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Effects of Fluticasone on Systemic Markers of Inflammation in Chronic Obstructive Pulmonary Disease

James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research; Department of Medicine (Pulmonary Division), University of British Columbia, Vancouver, British Columbia; Department of Medicine, Pulmonary Division, University of Alberta, Edmonton; and Wetaskiwin General Hospital, Wetaskiwin, Alberta, Canada

Correspondence and requests for reprints should be addressed to S. F. Paul Man, M.D., James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, St. Paul's Hospital, 1081 Burrard Street, Vancouver, BC, V6Z 1Y6 Canada. E-mail: pman{at}providencehealth.bc.ca

Systemic inflammation is present in chronic obstructive pulmonary disease (COPD), which has been linked to cardiovascular morbidity and mortality. We determined the effects of oral and inhaled corticosteroids on serum markers of inflammation in patients with stable COPD. We recruited 41 patients with mild to moderate COPD. After 4 weeks during which inhaled corticosteroids were discontinued, patients were assigned to fluticasone (500 mcg twice a day), oral prednisone (30 mg/day), or placebo over 2 weeks, followed by 8 weeks of fluticasone at 500 mcg twice a day and another 8 weeks at 1,000 mcg twice a day. Withdrawal of inhaled corticosteroids increased baseline C-reactive protein (CRP) levels by 71% (95% confidence interval [CI], 16–152%). Two weeks with inhaled fluticasone reduced CRP levels by 50% (95% CI, 9–73%); prednisone reduced it by 63% (95% CI, 29–81%). No significant changes were observed with the placebo. An additional 8 weeks of fluticasone were associated with CRP levels that were lower than those at baseline (a 29% reduction; 95% CI, 7–46%). Inhaled and oral corticosteroids are effective in reducing serum CRP levels in patients with COPD and suggest their potential use for improving cardiovascular outcomes in COPD.

Key Words: chronic obstructive pulmonary disease • corticosteroid • C-reactive protein • fluticasone • prednisone

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