title: PON1, a new biomarker of cardiovascular disease, is low in patients with systemic vasculitis.
abstract: OBJECTIVE
  Because systemic vasculitis (SV) predisposes to atherosclerosis, and high-density lipoprotein (HDL) prevents atherosclerosis by "reverse cholesterol transport" and by inhibiting low-density lipoprotein (LDL) oxidation thanks to apolipoprotein A-I (Apo-AI) and paraoxonase 1 (PON1), we assessed whether LDL oxidation was increased in SV and associated with less PON1 activity.
  
  
  METHODS
  The sera of 33 patients with active SV (ASV), 32 in full remission of SV (RSV) and 20 healthy subjects (HS) were analyzed for C-reactive protein (CRP), high-sensitivity-CRP, lipids, lipoproteins, apolipoproteins, PON1 activity, LDL-immune complexes (LDL-IC), and auto-antibodies to oxidized-LDL (ox-LDL), and anticardiolipin antibodies.
  
  
  RESULTS
  CRP was higher in ASV than RSV and HS, and negatively correlated with HDL-cholesterol and Apo-AI. Autoantibodies to ox-LDL and highly oxidized malondialdehyde-LDL were higher in RSV than ASV and HS (P<0.05). LDL-IC titers were higher in ASV than RSV and HS (P<0.05). PON1 activity was lower in ASV and RSV than HS (P=0.02). A trend toward a negative correlation between basal PON1 activity and anti-MDA-LDL antibodies (P=0.06) was observed.
  
  
  CONCLUSIONS
  Inflammatory markers in SV were associated with a modified lipoprotein profile, which could lower PON1 activity and contribute to increased ox-LDL titers and accelerated atherosclerosis development.
authors.affiliation: Department of Nephrology and Internal Medicine, Hospital of Valenciennes, Valenciennes, France.
authors.forename: Thomas
authors.initials: T
authors.lastname: Quéméneur
authors.forename: Françoise
authors.initials: F
authors.lastname: Martin-Nizard
authors.forename: Abdelmejid
authors.initials: A
authors.lastname: Kandoussi
authors.forename: Xavier
authors.initials: X
authors.lastname: Kyndt
authors.forename: Philippe
authors.initials: P
authors.lastname: Vanhille
authors.forename: Eric
authors.initials: E
authors.lastname: Hachulla
authors.forename: Pierre-Yves
authors.initials: PY
authors.lastname: Hatron
authors.forename: Jean-Charles
authors.initials: JC
authors.lastname: Fruchart
authors.forename: Patrick
authors.initials: P
authors.lastname: Duriez
authors.forename: Marc
authors.initials: M
authors.lastname: Lambert
mesh_terms: D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood; D043303:Aryldialkylphosphatase / Q000097:blood*; D050197:Atherosclerosis / Q000097:blood / Q000276:immunology; D001323:Autoantibodies / Q000097:blood; D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism; D008076:Cholesterol, HDL / Q000097:blood; D005260:Female; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood / Q000276:immunology / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000031:analogs & derivatives / Q000097:blood / Q000276:immunology; D008875:Middle Aged; D018384:Oxidative Stress; D014657:Vasculitis / Q000097:blood* / Q000276:immunology*
chemical_list: D016632:Apolipoprotein A-I; D001323:Autoantibodies; D015415:Biomarkers; D008076:Cholesterol, HDL; D008077:Lipoproteins, LDL; C502964:malondialdehyde-low density lipoprotein, mouse; C099252:oxidized low density lipoprotein; D008315:Malondialdehyde; D002097:C-Reactive Protein; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human