title: Effects of a brief course of azithromycin on soluble cell adhesion molecules and markers of inflammation in survivors of an acute coronary syndrome: A double-blind, randomized, placebo-controlled study.
abstract: BACKGROUND
  The anti-chlamydial antibiotic, azithromycin, may improve outcome in patients who survive an acute coronary syndrome. The mechanisms are, however, poorly understood. The aims of this study were to define any relationship between Chlamydia pneumoniae seropositivity and levels of specific markers of endothelial activation (soluble cell adhesion molecules) and more general markers of inflammation (C-reactive protein [CRP] and interleukin-6 [IL-6]) and to assess whether azithromycin had any effect on such markers.
  
  
  METHODS
  Patients who survived an acute coronary syndrome were randomized to receive treatment with azithromycin (n = 72) or placebo (n = 69) for 5 days. Before therapy, C pneumoniae IgA and IgG titers were checked, with serum levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1, soluble E-selectin (sE-selectin), soluble P-selectin, high-sensitivity CRP, and IL-6. They were rechecked 3 months later.
  
  
  RESULTS
  There were no significant correlations between C pneumoniae titers and levels of CRP, IL-6, or soluble cell adhesion molecules. However, azithromycin treatment significantly reduced mean sICAM-1 levels (P =.006). This effect was more marked in patients with elevated titers of C pneumoniae IgA and IgG. Soluble E-selectin levels were also reduced in patients who were seropositive, but no effects were seen on other endothelial or inflammatory markers.
  
  
  CONCLUSIONS
  After an acute coronary syndrome, a 5-day course of azithromycin reduces levels of sICAM-1, a marker of endothelial cell activation. Although these data suggest a potentially beneficial role for azithromycin, they should be interpreted with caution.
authors.affiliation: Department of Cardiology the Royal Infirmary of Edinburgh, Edinburgh, Scotland, UK. g.hillis@abdn.ac.uk
authors.forename: Graham S
authors.initials: GS
authors.lastname: Hillis
authors.forename: Claire V
authors.initials: CV
authors.lastname: Pearson
authors.forename: Scott A
authors.initials: SA
authors.lastname: Harding
authors.forename: Sheena
authors.initials: S
authors.lastname: Sutherland
authors.forename: Christopher A
authors.initials: CA
authors.lastname: Ludlam
authors.forename: John C
authors.initials: JC
authors.lastname: Marioni
authors.forename: Robin J
authors.initials: RJ
authors.lastname: Prescott
authors.forename: Keith A A
authors.initials: KA
authors.lastname: Fox
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Flapan
mesh_terms: D000368:Aged; D000900:Anti-Bacterial Agents / Q000494:pharmacology / Q000627:therapeutic use*; D000907:Antibodies, Bacterial / Q000097:blood; D017963:Azithromycin / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis / Q000187:drug effects; D015815:Cell Adhesion Molecules / Q000097:blood / Q000187:drug effects*; D023521:Chlamydophila Infections / Q000150:complications / Q000188:drug therapy*; D016993:Chlamydophila pneumoniae / Q000276:immunology / Q000302:isolation & purification; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood / Q000187:drug effects; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000150:complications / Q000188:drug therapy*
chemical_list: D000900:Anti-Bacterial Agents; D000907:Antibodies, Bacterial; D015415:Biomarkers; D015815:Cell Adhesion Molecules; D018836:Inflammation Mediators; D015850:Interleukin-6; D018799:Intercellular Adhesion Molecule-1; D017963:Azithromycin; D002097:C-Reactive Protein