Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose . Patients with systemic lupus erythematosus (SLE) have an increased risk of cardiovascular disease (CVD), which may be due to an increased prevalence of atherosclerosis. Atherosclerosis is recognized as being associated with chronic inflammation. SLE is characterized by activation of the innate immune system and an increased expression of type I interferon (IFN) leading to chronic inflammation. Galectin-3 binding protein(G3BP) is a putative marker of IFN activation and has recently been shown to be increased in plasma of SLE patients. The objective of this study was to quantify plasma G3BP and determine the association of G3BP and atherosclerosis in SLE.
Methods . In a population-based predominantly Caucasian cohort we recruited 80 SLE patients. Atherosclerotic burden was assessed by cardiac CT scan for coronary calcium score (CAC) and carotid duplex for carotid intima-media thickness (IMT) and plaque using the ARIC study plaque definition. The presence of atherosclerosis was defined by a CAC > 0 and/or carotid plaque. A total of 38 patients were found to be negative for atherosclerosis and 42 patients were found to be positive. The concentration of galectin-3 binding protein (G3BP, 90k/Mac-2 BP) was determined in plasma samples by a commercially available sandwich-type enzyme-linked immunosorbent assay (eBioscience). Samples were diluted 1:100 and concentrations were determined by extrapolation to standard curves obtained with known concentrations of G3BP.
Results . Mean plasma galectin-3-binding protein in the entire study population was 59.54 ng/ml. Plasma galectin-3-binding protein did not significantly differ between SLE patients with atherosclerosis and without atherosclerosis. G3BP levels were significantly correlated with disease activity as expressed by SLEDAI (P=0.02).
Conclusion . The inflammatory marker galectin-3-binding protein is not significantly associated with atherosclerosis, but we confirm its association with disease activity in SLE patients.
Disclosure:
S. Kay,
None;
N. Heegaard,
None;
A. Voss,
None.
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