title: Accelerated atherosclerosis in patients with Wegener's granulomatosis.
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.
authors.affiliation: Department of Clinical Immunology, University Hospital, PO Box 30.001, 9700 RB Groningen, Netherlands. k.de.leeuw@int.azg.nl
authors.forename: K
authors.initials: K
authors.lastname: de Leeuw
authors.forename: J-S
authors.initials: JS
authors.lastname: Sanders
authors.forename: C
authors.initials: C
authors.lastname: Stegeman
authors.forename: A
authors.initials: A
authors.lastname: Smit
authors.forename: C G
authors.initials: CG
authors.lastname: Kallenberg
authors.forename: M
authors.initials: M
authors.lastname: Bijl
mesh_terms: D000328:Adult; D000368:Aged; D001161:Arteriosclerosis / Q000097:blood / Q000209:etiology* / Q000473:pathology; D001327:Autoimmune Diseases / Q000097:blood / Q000150:complications* / Q000473:pathology; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000209:etiology; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging / Q000473:pathology; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D014890:Granulomatosis with Polyangiitis / Q000097:blood / Q000150:complications* / Q000473:pathology; D006801:Humans; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000097:blood; D020780:Matrix Metalloproteinase 9 / Q000097:blood; D008875:Middle Aged; D012307:Risk Factors; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000097:blood; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology; D017540:Tunica Media / Q000000981:diagnostic imaging / Q000473:pathology; D014463:Ultrasonography
chemical_list: D019715:Tissue Inhibitor of Metalloproteinase-1; D002097:C-Reactive Protein; D019278:Matrix Metalloproteinase 3; D020780:Matrix Metalloproteinase 9