title: Traditional risk factor assessment does not capture the extent of cardiovascular risk in systemic lupus erythematosus.
abstract: BACKGROUND
  Systemic lupus erythematosus (SLE) is associated with accelerated atherosclerosis. However, the degree of endothelial dysfunction and its relationship to traditional and novel cardiovascular risk factors have not been examined in SLE.
  
  
  METHODS
  In a case-control design, 35 patients with clinically stable SLE and 35 control subjects matched for age, sex, body mass index and smoking status were studied. Arterial elasticity, lipid profile, homocysteine, measures of inflammation and oxidative stress were determined.
  
  
  RESULTS
  Among traditional vascular risk factors, there was a nonsignificant trend towards lower blood pressure in the control subjects, whereas low-density lipoprotein (LDL) cholesterol levels were significantly lower in the SLE group (2.5 vs 3.3 mmol/L, P < 0.001). Patients with SLE had significantly lower small artery elasticity (SAE; 4.9 vs 7.0 ml/mmHg x 100, P < 0.001) and higher plasma homocysteine (11.4 vs 8.3 mmol/L, P = 0.002) than control subjects. Levels of serum sVCAM-1 (614 vs 494 ng/mL, P = 0.002), oxidized LDL (144 vs 97, P < 0.001) and CD40 ligand (4385 vs 1373 pg/ml, P = 0.001) were significantly higher in SLE. Oxidized LDL levels, older age at SLE diagnosis and higher disease damage scores correlated inversely with SAE but not traditional risk factors.
  
  
  CONCLUSIONS
  Impaired endothelial function as shown by decreased SAE, and an adverse profile of novel proatherogenic and prothrombotic vascular disease risk factors were prevalent in clinically quiescent SLE. These findings show the vulnerability of patients with SLE for atherosclerosis, and emphasize that assessments based on traditional risk factors alone may be inadequate.
authors.affiliation: Department of Medicine, The University of Melbourne, St. Vincent's Hospital, Melbourne, Victoria, Australia.
authors.forename: A B
authors.initials: AB
authors.lastname: Lee
authors.forename: T
authors.initials: T
authors.lastname: Godfrey
authors.forename: K G
authors.initials: KG
authors.lastname: Rowley
authors.forename: C S
authors.initials: CS
authors.lastname: Karschimkus
authors.forename: G
authors.initials: G
authors.lastname: Dragicevic
authors.forename: E
authors.initials: E
authors.lastname: Romas
authors.forename: L
authors.initials: L
authors.lastname: Clemens
authors.forename: A M
authors.initials: AM
authors.lastname: Wilson
authors.forename: M
authors.initials: M
authors.lastname: Nikpour
authors.forename: D L
authors.initials: DL
authors.lastname: Prior
authors.forename: J D
authors.initials: JD
authors.lastname: Best
authors.forename: A J
authors.initials: AJ
authors.lastname: Jenkins
mesh_terms: D000328:Adult; D001158:Arteries / Q000503:physiopathology*; D001794:Blood Pressure; D019013:CD40 Antigens / Q000097:blood; D016022:Case-Control Studies; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000209:etiology*; D004548:Elasticity; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006710:Homocysteine / Q000097:blood; D006801:Humans; D016015:Logistic Models; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012307:Risk Factors; D012720:Severity of Illness Index; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D019013:CD40 Antigens; D008078:Cholesterol, LDL; D019010:Vascular Cell Adhesion Molecule-1; D006710:Homocysteine