as vocal cord dysfunction, vocal cord paralysis, thyroid enlargement, or a soft tissue mass (eg, malignant tumor).
- Upper airway
- Look for evidence of erythematous or boggy turbinates or the presence of polyps from sinusitis, allergic rhinitis, or upper respiratory tract infection.
- Any type of nasal obstruction may result in worsening of asthma or symptoms of exercise-induced bronchospasm.
- Skin: Observe for the presence of atopic dermatitis, eczema, or other manifestations of allergic skin conditions.
Causes
- Factors that can contribute to asthma or airway hyperreactivity may include any of the following:
- Environmental allergens: House dust mites, animal allergens (especially cat and dog), cockroach allergens, and fungi are most commonly reported.
- Viral respiratory tract infections
- Exercise; hyperventilation
- Gastroesophageal reflux disease
- Chronic sinusitis or rhinitis
- Aspirin or nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity, sulfite sensitivity
- Use of beta-adrenergic receptor blockers (including ophthalmic preparations)
- Obesity: Based on a prospective cohort study of 86,000 patients, those with an elevated body mass index are more likely to have asthma.
- Environmental pollutants, tobacco smoke
- Occupational exposure
- Irritants (eg, household sprays, paint fumes)
- Various high and low molecular weight compounds: A variety of high and low molecular weight compounds are associated with the development of occupational asthma, such as insects, plants, latex, gums, diisocyanates, anhydrides, wood dust, and fluxes.
- Emotional factors or stress
- Perinatal factors: Prematurity and increased maternal age increase the risk for asthma; breastfeeding has not been definitely shown to be protective. Both maternal smoking and prenatal exposure to tobacco smoke also increase the risk of developing asthma.
- Factors that contribute to exercise-induced bronchospasm symptoms (in both people with asthma and athletes) include the following:
- Exposure to cold or dry air
- Environmental pollutants (eg, sulfur, ozone)
- level of bronchial hyperreactivity
- Chronicity of asthma and symptomatic control
- Duration and intensity of exercise
- Allergen exposure in atopic individuals
- Coexisting respiratory infection
More on Asthma |
 Overview: Asthma |
| Differential Diagnoses & Workup: Asthma |
| Treatment & Medication: Asthma |
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References
[Guideline] National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the diagnosis and management of asthma. NIH Publication No. 97-4051. NIH Publication. 1997;[Full Text].
[Guideline] National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma. NIH Publication No. 07-4051. 2007.
McFadden ER Jr. Exercise-induced airway obstruction. Clin Chest Med. Dec 1995;16(4):671-82. [Medline].
Randolph C. Exercise-induced asthma: update on pathophysiology, clinical diagnosis, and treatment. Curr Probl Pediatr. Feb 1997;27(2):53-77. [Medline].
[Guideline] National Heart, Lung, and Blood Institute. Global Strategy for Asthma Management and Prevention. NIH Publication. 2008;[Full Text].
[Guideline] Williams SG, Schmidt DK, Redd SC, Storms W. Key clinical activities for quality asthma care. Recommendations of the National Asthma Education and Prevention Program. MMWR Recomm Rep. Mar 28 2003;52:1-8. [Medline].
[Guideline] National Heart, Lung, and Blood Institute. Education for a partnership in asthma care. Expert panel report 3: guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program (NAEPP). Aug 2007;[Full Text].
[Guideline] National Heart, Lung, and Blood Institute. Managing asthma long term-special situations. Expert panel report 3: guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program (NAEPP). Aug 2007;[Full Text].
[Guideline] National Heart, Lung, and Blood Institute. Managing exacerbations of asthma. Expert panel report 3: guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program (NAEPP). Aug 2007;[Full Text].
[Guideline] National Heart, Lung, and Blood Institute. Measures of asthma assessment and monitoring. Expert panel report 3: guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program (NAEPP). Aug 2007;[Full Text].
[Guideline] National Heart, Lung, and Blood Institute. Medications. Expert panel report 3: guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program (NAEPP). Aug 2007;[Full Text].
[Guideline] National Heart, Lung, and Blood Institute. Managing asthma long term in children 0-4 years of age and 5-11 years of age. Expert panel report 3: guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program (NAEPP). Aug 2007;[Full Text].
[Guideline] National Heart, Lung, and Blood Institute. Managing asthma long term in youths >=12 years of age and adults. Expert panel report 3: guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program (NAEPP). Aug 2007;[Full Text].
Busse WW, Calhoun WF, Sedgwick JD. Mechanism of airway inflammation in asthma. Am Rev Respir Dis. Jun 1993;147(6 Pt 2):S20-4. [Medline].
Henderson WR Jr. Role of leukotrienes in asthma. Ann Allergy. Mar 1994;72(3):272-8. [Medline].
Horwitz RJ, Busse WW. Inflammation and asthma. Clin Chest Med. Dec 1995;16(4):583-602. [Medline].
Sears MR. Consequences of long-term inflammation. The natural history of asthma. Clin Chest Med. Jun 2000;21(2):315-29. [Medline].
Centers for Disease Control and Prevention. Asthma--United States, 1982-1992. MMWR Morb Mortal Wkly Rep. Jan 6 1995;43(51-52):952-5. [Medline].
Sly RM. Changing asthma mortality. Ann Allergy. Sep 1994;73(3):259-68. [Medline].
Burrows B, Barbee RA, Cline MG, Knudson RJ, Lebowitz MD. Characteristics of asthma among elderly adults in a sample of the general population. Chest. Oct 1991;100(4):935-42. [Medline].
Martin AJ, Landau LI, Phelan PD. Lung function in young adults who had asthma in childhood. Am Rev Respir Dis. Oct 1980;122(4):609-16. [Medline].
Irwin RS, Curley FJ, French CL. Chronic cough. The spectrum and frequency of causes, key components of the diagnostic evaluation, and outcome of specific therapy. Am Rev Respir Dis. Mar 1990;141(3):640-7. [Medline].
Bacci E, Cianchetti S, Bartoli M, et al. Low sputum eosinophils predict the lack of response to beclomethasone in symptomatic asthmatic patients. Chest. Mar 2006;129(3):565-72. [Medline].
Green RH, Brightling CE, McKenna S, et al. Asthma exacerbations and sputum eosinophil counts: a randomised controlled trial. Lancet. Nov 30 2002;360(9347):1715-21. [Medline].
[Best Evidence] Nair P, Pizzichini MM, Kjarsgaard M, et al. Mepolizumab for prednisone-dependent asthma with sputum eosinophilia. N Engl J Med. Mar 5 2009;360(10):985-93. [Medline].
Enright PL, Lebowitz MD, Cockroft DW. Physiologic measures: pulmonary function tests. Asthma outcome. Am J Respir Crit Care Med. Feb 1994;149(2 Pt 2):S9-18; discussion S19-20. [Medline].
Crapo RO, Casaburi R, Coates AL, et al. Guidelines for methacholine and exercise challenge testing-1999. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, July 1999. Am J Respir Crit Care Med. Jan 2000;161(1):309-29. [Medline].
Smith AD, Cowan JO, Brassett KP, Herbison GP, Taylor DR. Use of exhaled nitric oxide measurements to guide treatment in chronic asthma. N Engl J Med. May 26 2005;352(21):2163-73. [Medline].
[Guideline] Reddel HK, Taylor DR, Bateman ED, et al. An official American Thoracic Society/european Respiratory Society statement: asthma control and exacerbations: standardizing endpoints for clinical asthma trials and clinical practice. Am J Respir Crit Care Med. Jul 1 2009;180(1):59-99. [Medline].
National Heart, Lung, and Blood Institute. NAEPP Working Group Report: Considerations for Diagnosing and Managing Asthma in the Elderly. NIH Publication No. 96-3662. National Institutes of Health; 1996. [Full Text].
[Best Evidence] Castro M, Rubin AS, Laviolette M, et al. Effectiveness and safety of bronchial thermoplasty in the treatment of severe asthma: a multicenter, randomized, double-blind, sham-controlled clinical trial. Am J Respir Crit Care Med. Jan 15 2010;181(2):116-24. [Medline].
Kingston HG, Hirshman CA. Perioperative management of the patient with asthma. Anesth Analg. Sep 1984;63(9):844-55. [Medline].
Abramson MJ, Puy RM, Weiner JM. Is allergen immunotherapy effective in asthma? A meta-analysis of randomized controlled trials. Am J Respir Crit Care Med. Apr 1995;151(4):969-74. [Medline].
Camargo CA Jr, Weiss ST, Zhang S, Willett WC, Speizer FE. Prospective study of body mass index, weight change, and risk of adult-onset asthma in women. Arch Intern Med. Nov 22 1999;159(21):2582-8. [Medline].
Barnes PJ. Inhaled glucocorticoids for asthma. N Engl J Med. Mar 30 1995;332(13):868-75. [Medline].
Djukanovic R, Wilson JW, Britten KM, et al. Effect of an inhaled corticosteroid on airway inflammation and symptoms in asthma. Am Rev Respir Dis. Mar 1992;145(3):669-74. [Medline].
McFadden ER Jr, Hejal RB. The pathobiology of acute asthma. Clin Chest Med. Jun 2000;21(2):213-24, vii. [Medline].
Rowe BH, Keller JL, Oxman AD. Effectiveness of steroid therapy in acute exacerbations of asthma: a meta-analysis. Am J Emerg Med. Jul 1992;10(4):301-10. [Medline].
Rowe BH, Edmonds ML, Spooner CH, Diner B, Camargo CA Jr. Corticosteroid therapy for acute asthma. Respir Med. Apr 2004;98(4):275-84. [Medline].
Nayak A. A review of montelukast in the treatment of asthma and allergic rhinitis. Expert Opin Pharmacother. Mar 2004;5(3):679-86. [Medline].
Nelson HS. Advair: combination treatment with fluticasone propionate/salmeterol in the treatment of asthma. J Allergy Clin Immunol. Feb 2001;107(2):398-416. [Medline].
[Best Evidence] Cates CJ, Lasserson TJ, Jaeschke R. Regular treatment with formoterol and inhaled steroids for chronic asthma: serious adverse events. Cochrane Database Syst Rev. Apr 15 2009;CD006924. [Medline].
Bailey WC, Richards JM Jr, Brooks CM, Soong SJ, Windsor RA, Manzella BA. A randomized trial to improve self-management practices of adults with asthma. Arch Intern Med. Aug 1990;150(8):1664-8. [Medline].
Ignacio-Garcia JM, Gonzalez-Santos P. Asthma self-management education program by home monitoring of peak expiratory flow. Am J Respir Crit Care Med. Feb 1995;151(2 Pt 1):353-9. [Medline].
Kotses H, Bernstein IL, Bernstein DI, et al. A self-management program for adult asthma. Part I: Development and evaluation. J Allergy Clin Immunol. Feb 1995;95(2):529-40. [Medline].
Nathan RA, Sorkness CA, Kosinski M, et al. Development of the asthma control test: a survey for assessing asthma control. J Allergy Clin Immunol. Jan 2004;113(1):59-65. [Medline].
[Best Evidence] Coffman JM, Cabana MD, Yelin EH. Do school-based asthma education programs improve self-management and health outcomes?. Pediatrics. Aug 2009;124(2):729-42. [Medline].
Hamilos DL. Gastroesophageal reflux and sinusitis in asthma. Clin Chest Med. Dec 1995;16(4):683-97. [Medline].
Harding SM, Guzzo MR, Richter JE. The prevalence of gastroesophageal reflux in asthma patients without reflux symptoms. Am J Respir Crit Care Med. Jul 2000;162(1):34-9. [Medline].
Harding SM, Sontag SJ. Asthma and gastroesophageal reflux. Am J Gastroenterol. Aug 2000;95(8 Suppl):S23-32. [Medline].
Kiljander TO, Salomaa ER, Hietanen EK, Terho EO. Gastroesophageal reflux in asthmatics: A double-blind, placebo-controlled crossover study with omeprazole. Chest. Nov 1999;116(5):1257-64. [Medline].
Morris MJ, Deal LE, Bean DR, Grbach VX, Morgan JA. Vocal cord dysfunction in patients with exertional dyspnea. Chest. Dec 1999;116(6):1676-82. [Medline].
Chan-Yeung M. 2003 Christie Memorial lecture. Occupational asthma--the past 50 years. Can Respir J. Jan-Feb 2004;11(1):21-6. [Medline].
Chan-Yeung M. Assessment of asthma in the workplace. ACCP consensus statement. American College of Chest Physicians. Chest. Oct 1995;108(4):1084-117. [Medline].
National Heart, Lung, and Blood Institute. Executive Summary: Management of Asthma During Pregnancy. NIH Publication No. 92-3279a. National Institutes of Health; 1992.
[Guideline] Dombrowski MP, Schatz M. ACOG practice bulletin: clinical management guidelines for obstetrician-gynecologists number 90, February 2008: asthma in pregnancy. Obstet Gynecol. Feb 2008;111(2 Pt 1):457-64. [Medline].
[Best Evidence] Castro M, Rubin AS, Laviolette M, et al. Effectiveness and safety of bronchial thermoplasty in the treatment of severe asthma: a multicenter, randomized, double-blind, sham-controlled clinical trial. Am J Respir Crit Care Med. Jan 15 2010;181(2):116-24. [Medline].
Juniper EF, Buist AS, Cox FM, Ferrie PJ, King DR. Validation of a standardized version of the Asthma Quality of Life Questionnaire. Chest. May 1999;115(5):1265-70. [Medline].
Lahdensuo A, Haahtela T, Herrala J, et al. Randomised comparison of guided self management and traditional treatment of asthma over one year. BMJ. Mar 23 1996;312(7033):748-52. [Medline].
Laitinen LA, Laitinen A, Haahtela T. A comparative study of the effects of an inhaled corticosteroid, budesonide, and a beta 2-agonist, terbutaline, on airway inflammation in newly diagnosed asthma: a randomized, double-blind, parallel-group controlled trial. J Allergy Clin Immunol. Jul 1992;90(1):32-42. [Medline].
O'Byrne PM, Parameswaran K. Pharmacological management of mild or moderate persistent asthma. Lancet. Aug 26 2006;368(9537):794-803. [Medline].
Strunk RC, Weiss ST, Yates KP, Tonascia J, Zeiger RS, Szefler SJ. Mild to moderate asthma affects lung growth in children and adolescents. J Allergy Clin Immunol. Nov 2006;118(5):1040-7. [Medline].
Suissa S, Ernst P, Boivin JF, et al. A cohort analysis of excess mortality in asthma and the use of inhaled beta-agonists. Am J Respir Crit Care Med. Mar 1994;149(3 Pt 1):604-10. [Medline].
Woolcock A, Lundback B, Ringdal N, Jacques LA. Comparison of addition of salmeterol to inhaled steroids with doubling of the dose of inhaled steroids. Am J Respir Crit Care Med. May 1996;153(5):1481-8. [Medline].
Keywords
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