Abstract
Inhaled corticosteroid is the first choice antiinflammatory therapy for chronic asthma. International guidelines are based upon data obtained in the non-smokers with asthma. The objective of this review is to highlight the interaction between cigarette smoking and metabolism of steroids and to consider the consequences of such an interaction on clinical and respiratory function. The mechanisms of corticosteroid resistance induced by cigarette smoking results of overexpression of glucocorticoid receptor beta, increased activation of pro-inflammatory transcription factors (nuclear factor-kappaB) and cytokines (IL-4, IL-8, TNF-alpha) or reduced histone deacetylase activity. Compared with non smokers with asthma, inhaled corticosteroids in smokers with asthma does not improve asthma control, lung function and bronchial obstruction. Active smoking impairs the efficacy of short-term oral corticosteroid treatment. Smoking cessation is the highest priority in smokers with asthma.
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