No abstract

The study was designed to assess the effect of cigarette smoking on the therapeutic response to oral corticosteroids in chronic stable asthma. We performed a randomized, placebo-controlled, crossover study with prednisolone (40 mg daily) or placebo for 2 weeks in smokers with asthma, ex-smokers with asthma, and never-smokers with asthma. All subjects had reversibility in FEV 1 after nebulized albuterol of 15% or more and a mean postbronchodilator FEV 1 % predicted of more than 80%. Efficacy was assessed using FEV 1 , daily PEF, and an asthma control score. There was a significant improvement after oral prednisolone compared with placebo in FEV 1 , ml (mean difference, 237; 95% confidence intervals, 43, 231; p ϭ 0.019), morning PEF L/m (mean difference, 36.8; 95% confidence intervals (CI), 11, 62; p ϭ 0.006), and asthma control score (mean difference, Ϫ0.72; 95% CI, Ϫ1.2, Ϫ0.3; p ϭ 0.004) in never-smokers with asthma but no change in smokers with asthma (mean differences of 47, 6.5, and Ϫ0.05 with p values of 0.605, 0.47, and 0.865, respectively). Ex-smokers with asthma had a significant improvement in morning and night PEF (mean difference, 29.1; CI, 2.3, 56; p ϭ 0.04 and 52.4; CI, 26, 79; p ϭ 0.003, respectively), but not in FEV 1 or asthma control score. We conclude that active smoking impairs the efficacy of short-term oral corticosteroid treatment in chronic asthma.Active cigarette smoking is common in adult patients with asthma, with over 20% being current smokers (1, 2). A recent survey of adults presenting to emergency departments with acute asthma revealed that 35% were cigarette smokers (3). Current smokers with asthma, compared with never-smokers, have more severe asthma symptoms (1, 2), an accelerated decline in lung function (4), an increase in hospitalization rates for asthma (5), and increased mortality after a near-fatal asthma attack (6). A further 22-43% of adults with asthma are ex-smokers (1, 2).There is relatively little information on the influence of cigarette smoking on the therapeutic effect of asthma medications. Corticosteroids are currently the best antiinflammatory therapy available for the treatment of asthma and are recommended in international guidelines (7). The evidence for these recommendations is based on clinical trials that have been undertaken largely in nonsmoking patients with asthma. In a randomized controlled trial, we recently found that active cigarette smoking impaired the efficacy of short-term inhaled corticosteroid treatment in steroid-naïve patients with asthma (8). This result confirmed an earlier uncontrolled study that reported a reduced response to inhaled corticosteroids in terms of airway function

No abstract

Cough severity and sputum ECP levels are modestly reduced by inhaled corticosteroids in patients with chronic cough persisting for more than 1 year. LTB(4), Cys-LT, PGE(2), IL-8, myeloperoxidase, and TNF-alpha levels are unaltered by this therapy. This raises the possibility that drugs targeted to reduce the effects of these mediators might be of benefit in chronic persistent cough.

IL-15 and IL-13 production appears to be reciprocally regulated by steroid therapy in asthma patients. The steroid-associated increase in IL-15 may regulate a fundamental shift away from an inflammatory Th2-type environment in asthma and may be an essential component of the cytokine modulation underlying the therapeutic benefit of corticosteroids in this condition.