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Ann Rheum Dis 64:753-759 doi:10.1136/ard.2004.029033
  • Extended report

Accelerated atherosclerosis in patients with Wegener’s granulomatosis

  1. K de Leeuw1,
  2. J-S Sanders1,
  3. C Stegeman2,
  4. A Smit3,
  5. C G Kallenberg1,
  6. M Bijl1
  1. 1Department of Clinical Immunology, University Hospital, Groningen, Netherlands
  2. 2Department of Nephrology, University Hospital, Groningen
  3. 3Department of Vascular diseases, University Hospital, Groningen
  1. Correspondence to:
    MsKarina de Leeuw
    Department of Internal Medicine, Division of Clinical Immunology, University Hospital, PO Box 30.001, 9700 RB Groningen, Netherlands; k.de.leeuwint.azg.nl
  • Accepted 10 September 2004
  • Published Online First 16 September 2004

Abstract

Background: Several autoimmune disorders are complicated by excess cardiovascular disease. In addition to traditional risk factors, non-traditional risk factors such as endothelial activation and excessive vascular remodelling might be determinants of the progression of atherosclerosis in patients with an autoimmune disease.

Objective: To evaluate whether patients with Wegener’s granulomatosis (WG) have an increased prevalence of atherosclerosis and to determine predisposing factors.

Methods: 29 WG patients (19 men; mean (SD) age, 53 (14) years) with inactive disease and 26 controls (16 men; age 53 (15) years) were studied. Common carotid intima–media thickness (IMT) was measured by ultrasound. In all individuals traditional risk factors for cardiovascular disease were determined. High sensitivity C reactive protein (hsCRP) was measured. Endothelial activation was assessed by measuring thrombomodulin, vascular cell adhesion molecule-1, and von Willebrand factor. As a marker of vascular remodelling matrix metalloproteinases (MMP-3 and MMP-9) and TIMP-1 were measured.

Results: IMT was increased in WG patients compared with controls (p<0.05). No differences in traditional risk factors and endothelial activation markers between patients and controls were found. Levels of hsCRP, MMPs, and TIMP-1 were increased in WG patients (p<0.05).

Conclusions: Increased IMT found in WG patients cannot be explained by an increased prevalence of traditional risk factors. Although endothelial activation markers in WG patients with inactive disease were not increased, the raised levels of hsCRP, MMPs, and TIMP-1 suggest that enhanced inflammation and excessive vascular remodelling are contributing factors in the development of accelerated atherosclerosis in WG.

Footnotes