December 29, 2009
Women with systemic lupus erythematosus (SLE) have increased atherosclerosis.
Identification of at-risk patients and the etiology underlying atherosclerosis in SLE remains
elusive. Normal HDL lose antioxidant capacity during inflammation, and these dysfunctional
HDL might predispose to atherosclerosis. The aim of this study is to determine whether
dysfunctional pro-inflammatory HDL (piHDL) is associated with subclinical atherosclerosis in
276 SLE women had carotid artery ultrasound to identify plaques and measure intimamedia
thickness (IMT). Antioxidant function of HDL was measured as change in oxidation of
LDL after addition of subject HDL. Two anti-inflammatory HDL components, paraoxonase and
apolipoprotein A-1, were also measured.
Results: 48.2% of patients had piHDL. 86.7% of subjects with plaque had piHDL, versus 40.7%
without (p<0.001). Patients with piHDL also had higher IMT (p<0.001). After multivariate
analysis, the only significant factors associated with plaque were piHDL, (OR 16.5, p<0.001),
age (OR 1.1, p<0.001), and tobacco use (OR 6.4, p=0.03). Factors associated with IMT
measurements in the highest quartile were piHDL (OR 2.6, p=0.01), age (OR 1.1, p<0.001),
body mass index (OR 1.08, p=0.01), and lifetime prednisone dose > 20g (OR 2.7, p=0.04);
hydroxychloroquine was protective against high IMT (OR 0.4, p=0.03). Paraoxonase activity
was inversely associated with IMT (r=-0.32, p=0.001), but there was no association between
plaque and paraoxonase or apolipoprotein A-1 levels.
Dysfunctional piHDL greatly increases risk for subclinical atherosclerosis
in SLE; they associate with increased prevalence of carotid plaque and with high IMT. The
presence of piHDL may help identify patients at risk for atherosclerosis.