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Effects of short-term treatment with atorvastatin in smokers with asthma - a randomized controlled trialAbstract: Seventy one smokers with mild to moderate asthma were recruited to a randomized double-blind parallel group trial comparing treatment with atorvastatin (40 mg per day) versus placebo for 4 weeks. After 4 weeks treatment inhaled beclometasone (400 μg per day) was added to both treatment arms for a further 4 weeks. The primary outcome was morning peak expiratory flow after 4 weeks treatment. Secondary outcome measures included indices of asthma control and airway inflammation.At 4 weeks, there was no improvement in the atorvastatin group compared to the placebo group in morning peak expiratory flow [-10.67 L/min, 95% CI -38.70 to 17.37, p = 0.449], but there was an improvement with atorvastatin in asthma quality of life score [0.52, 95% CI 0.17 to 0.87 p = 0.005]. There was no significant improvement with atorvastatin and inhaled beclometasone compared to inhaled beclometasone alone in outcome measures at 8 weeks.Short-term treatment with atorvastatin does not alter lung function but may improve asthma quality of life in smokers with mild to moderate asthma.Clinicaltrials.gov identifier: NCT00463827Smokers with asthma have poor symptom control, accelerated decline in lung function and an attenuated response to inhaled corticosteroids compared to non-smokers with asthma[1-4]. Optimum medical therapy for smokers with asthma has not been established. There is an unmet need for alternative or additional drugs for smokers with asthma who are unable to stop smoking.In addition to reducing cholesterol biosynthesis by inhibiting 3-hydroxy-3-methylgluteryl coenzyme A (HMG-CoA) reductase, statins have pleiotropic anti-inflammatory effects[5] that may be beneficial in the treatment of chronic inflammatory diseases[5,6]. Preclinical in vitro and in vivo studies, including experimental models of allergic lung inflammation[7,8], have shown that statins reduce components of airway inflammation potentially relevant to the pathogenesis of asthma. Despite preliminary data showing an ab
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