Abstract
Objective
Inflammatory disease activity in patients with systemic lupus erythematosus (SLE) may affect the development of atherosclerosis, contributing to their increased risk of cardiovascular disease (CVD). This process may be mediated by anti–apolipoprotein A‐I (anti–Apo A‐I), anti–high‐density lipoprotein (anti‐HDL), and anti–C‐reactive protein (anti‐CRP) autoantibodies. We undertook this study to examine whether levels of these antibodies rise in association with increased SLE disease activity.
Methods
IgG anti–Apo A‐I, anti‐HDL, and anti‐CRP levels were measured in serum from the following groups: 39 patients with persistently high disease activity (British Isles Lupus Assessment Group [BILAG] A or B score) over the previous 2 years, 42 patients with persistently low disease activity (no BILAG A or B scores) over the previous 2 years, 34 healthy controls, 25 individual patients from whom paired samples (at time of disease flare and quiescence) were obtained and compared, 16 patients with newly diagnosed lupus nephritis from whom multiple samples were obtained and who were followed up prospectively for up to 2 years, and 24 patients with SLE who had experienced CVD events.
Results
Serum levels of IgG anti–Apo A‐I, anti‐HDL, and anti‐CRP were higher in patients with SLE than in controls. Anti–Apo A‐I and anti‐HDL levels, but not anti‐CRP levels, were higher in patients with persistently high disease activity than in those with low disease activity. Mean levels of the 3 autoantibodies in patients who had experienced CVD events lay between the mean levels in the high and low disease activity groups. Only levels of anti–Apo A‐I were significantly higher in samples obtained from individual patients during disease flares than in samples obtained during disease quiescence. In the lupus nephritis patients, anti–Apo A‐I and anti‐HDL levels correlated with serum levels of high avidity IgG anti–double‐stranded DNA.
Conclusion
Persistent disease activity is associated with a significant increase in IgG anti–Apo A‐I and anti‐HDL in patients with SLE.