Asthma in Children
- LAST REVIEWED: 15 June 2015
- LAST MODIFIED: 29 May 2014
- DOI: 10.1093/obo/9780199756797-0108
- LAST REVIEWED: 15 June 2015
- LAST MODIFIED: 29 May 2014
- DOI: 10.1093/obo/9780199756797-0108
Asthma has puzzled and confused humanity for a long time. It was only recognized as a unique illness toward the end of the 19th century and its links to allergy (for about half the cases of asthma) were not established until the early 1900s. The epidemiological explosion in asthma cases occurred in most developed countries from the second half of the 20th century, particularly the last quarter of that century. Even though asthma presents with considerable individual variability, certain clinical features including intermittent dyspnea and wheezing generally allow its recognition. Attempts to use these features to precisely define asthma, however, have not been successful. The most concise and useful description of asthma is “variable airflow obstruction.” The diagnosis is made by recognition of a pattern of one or more characteristic symptoms including wheeze, cough, chest tightness, and dyspnea and is best confirmed by evidence of variable or reversible airflow obstruction accompanying symptoms. Continuing allergic airway inflammation beginning in the first three years of life contributes to airway hyperresponsiveness and impairment of lung function at school age. Thus, asthma begins in early childhood, with a higher incidence and earlier onset in males. Immune and lung development occur largely in utero and during early childhood. Research continues to delineate early immunophenotypes and early airway response outcomes among children predisposed to asthma (atopic and nonatopic).
National Heart Lung Blood Institute 2007, Global Initiative for Asthma 2012, British Guideline on the Management of Asthma 2012, and Guia Espanola Para EL Manejo Asma 2009 (Spanish Guideline on the Management of Asthma) all define asthma as a chronic inflammatory disorder of the airways with variable airflow obstruction. According to Umetsu, et al. 2002 and von Mutius 2009, asthma is a complex trait caused by multiple environmental factors in combination with more than one hundred major and minor susceptibility genes and has many different forms or phenotypes. Kim, et al. 2010 reported that there are several different forms of asthma (allergic, non-allergic, and intrinsic). First, allergic asthma, which constitutes about half the cases, can be induced by allergens that include house dust mite, pollen, ragweed, cockroach, and mold along with the involvement of genes such as IL-13R, IL-4, FceRIa, and HLA through mediation by TH2 immune responses. Second, non-allergic asthma can also be caused by several factors such as ozone, cigarette smoke, diesel particles, infection, aspirin, exercise, and cold air with the involvement of genes such as HAVcr1 (TIM1), CD14, and IL-10. So, non-TH2 cells and various immune cells other than TH2 cells contribute to non-allergic asthma. Third, ADAM33 gene is implicated in the intrinsic asthma. Weinberger and Abu-Hasan 2006 emphasizes the role of viral respiratory infections as one of the most important causes of asthma exacerbation and also as a contributor to the development of asthma. Treatment involves using quick-relief inhalers and long-term control medications along with environmental control.
British Guideline on the Management of Asthma. 2012. British guideline on the management of asthma (2012 revised edition). London: British Thoracic Society.
This guideline provides recommendations based on current evidence for best practice in the management of asthma. It makes recommendations on management of adults, including pregnant women, adolescents, and children with asthma. It considers asthma management in all patients with a diagnosis of asthma irrespective of age or gender.
Global Initiative for Asthma. 2012. Global Strategy for Asthma Management and Prevention (2012 updated edition), a joint project between National Institutes of Health and World Health Organization. Bethesda, MD: National Institutes of Health.
Global Initiative for Asthma (GINA) works with health professionals around world to reduce asthma prevalence, morbidity, and mortality. Through various resources, projects such as Asthma Control Challenge to reduce hospitalizations, and events such as World Asthma Day, GINA is working to improve lives of people with asthma worldwide.
Guia Espanola Para El Manejo Asma. 2009. Spanish guideline on the management of asthma. Archivos de Bronconeumologia 45 (Suppl. 7): 2–35.
The direct factors for asthma exacerbations are 1) viral respiratory infection, 2) tobacco, 3) cold and humid conditions, 4) allergens, and 5) air pollution. The indirect factors are 1) physical exercise, 2) food allergens and additives, 3) pregnancy, 4) storms and thermal inversion, 5) drugs, 6) sinusitis, 7) menstruation, and 8) gastro-esophageal reflux.
Kim, H. Y., R. H. DeKruyff, D. T. Umetsu. 2010. The many paths to asthma: Phenotypes shaped by innate and adaptive immunity. Nature Immunology 11.7: 577–584.
Asthma is associated with multiple environmental factors in combination with more than one hundred major and minor susceptibility genes and has many different forms or phenotypes. They include allergic asthma, severe steroid-resistant asthma and asthma induced by exposure to air pollution, cigarette smoke, diesel exhaust, obesity, aspirin and exercise.
National Heart Lung Blood Institute. 2007. Expert panel report 3: Guidelines for the diagnosis and management of asthma. Bethesda, MD: National Institutes of Health.
The National Heart Lung Blood Institute (NHLBI) emphasizes importance of asthma control and introduces new approaches for monitoring asthma. It added an expanded section on childhood asthma, new guidance on medications, new recommendations on patient education in settings beyond physician’s office, and environmental control.
Umetsu, D. T., J. J. McIntire, O. Akbari, C. Macaubas, R. H. DeKruyff. 2002. Asthma: An epidemic of dysregulated immunity. Nature Immunology 3.8: 715–720.
Infections may normally induce the development of regulatory T (T(R)) cells and protective immunity that limit airway inflammation and promote tolerance to respiratory allergens. In the absence of such infections, T(H)2 cells—which are developmentally related to T(R) cells—develop and coordinate the development of asthmatic inflammation.
von Mutius, E. 2009. Gene-environment interactions in asthma. J Allergy Clin Immunol 123:3–11.
Asthma is a complex disease and its incidence is determined by an intricate interplay of genetic and environmental factors. The identification of novel genes for asthma suggests that many genes with small effects rather than few genes with strong effects contribute to the development of asthma.
Weinberger, M., and M. Abu-Hasan. 2006. Asthma in the pre-school child. In Kendig’s disorders of the respiratory tract in children. 7th ed. Edited by V. Chernick, T. F. Boat, R. W. Wilmott, and A. Bush, 795–809. Philadelphia: Saunders Elsevier.
While asthma can begin at almost any age, it most commonly begins in infancy with a viral respiratory infection that causes the lower airway inflammatory disease with consequent wheezing and coughing that is commonly known as bronchiolitis. The most common of this initial wheezing episode is respiratory syncytial virus (RSV).
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