Impaired serum cholesterol efflux capacity in rheumatoid arthritis and systemic lupus erythematosus. Issue 3 (5th April 2013)

• Record Type: Journal Article
• Authors: Ronda, Nicoletta; Favari, Elda; Borghi, Maria Orietta; Ingegnoli, Francesca; Gerosa, Maria; Chighizola, Cecilia; Zimetti, Francesca; Adorni, Maria Pia; Bernini, Franco; Meroni, Pier Luigi
• Is Part Of: Annals of the rheumatic diseases. Volume 73:Issue 3(2014)
• Page Start: 609
• Page End: 615
• Publication Date: 2013-04-05
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2012-202914
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Objectives: The marked cardiovascular risk in autoimmune diseases is only partly explained. The capacity of high-density lipoproteins (HDL) to promote cell cholesterol efflux is a property with a well-known anti-atherogenic significance, but is also involved in functional modulation of endothelial and immune cells. The aim of this work was to evaluate HDL functionality with respect to cell cholesterol efflux in rheumatoid arthritis (RA) and systemic lupus erythemathosus (SLE) patients. Methods: We evaluated serum cholesterol efflux capacity (CEC) of apoB-depleted serum, which mainly reflects HDL activity, from 30 RA and 30 SLE patients, and from 30 healthy controls by radioisotopic ex-vivo systems discriminating between the specific pathways of cholesterol efflux. Results: RA patients presented impairment of ATP-binding cassette G1-mediated CEC that correlated with disease activity. SLE patients showed a more complex pattern of modifications unrelated to disease activity, with marked reduction of ATP-binding cassette G1-mediated CEC and impairment of ATP-binding cassette A1-mediated CEC. The relationship between specific pathways of CEC values and serum total HDL differed between groups and there was no relationship with autoantibody profile or current therapy. Conclusions: CEC is impaired in RA and SLE, with a specific mechanism pattern in each disease not depending on serum HDL levels. These findings provide a new mechanism for the increased atherosclerotic risk in RA and SLE patients.