title: An antiinflammatory effect of salmeterol, a long-acting beta(2) agonist, assessed in airway biopsies and bronchoalveolar lavage in asthma.
abstract: The addition of long-acting beta(2) agonists to inhaled corticosteroid (ICS) therapy in symptomatic patients with asthma improves clinical status more than increasing the dose of ICS. It has been suggested that these benefits could be at the cost of an increase in airway inflammation, but few histopathological studies have been performed in the relevant group. In a double-blind, parallel-group, placebo-controlled study, we randomly assigned 50 symptomatic patients with asthma who were receiving ICS (range, 100 -500 microgram/d) to 12 wk of supplementary treatment with salmeterol (50 microgram twice daily) or fluticasone (100 microgram twice daily) or placebo. Bronchial biopsies and BAL were obtained from 45 patients before and after treatment and analyzed. After treatment with salmeterol there was no deterioration of airway inflammation as assessed by mast cells, lymphocytes, or macrophages in BAL or biopsies, but rather a significant fall in EG1-positive eosinophils in the lamina propria (from a median 18.3 to 7.6 cells/mm, p = 0.01), which was not seen after treatment with fluticasone. The only cellular effect of added fluticasone was a decrease in BAL lymphocyte activation. There was a concurrent improvement in clinical status, more marked with salmeterol than with increased ICS. Thus, adding salmeterol to ICS is not associated with increased "allergic" airway inflammation, but conversely with a complementary antieosinophil effect.
authors.affiliation: Department of Respiratory Medicine, Alfred Hospital and Monash University Medical School, Prahran, Melbourne, Australia.
authors.forename: X
authors.initials: X
authors.lastname: Li
authors.forename: C
authors.initials: C
authors.lastname: Ward
authors.forename: F
authors.initials: F
authors.lastname: Thien
authors.forename: R
authors.initials: R
authors.lastname: Bish
authors.forename: T
authors.initials: T
authors.lastname: Bamford
authors.forename: X
authors.initials: X
authors.lastname: Bao
authors.forename: M
authors.initials: M
authors.lastname: Bailey
authors.forename: J W
authors.initials: JW
authors.lastname: Wilson
authors.forename: E
authors.initials: E
authors.lastname: Haydn Walters
mesh_terms: D000318:Adrenergic beta-Agonists / Q000627:therapeutic use*; D000420:Albuterol / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000730:Androstadienes / Q000627:therapeutic use; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D001707:Biopsy, Needle; D001980:Bronchi / Q000473:pathology*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology*; D004311:Double-Blind Method; D004804:Eosinophils / Q000473:pathology; D000068298:Fluticasone; D005541:Forced Expiratory Volume; D006801:Humans; D007249:Inflammation; D008214:Lymphocytes / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008407:Mast Cells / Q000473:pathology; D010366:Peak Expiratory Flow Rate; D000068299:Salmeterol Xinafoate
chemical_list: D000318:Adrenergic beta-Agonists; D000730:Androstadienes; D018927:Anti-Asthmatic Agents; D000893:Anti-Inflammatory Agents; D000068299:Salmeterol Xinafoate; D000068298:Fluticasone; D000420:Albuterol