Serum lipoprotein‐associated phospholipase A2 activity in Chinese patients with systemic lupus erythematosus

Abstract

BackgroundFew studies have explored the association between lipoprotein‐associated phospholipase A2 (Lp‐PLA2) and systemic lupus erythematosus (SLE). However, most of these studies have investigated only European patient populations and have come to contradictory conclusions. Furthermore, few studies have been conducted on Chinese patient groups. This study aimed to explore the association between serum Lp‐PLA2 activity and SLE in a Chinese patient group.MethodsSerum Lp‐PLA2 activity was detected in 154 SLE patients and 55 age‐, sex‐, and body mass index‐matched healthy controls. Information concerning the anthropometric data, clinical manifestations, SLE Disease Activity Index 2000 (SLEDAI‐2K), complement C3 (C3), and complement C4 (C4) erythrocyte sedimentation rate (ESR), and autoantibodies were evaluated.ResultsThe average level of serum Lp‐PLA2 activity was 221 ± 56 U/L in SLE patients compared with 160 ± 37 U/L in healthy controls (p < 0.001). SLE patients that presented with nephritis, anemia, and fibrinolytic abnormality had higher serum Lp‐PLA2 activity than SLE patients who did not present with these symptoms (p < 0.05), and the levels of serum Lp‐PLA2 activity correlated with the severity of the clinical manifestations (p < 0.001). There was no correlation between serum Lp‐PLA2 activity and serum autoantibodies levels (p > 0.05). According to Spearman’s rank correlation coefficient, ESR, SLEDAI‐2K, C3, and C4 significantly correlated with serum Lp‐PLA2 activity (p < 0.001). According to binary logistic regression, Lp‐PLA2 activity was independently associated with active SLE in patients (OR 1.049; 95% CI: 1.025–1.073, p < 0.001).ConclusionsSerum Lp‐PLA2 activity is associated with some clinical manifestations (nephritis, anemia, and fibrinolytic abnormality) in SLE patients, and its activity may contribute to the development of SLE disease. These findings provide new insight into the pathogenesis of SLE.