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Atorvastatin as add-on therapy to ICSs offers no short-term improvement in asthma control, researchers report

Monday, December 01 2008 | Comments
Evidence Grade 2 What's This?
Adults with mild to moderate atopic asthma who use inhaled corticosteroids (ICSs) experience no short-term improvement in asthma control with the addition of atorvastatin, although it does appear to reduce sputum macrophage counts, new data demonstrate.

The authors explained that in addition to cholesterol-lowering properties,  statins also have anti-inflammatory effects.  Results of one investigation showed that patients with rheumatoid arthritis who were treated with atorvastatin demonstrated improvement in clinical outcome measures associated with a reduction in certain inflammatory biomarkers. To determine whether the addition of atorvastatin to ICSs improves lung function and airway inflammation in adults with atopic asthma, they conducted a randomized controlled trial that included 54 affected patients.

The participants were using <=1,000 mcg beclomethasone-equivalent daily and no other asthma medication other than a short-acting beta-2 agonist. The 24-week study involved a 2-week run-in period followed by randomization to either 40 mg/day atorvastatin as add-on therapy or placebo for 8 weeks and then crossover to the other treatment arm after a 6-week washout period. Throughout the study, patients recorded morning and evening peak expiratory flow (PEF) measurements and symptoms; they also underwent spirometry during office visits at regular intervals. Before and after each treatment period, the patients completed a validated asthma control questionnaire (ACQ) and an asthma quality of life questionnaire (AQLQ) in addition to providing blood samples and induced sputum for testing.

The study's primary outcome was morning PEF.

The results showed that at 8 weeks the change in mean morning PEF relative to baseline did not significantly differ between the atorvastatin and placebo treatment periods; the mean difference was only -0.5 L/minute (P=.921). There also was no significant difference between atorvastatin add-on therapy and placebo with regard to other lung function measures such as evening PEF or airway responsiveness to methacholine. ACQ and AQLQ scores also did not significantly differ.

However, the absolute sputum macrophage count was statistically significantly reduced after treatment with atorvastatin as compared with placebo (mean absolute difference, -449,000 cells; 95% CI, -801,000 to -97,000; P=.029). In addition, the sputum concentration of leukotriene B4 was significantly reduced (mean difference, -88.1 pg/mL; 95% CI, -156.4 pg/mL to -19.9 pg/mL; P=.014). Sputum concentrations of other inflammatory cytokines and mediators were similar after atorvastatin and placebo periods.

"The reduction in the sputum macrophage count suggests potential areas for investigation of atorvastatin in chronic lung disease in which activated alveolar macrophages have been implicated in the pathogenesis, such as [chronic obstructive pulmonary disease]," the investigators concluded. (Hothersall EJ, et al. Thorax 2008;63:1070-1075.)

This information concerns a use that has not been approved by the Food and Drug Administration.

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