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 SLE.
276 SLE women had carotid artery ultrasound to identify plaques and measure intima-media 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.
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 16.1, p<0.001), age (OR 1.2, p<0.001), hypertension (OR 3.0, p=0.04), dyslipidemia (OR 3.4, p=0.04), and mixed racial background (OR 8.3, p=0.04). Factors associated with IMT measurements in the highest quartile were piHDL (OR 2.5, p=0.02), age (OR 1.1, p<0.001), body mass index (OR 1.07, p=0.04), lifetime prednisone dose > 20g (OR 2.8, p=0.04), and African American race (OR 8.3, p=0.001).
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.