2019 Volume 249 Issue 1 Pages 1-7
A defect in clearance of apoptotic materials is pivotal in the pathogenesis of systemic lupus erythematosus (SLE). Protein S participates in the removal of apoptotic remnants and the anticoagulation pathway. The aim of the study was to clarify the relationship between plasma levels of free protein S and the disease activity or subclinical atherosclerosis in SLE. Free protein S was measured by an enzyme-linked immunosorbent assay, and patients were classified into two groups of free protein S levels: low (< 50%) and normal (≥ 50%). One hundred-eleven Korean female patients with SLE were enrolled, and the levels of free protein S were 67.4 ± 19.7%. Carotid plaque was detected in 25 (22.5%) patients. Twenty-one patients with low free protein S had lower hemoglobin (11.4 ± 1.4 vs. 12.5 ± 1.4 g/dL) and lymphocytes (1,221 ± 609 vs. 1,720 ± 1,097/µL), higher erythrocyte sedimentation rate (30.1 ± 20.6 vs. 20.8 ± 17.8 mm/h), and lower complement 3 (80.8 ± 27.6 vs. 103.4 ± 25.8 mg/dL) and complement 4 (15.6 ± 10.4 vs. 21.5 ± 7.6 mg/dL) than those with normal protein S. There was no significant difference in the proportion of patients with increased carotid artery intima-media thickness (> 4.6 mm) or with carotid artery plaque between two groups. The low levels of free protein S were associated with hemoglobin (OR = 0.64, p = 0.04) and complement 3 (OR = 0.96, p = 0.005). Free protein S is correlated with disease activity, but not with subclinical atherosclerosis in SLE.
