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Prevention of the continuum of bronchial asthma
EDITOR'S C O L U M N
Prevention of the continuum of bronchial asthma ASTHMA 1S A heterogenous disease. Through the years much has been learned about its clinical nature, mechanisms, and t h e pathways leading to status asthmaticus; more is being learned by intense study of asymptomatic patients. For example, the chemical mediators, histamine and neutrophil chemotactic factor, are released and measurable in the sera of patients with allergen-induced and exercise-induced asthma, but not after methacholineinduced bronchoconstriction in these patients) There are multifactorial precipitators that cause symptoms in some, but usually different, patients. Aerosolized methacholine can even identify the patient free of asthma for several years, whereas patients reacting to aerosolized histamine are more likely to have severe asthma with bronchial hyperreactivity and thus respond to most stimuli. Pediatricians know that these patients also include responders and nonresponders to various types of medications. Each of these variables has the potential for contributing to the subclassification of asthmatic patients in the future. One classification based on severity, principally the frequency of breathlessness, has been evolving over the past 25 years. 2 In addition, for reasons not always apparent, many children progress steadily through these various classes, from subclinical asthma through mild episodic asthma to continuing asthma and then to intractable asthma (chronic unremitting asthma). Rarely a child develops irreversible asthma. All can develop acute severe asthma at any time. The 1960s brought the development of techniques to prevent death from status asthmaticus, and in the 1970s the application of pharmacokinetic principles resulted in less acute severe asthma. It is increasingly apparent that in the 1980s additional methods to halt the progression of this disease will be developed. The article by Kraemer et al. in this issue of the Journal is an important contribution to this process. These investigators classified their patients by two methods. Patients were ranked by severity of disease, and then each was grouped by pulmonary function tests into those with hyperinflation, those with air flow obstruction, and those with both abnormalities. The response to a single dose of bronchodilator was then evaluated. Without prior classification, the results would have been equivocal and meaningless. Although the interpretation and conclusions
will be subjected to considerable debate, the results are quite clear. Two thirds of asymptomatie asthmatic children in the "interval phase," that is between episodes, may have residual hyperinflation unresponsive to a single dose of albuterol. Implications for long-term therapy obviously exist but need to be evaluated in similar, well-defined populations. It is apparent that two weeks after the last episode a significant latent component of asthma persists. The occurrence of chronic hyperinflation has been known since 1958. 3 This subject also has been comprehensively reviewed,4 yet classification of the study subjects has been a continuing problem. This situation is complicated by the occurrence of similar pulmonary sequelae after viral infections, such as bronchiolitis,5 which asthmatic children also acquire.
See related article, p. 347.
The essence of pediatrics is prevention, and care must be taken to observe asthmatic children for several months after each acute episode to minimize the effect of the residual injury or of latent disease.
Herbert C. Mansmann, Jr., M.D. Professor of Pediatrics Associate Professor of Medicine Jefferson Medical College Thomas Jefferson University Philadelphia, Pennsylvania REFERENCES 1. Lee TH, Brown MJ, Nagy L, Causon R, Walport MJ, Kay AB: Exercise-induced release of histamine and neutrophil chemotactic factor in atopic asthmatics. J Allergy Clin Immunol 70:73, 1982. 2. Mansmann HC Jr: The evaluation, control, and modification of continuing asthma. Clin Chest Med 1:339, 1980. 3. Kraepelien S, Engstr6m I, Karlberg P: Respiratory studies in children. II. Lung volumes in symptom-free asthmatic children, 6-14 years of age. Acta Paediatr Scand 47:399, 1958. 4. McFadden ER Jr: The chronicity of acute attacks of asthma: Mechanical and therapeutic implications. J Allergy Clin ImmunoI 56:18, 1975. 5. Kaltan M, Keens TG, Lapierre JG, Levison H, Bryan AC, Reilly BJ: Pulmonary function abnormalities in symptom-free children after bronchiolitis. Pediatrics 59:683, 1977.
The Journal o f P E D I A T R I CS Vol. 102, No. 3, 1983
391
Prevention of the continuum of bronchial asthma ASTHMA 1S A heterogenous disease. Through the years much has been learned about its clinical nature, mechanisms, and t h e pathways leading to status asthmaticus; more is being learned by intense study of asymptomatic patients. For example, the chemical mediators, histamine and neutrophil chemotactic factor, are released and measurable in the sera of patients with allergen-induced and exercise-induced asthma, but not after methacholineinduced bronchoconstriction in these patients) There are multifactorial precipitators that cause symptoms in some, but usually different, patients. Aerosolized methacholine can even identify the patient free of asthma for several years, whereas patients reacting to aerosolized histamine are more likely to have severe asthma with bronchial hyperreactivity and thus respond to most stimuli. Pediatricians know that these patients also include responders and nonresponders to various types of medications. Each of these variables has the potential for contributing to the subclassification of asthmatic patients in the future. One classification based on severity, principally the frequency of breathlessness, has been evolving over the past 25 years. 2 In addition, for reasons not always apparent, many children progress steadily through these various classes, from subclinical asthma through mild episodic asthma to continuing asthma and then to intractable asthma (chronic unremitting asthma). Rarely a child develops irreversible asthma. All can develop acute severe asthma at any time. The 1960s brought the development of techniques to prevent death from status asthmaticus, and in the 1970s the application of pharmacokinetic principles resulted in less acute severe asthma. It is increasingly apparent that in the 1980s additional methods to halt the progression of this disease will be developed. The article by Kraemer et al. in this issue of the Journal is an important contribution to this process. These investigators classified their patients by two methods. Patients were ranked by severity of disease, and then each was grouped by pulmonary function tests into those with hyperinflation, those with air flow obstruction, and those with both abnormalities. The response to a single dose of bronchodilator was then evaluated. Without prior classification, the results would have been equivocal and meaningless. Although the interpretation and conclusions
will be subjected to considerable debate, the results are quite clear. Two thirds of asymptomatie asthmatic children in the "interval phase," that is between episodes, may have residual hyperinflation unresponsive to a single dose of albuterol. Implications for long-term therapy obviously exist but need to be evaluated in similar, well-defined populations. It is apparent that two weeks after the last episode a significant latent component of asthma persists. The occurrence of chronic hyperinflation has been known since 1958. 3 This subject also has been comprehensively reviewed,4 yet classification of the study subjects has been a continuing problem. This situation is complicated by the occurrence of similar pulmonary sequelae after viral infections, such as bronchiolitis,5 which asthmatic children also acquire.
See related article, p. 347.
The essence of pediatrics is prevention, and care must be taken to observe asthmatic children for several months after each acute episode to minimize the effect of the residual injury or of latent disease.
Herbert C. Mansmann, Jr., M.D. Professor of Pediatrics Associate Professor of Medicine Jefferson Medical College Thomas Jefferson University Philadelphia, Pennsylvania REFERENCES 1. Lee TH, Brown MJ, Nagy L, Causon R, Walport MJ, Kay AB: Exercise-induced release of histamine and neutrophil chemotactic factor in atopic asthmatics. J Allergy Clin Immunol 70:73, 1982. 2. Mansmann HC Jr: The evaluation, control, and modification of continuing asthma. Clin Chest Med 1:339, 1980. 3. Kraepelien S, Engstr6m I, Karlberg P: Respiratory studies in children. II. Lung volumes in symptom-free asthmatic children, 6-14 years of age. Acta Paediatr Scand 47:399, 1958. 4. McFadden ER Jr: The chronicity of acute attacks of asthma: Mechanical and therapeutic implications. J Allergy Clin ImmunoI 56:18, 1975. 5. Kaltan M, Keens TG, Lapierre JG, Levison H, Bryan AC, Reilly BJ: Pulmonary function abnormalities in symptom-free children after bronchiolitis. Pediatrics 59:683, 1977.
The Journal o f P E D I A T R I CS Vol. 102, No. 3, 1983
391