Microvascular function is preserved in newly diagnosed rheumatoid arthritis and low systemic inflammatory activity

Microvascular function is preserved in newly diagnosed rheumatoid arthritis and low systemic inflammatory activity

  • نوع فایل : کتاب
  • زبان : انگلیسی
  • مؤلف : Izhar C. van Eijk & Erik H. Serné & Ben A. C. Dijkmans & Yvo Smulders & Michael Nurmohamed
  • چاپ و سال / کشور: 2011

Description

Rheumatoid arthritis (RA) is associated with increased cardiovascular morbidity and mortality. Microvascular function has been linked to several risk factors for cardiovascular disease and may be affected in RA. It is, however, presently unknown at what point in the disease course the abnormalities in microvascular function occur. We determined whether microvascular function is already disturbed in early disease-modifying antirheumatic drugs (DMARD)-naive RA patients with low systemic inflammation. Fifteen consecutive RA patients with a median symptom duration of 5 months, a C-reactive protein level of .20 mg/l and without a history of cardiovascular disease, and age 15 and sex-matched healthy controls were recruited. Endothelium-dependent and endotheliumindependent vasodilatation in skin was 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. CRP and ESR levels were mildly, but significantly elevated in patients compared to controls. No differences in both endothelium-dependent vasodilatation and capillary recruitment were observed between groups [709% (95% CI, 457.961%) vs 797% (95% CI, 556. 1,037%), P = 0.59 and 37% (95% CI, 26.47%) vs 41% (95% CI, 31.50%), P=0.59, respectively]. Skin microvascular function is preserved in early, DMARD-naive RA patients with moderately active RA but low systemic inflammatory activity. Both the extent of the systemic inflammation and disease duration, therefore, may be important determinants of microvascular dysfunction and subsequent increased risk for cardiovascular disease.
Clin Rheumatol (2011) 30:1113–1118 eceived: 27 December 2010 / Revised: 13 March 2011 / Accepted: 4 April 2011 / Published online: 13 April 2011
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