title: Microvascular function is impaired in ankylosing spondylitis and improves after tumour necrosis factor alpha blockade.
abstract: OBJECTIVE
  Ankylosing spondylitis (AS) is associated with increased cardiovascular morbidity and mortality. Microvascular function has been linked to several risk factors for cardiovascular disease. Inflammation in AS may cause microvascular dysfunction. To test this, we assessed microvascular function in (a) patients with AS compared to healthy controls and (b) patients with AS before and after 1 month of anti-tumour necrosis factor (TNF)alpha treatment with etanercept.
  
  
  METHODS
  A total of 15 consecutive patients with AS, who were scheduled for etanercept treatment according to the Assessment in Ankylosing Spondylitis (ASAS) group guidelines, and 12 healthy controls matched for age and sex, were recruited. Endothelium-dependent and independent vasodilatation in skin were evaluated with laser Doppler fluxmetry after iontophoresis of acetylcholine and sodium nitroprusside, respectively. Videomicroscopy was used to measure recruitment of skin capillaries after arterial occlusion.
  
  
  RESULTS
  Compared to healthy controls, patients with AS had impaired endothelium-dependent vasodilatation and capillary recruitment. Following anti-TNFalpha treatment, microvascular function improved significantly for endothelium-dependent vasodilatation (p = 0.03) and capillary recruitment (p = 0.006). A significant correlation was observed between changes in endothelium-dependent vasodilatation and changes in erythrocyte sedimentation rate (ESR) (r = -0.56; p = 0.03).
  
  
  CONCLUSIONS
  Microvascular dysfunction is present in patients with AS with active disease, but improves as inflammation regresses after TNFalpha blockade.
authors.affiliation: Department of Rheumatology, Jan van Breemen Institute, Amsterdam, The Netherlands.
authors.forename: I C
authors.initials: IC
authors.lastname: van Eijk
authors.forename: M J L
authors.initials: MJ
authors.lastname: Peters
authors.forename: E H
authors.initials: EH
authors.lastname: Serné
authors.forename: I E
authors.initials: IE
authors.lastname: van der Horst-Bruinsma
authors.forename: B A C
authors.initials: BA
authors.lastname: Dijkmans
authors.forename: Y M
authors.initials: YM
authors.lastname: Smulders
authors.forename: M T
authors.initials: MT
authors.lastname: Nurmohamed
mesh_terms: D000109:Acetylcholine; D000328:Adult; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D008297:Male; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology; D008875:Middle Aged; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012867:Skin / Q000098:blood supply*; D013167:Spondylitis, Ankylosing / Q000188:drug therapy / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents
chemical_list: D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D014665:Vasodilator Agents; D002097:C-Reactive Protein; D000109:Acetylcholine; D000068800:Etanercept