title: Complement system and small HDL particles are associated with subclinical atherosclerosis in SLE patients.
abstract: BACKGROUND
  The complement system is involved in the pathogenic course of SLE. These patients exhibit metabolic disturbances in lipoprotein metabolism characterized by a pro-inflammatory status and an accelerated atherosclerosis. The aim of this study is to investigate whether levels of the complement are associated to the presence of subclinical atherosclerosis, lipid and glucose metabolism and inflammatory markers in SLE patients.
  
  
  METHODS
  Sixty-nine consecutive patients with SLE were recruited for the study. Fasting venous blood samples were collected on the same day as the measurements of cIMT were performed. Total plasma lipids and the distribution of subclasses of lipoproteins were analyzed by nuclear magnetic resonance spectroscopy.
  
  
  RESULTS
  We found direct correlations between cIMT values and the levels of C3, C4 and CH50. In multivariate analyses, the mean cIMT from the three territories were predicted by age (β = 0.005, 95% CI: 0.002-0.007, P < 0.001) and the functional hemolytic assay of the complement activity CH50 (β = 0.003, 95% CI: 0.001-0.006, P < 0.0013). The complement components were associated with BMI, SBP and levels of glucose. Small, dense HDL particles also correlated with the three complement components C3, C4 and CH50 in bivariate analyses. In multivariate analyses small HDL particles predicted levels of C3: β = 0.024, 95% CI: 0.013-0.035, P < 0.001; and C4: β = 0.005, 95% CI: 0.002-0.008, P = 0.006.
  
  
  CONCLUSIONS
  Activation of the complement system measured by functional assay CH50 is related to subclinical atherosclerosis in quiescent lupus patients and is activated by the small dense HDL particles.
authors.affiliation: Internal Medicine Department, Hospital Universitari Sant Joan de Reus, Institut Investigació Sanitaria Pere Virgili (IISPV), Universitat Rovira i Virgili, Reus, Spain.
authors.forename: Sandra
authors.initials: S
authors.lastname: Parra
authors.forename: Gloria
authors.initials: G
authors.lastname: Vives
authors.forename: Raimon
authors.initials: R
authors.lastname: Ferré
authors.forename: Marta
authors.initials: M
authors.lastname: González
authors.forename: Montse
authors.initials: M
authors.lastname: Guardiola
authors.forename: Josep
authors.initials: J
authors.lastname: Ribalta
authors.forename: Antoni
authors.initials: A
authors.lastname: Castro
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000209:etiology / Q000276:immunology*; D059168:Carotid Intima-Media Thickness; D003176:Complement C3 / Q000032:analysis*; D003181:Complement C4 / Q000032:analysis*; D015941:Complement Hemolytic Activity Assay; D003165:Complement System Proteins / Q000032:analysis*; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood; D008075:Lipoproteins, HDL / Q000502:physiology*; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000276:immunology*; D008297:Male; D008875:Middle Aged
chemical_list: D003176:Complement C3; D003181:Complement C4; D008055:Lipids; D008075:Lipoproteins, HDL; D003165:Complement System Proteins