title: Impaired serum cholesterol efflux capacity in rheumatoid arthritis and systemic lupus erythematosus.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Pharmacy, University of Parma, , Parma, Italy.
authors.forename: Nicoletta
authors.initials: N
authors.lastname: Ronda
authors.forename: Elda
authors.initials: E
authors.lastname: Favari
authors.forename: Maria Orietta
authors.initials: MO
authors.lastname: Borghi
authors.forename: Francesca
authors.initials: F
authors.lastname: Ingegnoli
authors.forename: Maria
authors.initials: M
authors.lastname: Gerosa
authors.forename: Cecilia
authors.initials: C
authors.lastname: Chighizola
authors.forename: Francesca
authors.initials: F
authors.lastname: Zimetti
authors.forename: Maria Pia
authors.initials: MP
authors.lastname: Adorni
authors.forename: Franco
authors.initials: F
authors.lastname: Bernini
authors.forename: Pier Luigi
authors.initials: PL
authors.lastname: Meroni
mesh_terms: D064286:ATP Binding Cassette Transporter 1 / Q000502:physiology; D000070998:ATP Binding Cassette Transporter, Subfamily G, Member 1; D018528:ATP-Binding Cassette Transporters / Q000502:physiology; D000328:Adult; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000276:immunology; D001323:Autoantibodies / Q000097:blood; D001692:Biological Transport / Q000502:physiology; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood / Q000502:physiology; D005260:Female; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D051122:Scavenger Receptors, Class B / Q000097:blood / Q000502:physiology; D012720:Severity of Illness Index
chemical_list: C577836:ABCA1 protein, human; C419353:ABCG1 protein, human; D064286:ATP Binding Cassette Transporter 1; D000070998:ATP Binding Cassette Transporter, Subfamily G, Member 1; D018528:ATP-Binding Cassette Transporters; D001323:Autoantibodies; D008076:Cholesterol, HDL; C495124:SCARB1 protein, human; D051122:Scavenger Receptors, Class B; D002784:Cholesterol