title: Differences in responses upon corticosteroid therapy between smoking and non-smoking patients with COPD.
abstract: Inhaled corticosteroids have a high level of topical anti-inflammatory activity. However, in patients with COPD these drugs have been reported to exert limited effects. A reduction in histone deacetylase (HDAC) activity is suggested to prevent the anti-inflammatory action of corticosteroids. Cigarette smoke is known to reduce HDAC expression. The aim of this study is to compare the outcome of corticosteroid therapy in both smoking and non-smoking COPD patients. Twenty-three smoking patients and 18 ex-smoking patients with COPD were treated with inhaled corticosteroids for a period of 2 months. Blood and induced sputum samples were collected before and after treatment. Values of FEV(1) %-predicted did not change upon the therapy, but there was a trend to improve in the ex-smokers (63.1 -> 64.8%-pred.), compared with a decrease in the smokers (63.3 -> 61.6%-pred.). The levels of the pro-inflammatory cytokine IL-8 increased in the group of smokers from 379 +/-78 to 526 +/-118 ng/ml. Although not significant, a slight decrease from 382 +/-70 to 342 +/-62 ng/ml was observed in the group of ex-smokers. The neutrophil related elastase activity showed similar effects after steroid treatment, it went up from 36.4 +/-12.0 to 113.5 +/-9.7 nmol/l in smokers, and decreased from 346.2 +/-72.1 to 131.1 +/-6.5 nmol/l in ex-smokers with COPD. These results support the evidence that inhaled corticosteroids have no anti-inflammatory effects in COPD patients, but only when these patients are still smoking. Smoking cessation seems the best therapy for COPD patients.
authors.affiliation: Department of Respiratory Medicine, University of Antwerp, Belgium. Fransvan.Overveld@pmintl.com
authors.forename: F J
authors.initials: FJ
authors.lastname: Van Overveld
authors.forename: U
authors.initials: U
authors.lastname: Demkow
authors.forename: D
authors.initials: D
authors.lastname: Górecka
authors.forename: W A
authors.initials: WA
authors.lastname: De Backer
authors.forename: J
authors.initials: J
authors.lastname: Zieliński
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use*; D000368:Aged; D000418:Albumins / Q000378:metabolism; D000730:Androstadienes / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D019819:Budesonide / Q000627:therapeutic use*; D002452:Cell Count; D005260:Female; D000068298:Fluticasone; D005541:Forced Expiratory Volume; D006801:Humans; D016209:Interleukin-8 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000201:enzymology / Q000276:immunology; D010196:Pancreatic Elastase / Q000097:blood; D009195:Peroxidase / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000188:drug therapy*; D012907:Smoking; D016540:Smoking Cessation; D013183:Sputum / Q000737:chemistry / Q000166:cytology; D016896:Treatment Outcome
chemical_list: D000305:Adrenal Cortex Hormones; D000418:Albumins; D000730:Androstadienes; D000893:Anti-Inflammatory Agents; D016209:Interleukin-8; D019819:Budesonide; D000068298:Fluticasone; D009195:Peroxidase; D010196:Pancreatic Elastase