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Microvascular function is impaired in ankylosing spondylitis and improves after tumour necrosis factor α blockade
  1. I C van Eijk1,
  2. M J L Peters2,
  3. E H Serné3,
  4. I E van der Horst-Bruinsma2,
  5. B A C Dijkmans1,2,
  6. Y M Smulders3,
  7. M T Nurmohamed1,2,3
  1. 1
    Department of Rheumatology, Jan van Breemen Institute, Amsterdam, The Netherlands
  2. 2
    Department of Rheumatology, VU University Medical Center, Amsterdam, The Netherlands
  3. 3
    Department of Internal Medicine and ICaR-VU, VU University Medical Center, Amsterdam, The Netherlands
  1. Dr M T Nurmohamed, Jan van Breemen Institute, Dr Jan van Breemenstraat 2, 1056 AB Amsterdam, The Netherlands; m.nurmohamed{at}janvanbreemen.nl

Abstract

Objectives: 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)α 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-TNFα 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).

Conclusion: Microvascular dysfunction is present in patients with AS with active disease, but improves as inflammation regresses after TNFα blockade.

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Footnotes

  • Competing interests: None declared.

  • Ethics approval: All participants gave written informed consent and the study protocol was approved by the Institutional Ethics Committee of both hospitals.

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