RT Journal Article
SR Electronic
T1 Relations Between Autoantibodies Against Oxidized Low-Density Lipoprotein, Inflammation, Subclinical Atherosclerosis, and Cardiovascular Disease in Rheumatoid Arthritis
JF The Journal of Rheumatology
JO J Rheumatol
FD The Journal of Rheumatology
SP 1495
OP 1499
VO 35
IS 8
A1 MIKE J.L. PETERS
A1 VOKKO P. van HALM
A1 MICHAEL T. NURMOHAMED
A1 JAN DAMOISEAUX
A1 JAN WILLEM COHEN TERVAERT
A1 JOS W.R. TWISK
A1 BEN A.C. DIJKMANS
A1 ALEXANDRE E. VOSKUYL
YR 2008
UL http://www.jrheum.org/content/35/8/1495.abstract
AB Objective Rheumatoid arthritis (RA) is associated with an unexplained increased cardiovascular risk. Autoantibodies recognizing oxidized low-density lipoprotein (oxLDL-ab) are associated with atherosclerosis in the general population and have been reported in several autoimmune diseases. We investigated relations between oxLDL-ab, inflammation, subclinical atherosclerosis, and cardiovascular disease (CVD) in patients with RA. Methods In a nested case-control study, serum concentrations of oxLDL-ab were measured in 140 RA patients. Ultrasound examination of the carotid artery [i.e., carotid intima-media thickness (CIMT)] was performed in a third of these patients. Correlations were calculated for oxLDL-ab, C-reactive protein (CRP), and high-density lipoprotein (HDL) cholesterol. Regression analyses were used to examine associations between oxLDL-ab and prevalent CVD, and oxLDL-ab and CIMT. Results OxLDL-ab were positively correlated with CRP (r = 0.33, p < 0.001) and negatively correlated with HDL cholesterol (r = −0.28, p = 0.001). An indication for interaction was found (p = 0.09), suggesting that inflammation modifies the relation between HDL cholesterol and oxLDL-ab. OxLDL-ab were independently associated with intimal thickening, but not associated with prevalent CVD. Conclusion OxLDL-ab were strongly related with the degree of inflammation and may predispose to a higher risk for CVD, as they were independently associated with subclinical atherosclerosis in patients with RA.