
Editorial
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There is now clear evidence that asthma prevalence increased significantly, especially in developed countries, during the second part of the 20th century. What caused this increase is currently unknown. Recent reports from the United States and the United Kingdom suggest that asthma prevalence may have plateaued between 1995 and the first few years of the present century. This stabilization, and even some decrease in asthma prevalence, especially in countries with high baseline rates, was confirmed by the International Study of Asthma and Allergies in Children. The hospitalization rate for asthma (as a proportion of asthma patients) decreased significantly in the United States between 1980 and 1995, then remained stable between 2001 and 2004. However, the asthma death rate (as a proportion of subjects with asthma) did not decrease significantly during either of those periods. A better understanding of what determines the stable asthma death rate is urgently needed, especially since inhaled corticosteroids have been shown to prevent asthma deaths in persons who take them regularly.
Asthma is a heterogeneous disorder with multiple clinical phenotypes. Phenotypes can be grouped into clinical or physiological, trigger-defined, and inflammatory phenotypes. Treatment based on inflammatory phenotyping improves clinical measures of asthma morbidity. Further study of individual asthma phenotypes will improve understanding of their immunologic and pathologic characteristics and improve diagnosis and therapy. Because asthma is a common disorder with nonspecific presenting features, other disorders are often misdiagnosed as asthma. A high index of suspicion for alternative diagnoses must be maintained when evaluating a patient who presents with clinical features suggestive of asthma, particularly if the patient presents with atypical symptoms or fails to respond to therapy.
Diagnostic tests can only increase or decrease the probability of the asthma diagnosis, so a thorough history is very important. In patients with asthma-like symptoms, spirometric evidence of airway obstruction plus a large bronchodilator response makes asthma much more likely. However, normal spirometry is common in patients with mild asthma who are not symptomatic at the time of testing, and patients with poorly controlled asthma may lack substantial bronchodilator response. Inhalation challenge test often helps confirm asthma in patients with normal spirometry. Adult smokers with intermittent respiratory symptoms may have either asthma or chronic obstructive pulmonary disease (COPD). Normal post-bronchodilator spirometry rules out COPD. In patients with airway obstruction, a low diffusing capacity of the lung for carbon monoxide increases the probability of COPD and makes asthma much less likely. A high exhaled nitric oxide level makes allergic asthma more likely. Response to inhaled corticosteroids makes asthma more likely and COPD less likely.
Once the diagnosis of asthma is established, monitoring must be implemented to achieve asthma control. Because of the variability of asthma, monitoring is a long-term commitment to effectively adjust treatment and assure that therapy goals are met. This paper reviews the definition of asthma control, including the dimensions of impairment and risk, and the 2007 National Asthma Education and Prevention Program's Expert Panel Report 3, Guidelines for the Diagnosis and Management of Asthma, recommendations for periodic assessment and monitoring of effective control. New approaches to asthma monitoring, such as airway hyperresponsiveness, sputum eosinophils, exhaled nitric oxide, and pharmacogenetic measurements, will be critiqued.
Management of asthma requires attention to environmental exposures both indoors and outdoors. Americans spend most of their time indoors, where they have a greater ability to modify their environment. The indoor environment contains both pollutants (eg, particulate matter, nitrogen dioxide, secondhand smoke, and ozone) and allergens from furred pets, dust mites, cockroaches, rodents, and molds. Indoor particulate matter consists of particles generated from indoor sources such as cooking and cleaning activities, and particles that penetrate from the outdoors. Nitrogen dioxide sources include gas stoves, furnaces, and fireplaces. Indoor particulate matter and nitrogen dioxide are linked to asthma morbidity. The indoor ozone concentration is mainly influenced by the outdoor ozone concentration. The health effects of indoor ozone exposure have not been well studied. In contrast, there is substantial evidence of detrimental health effects from secondhand smoke. Guideline recommendations are not specific for optimizing indoor air quality. The 2007 National Asthma Education and Prevention Program asthma guidelines recommend eliminating indoor smoking and improving the ventilation. Though the guidelines state that there is insufficient evidence to recommend air cleaners, air cleaners and reducing activities that generate indoor pollutants may be sound practical approaches for improving the health of individuals with asthma. The guidelines are more specific about allergen avoidance; they recommend identifying allergens to which the individual is immunoglobin E sensitized and employing a multifaceted, comprehensive strategy to reduce exposure. Outdoor air pollutants that impact asthma include particulate matter, ozone, nitrogen dioxide, and sulfur dioxide, and guidelines recommend that individuals with asthma avoid exertion outdoors when these pollutants are elevated. Outdoor allergens include tree, grass, and weed pollens, which vary in concentration by season. Recommendations to reduce exposure include staying indoors, keeping windows and doors closed, using air conditioning and perhaps high-efficiency particulate arrestor (HEPA) air filters, and thorough daily washing to remove allergens from one's person.
Both short-acting and long-acting β agonists have been used for many years for the treatment of asthma. Short-acting β agonists are life-saving and their role as rescue agents is unquestioned, but regular use is not recommended because of safety concerns and the effectiveness of asthma-controller medications. Long-acting β agonists are effective controller medications but have safety issues, so their use should be restricted to patients who are not optimally controlled on first-line controllers such as inhaled corticosteroids. The effect of the β receptor genotype on β agonist response is unclear but could hold promise for proper patient management.
Asthma is a disorder of the lower airways, characterized by bronchial hyperresponsiveness and airflow limitation, the pathogenesis of which is yet to be fully understood. Regardless of its triggers, asthma's hallmark is a state of inflammation that, when uncontrolled, results in persistence of symptoms. Inhaled corticosteroids are established as the mainstay of asthma therapy. This paper examines what is currently available among this class of drugs, features of the ideal inhaled corticosteroid, the delivery systems, dose-response relationships, adverse effects, combination with long-acting β agonists, equipotent doses among the different types, and several special scenarios that involve the apparent incomplete or lack of response to treatment with inhaled corticosteroids among certain subgroups of patients, such as smokers and obese individuals, and we will discuss the scientific basis of such resistance and suggest alternative approaches to therapy.



