Current developments in the physiology and management of asthma.

Abstract

Introduction Asthma is one of the classic diseases recognized by Hippocrates over 2000 years ago, yet it remains a serious global health problem because it is still not yet well understood. Asthma prevalence is reported to be on the increase worldwide especially among children (Kemp, 2003). Fortunately, recent advances in science have improved our understanding of asthma and the ability to manage it effectively (GINA, 2004) although deaths from asthma far from disappearing, have become more frequent in some countries (Jackson et al, 1982). Previously, most information on the pathology of asthma was obtained from postmortem tissue. Macroscopically, in patients that died of asthma the lungs are over – inflated, with both large and small airways filled with plugs comprised of a mixture of mucus, serum proteins, inflammatory cells, and cell debris. Microscopically, the findings are usually of extensive infiltration of the airway lumen and wall with eosinophils and lymphocytes, vasodilatation, evidence of micro vascular leakage and epithelial disruption (Dunnil, 1960; Krait et al, 1996). More recently, studies of living subjects with asthma have involved endobronchial biopsies of patients with mild disease, which have generally reflected the findings at autopsy. However studies in patients with more severe asthma suggest that in addition to eosinophils and lymphocytes, neutrophils are also present and may play a role in more severe disease (Wenzel et al, 1997). Currently, the application of immunological and molecular biological techniques to asthma has greatly improved understanding of the disease. This has placed T – lymphocytes as pivotal cells in orchestrating the inflammatory response through the release of multifunctional cytokines (Robinson et al, 1992). In addition to potent mediators that contract airway smooth muscle, increase micro vascular leakage, activate different neurons and stimulate mucus secreting cells, a number of factors are released that have the capacity to produce structural changes in the airways or attract inflammatory cells to cause injury to the bronchial tissue. Chemokines have also been shown to play a crucial role in the recruitment of inflammatory cells to the airways (Bousquet et al, 2000).