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Review
. 2003 Feb;111(2 Suppl):S502-19.
doi: 10.1067/mai.2003.94.

6. Asthma

Robert F Lemanske Jr  1 , William W Busse
Affiliations
Review

6. Asthma

Robert F Lemanske Jr et al. J Allergy Clin Immunol. 2003 Feb.

Abstract

The increasing incidence and prevalence of asthma in many parts of the world continue to make it a global health concern. The heterogeneous nature of the clinical manifestations and therapeutic responses of asthma in both adult and pediatric patients indicate that it may be more of a syndrome rather than a specific disease entity. Numerous triggering factors including viral infections, allergen and irritant exposure, and exercise, among others, complicate both the acute and chronic treatment of asthma. Therapeutic intervention has focused on the appreciation that airway obstruction in asthma is composed of both bronchial smooth muscle spasm and variable degrees of airway inflammation characterized by edema, mucus secretion, and the influx of a variety of inflammatory cells. The presence of only partial reversibility of airflow obstruction in some patients indicates that structural remodeling of the airways may also occur over time. Choosing appropriate medications depends on the disease severity (intermittent, mild persistent, moderate persistent, severe persistent), extent of reversibility, both acutely and chronically, patterns of disease activity (exacerbations related to viruses, allergens, exercise, etc), and the age of onset (infancy, childhood, adulthood).

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Figures

Fig. 1
Fig. 1
One mechanism that initiates airway inflammation in antigen exposure in sensitized individuals. Antigen interaction with mast cell-bound, specific-IgE antibody results in release of preformed (histamine) and generated (leukotrienes) mediators along with cytokines [interleukins -4 and -5 and granulocyte macrophage-colony stimulating factor (GM-CSF)]. These various compounds can induce localized inflammatory cell influx and activation through the upregulation of various chemokines and adhesion molecules and recruitment of bone marrow cells (eg, eosinophils). (Modified and reproduced with permission from Busse WW, Lemanske RF Jr. N Engl J Med 2001;344:350-62.)
Fig. 2
Fig. 2
Stepwise approach for treating infants and young children (5 years of age and younger) with acute or chronic asthma (reproduced from www.nhlbi.nih.gov/guidelines/asthma/asthsumm.htm ).
Fig. 3
Fig. 3
Stepwise approach for treating asthma in adults and children older than 5 years of age (reproduced from www.nhlbi.nih.gov/guidelines/asthma/asthsumm.htm ).
Fig. 4
Fig. 4
Dosages for long-term control medications (reproduced from www.nhlbi.nih.gov/guidelines/ asthma/asthsumm.htm).
Fig. 5
Fig. 5
Estimated comparative daily dosages of inhaled corticosteroids (reproduced from www.nhlbi.nih.gov/guidelines/asthma/asthsumm.htm ).
Fig. 6
Fig. 6
Estimated severity of asthma exacerbations (reproduced from Murphy S, Bleecker ER, Boushey H, et al, editors. Guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program. II, 1-150. 1997. Bethesda, Md: National Institutes of Health).
Fig. 7
Fig. 7
Home treatment of asthma exacerbations (reproduced from Murphy S, Bleecker ER, Boushey H, et al, editors. Guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program. II, 1-150. 1997. Bethesda, Md: National Institutes of Health).
Fig. 8
Fig. 8
Hospital-based treatment of asthma exacerbations (reproduced from Murphy S, Bleecker ER, Boushey H, et al, editors. Guidelines for the diagnosis and management of asthma. National Asthma Education and Prevention Program. II, 1-150. 1997. Bethesda, Md: National Institutes of Health).
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