Introduction
Asthma is defined as the occurrence of dyspneic bronchospasmodic crises that are linked to bronchial hyperreactivity (BH). As an autoimmune disease, asthma is a chronic disturbance of immunological function that can be controlled to some extent but not eradicated by modern drug therapy. In other words, asthma does not just refer to the attacks. Instead, asthma is considered a chronic disturbance of the immune system. The attacks are the “tip of the iceberg.” Hence, any treatment aimed only at relaxing airways and relieving symptoms, be it orthodox or herbal, is superficial and will not change the chronicity of the disease (Germouty J. et al., 1988).
Asthma is an inflammatory chronic public health problem throughout the world affecting people of all ages, which can result in a variable restriction in the physical, emotional, and social aspects of a patient’s life (Bousquet et al. 1994). It is estimated that around 300 million people in the world currently have asthma (O’Byrne, 2006). The prevalence of asthma increases as communities adopt modern lifestyles and become urbanized ((Bousquet et al., 2003). With the proportion of the world’s population living in urban areas projected to increase from 45 to 59% in 2025, there is likely to be a marked increase in the number of people with asthma worldwide over the next two decades. It is estimated that there may be an additional 100 million people with asthma by 2025 (Masoli et al. 2004).
Asthma can be classified as extrinsic (allergic asthma) or intrinsic asthma. Although there has been some confusion with the terms, and some medical scientists feel that the classification is meaningless (Burrows et al., 1989), the differentiation is quite clear. Patients with extrinsic asthma comprise the majority of cases and exhibit a positive skin test to common aeroallergens and foods. Serum IgE levels are usually raised. However, extrinsic asthmatics can still be exacerbated by non-specific stimuli such as cold air and exercise. Intrinsic asthmatics have negative skin tests and chronic infection, and other factors are thought to play a role in the disease process. Intrinsic asthma is usually later in onset and more severe. Aspirin-sensitive asthma (ASA) is one form of intrinsic asthma. Both types of asthma show an increased family occurrence (Ulrik et al., 1992).
The confusion over this classification of asthma probably arises when etiology is considered. It is likely that allergy often plays a role in the development and exacerbation of intrinsic asthma. Similarly, factors such as infection and gastroesophageal reflux (GER) may contribute to extrinsic asthma. Hence, the above classification should serve only as a guide to the different kinds of factors that can operate in asthma; the classification is secondary to the identification of factors in each individual case (Burrows et al., 1989).
The Findings
Asthmatic lungs are characterized by epithelial cell loss, goblet cell hyperplasia, increased collagen deposition, mast cell degranulation, and inflammatory cell infiltration. Asthma is now primarily classified as an inflammatory disorder. The desquamation allows allergens to penetrate more easily and exposes irritant receptors (Burrows et al., 1989).
Pathophysiology
Bronchoalveolar lavage has revealed the presence of activated helper T-cells in asthmatic lungs. Helper T-cells can be divided into two main types: TH1 and TH2. TH1-cells produce cytokines which are characteristic of the immune response to bacterial infections. The cytokines produced by TH2-cells are characteristic of allergic responses and include interleukin-4, interleukin-5, and granulocyte-macrophage colony-stimulating factor (GM-CSF). Patients with extrinsic asthma have high levels of these cytokines. In other words, the TH2-cell compartment appears to be overactive. Interleukin-5 activates eosinophils, which are the characteristic inflammatory cells in asthma, and interleukin-4 encourages B-cells to produce IgE. So, for extrinsic asthma, the acute symptoms may largely be the work of mast cells, while chronic inflammation results from the action of TH2-cells on eosinophils. A similar but not identical process may be involved in intrinsic asthma, which is triggered by an unknown antigen, such as a virus or even self tissue. Some scientists feel that T-cell-modulated, eosinophilic bronchitis is the primary abnormality in asthma, while bronchospasm and hyperreactivity are secondary phenomena (Sur et al., 1993).
The characteristic inflammatory cells of asthma are mast cells and eosinophils. Other cells also participate in the inflammatory process. Neutrophils have been implicated in sudden onset fatal asthma and bronchiolar obstruction associated with house dust mite sensitivity. Platelets and monocyte/macrophages also play a role. In particular, platelet activation is a feature of the late inflammatory response to antigen challenge. Endothelial cells also participate in the pathogenic process (Tanizaki et al., 1992).
Treatment and Management
The National Asthma Education and Prevention Program (NAEPP) of the National Heart, Lung, and Blood Institute provides information and guidelines for the management of asthma symptoms, as does the Global Initiative for Asthma (GINA), an international collaboration between the National Institutes of Health (NIH) and the World Health Organization (GINA, 2006). Both the NAEPP and GINA guidelines recommend the long-term, daily use of preventive medication for patients with persistent asthma. Inhaled corticosteroids (ICS) are the recommended therapy for patients with persistent asthma, regardless of disease severity. When ICS fail to control asthma symptoms, additional medications should be added to the regimen, in a stepwise manner, until adequate symptom control (defined as no activity limitations, no nighttime awakenings, minimal use of rescue medications, minimal respiratory symptoms, infrequent exacerbations, no ED visits, minimal adverse reactions to medication, and improved lung function values) has been achieved (GINA, 2006).
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O’Byrne, Paul. Global Initiative for Asthma, Global Strategy For Asthma Management and Prevention, GINA Report, 2006. Web.
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