Background/Purpose: Leucine-rich a2-glycoprotein (LRG) is a plasma protein which contains leucine-rich repeats (LRRs). Though physiological functions of LRG have not been clarified yet, it has been reported that LRG could be a marker of granulocytic differentiation and its expression was up-regulated during neutrophil differentiation. LRG could show a significant increase in some inflammatory conditions, such as ulcerative colitis, in where serum LRG concentrations were well correlated with disease activity, and the expressions of LRG were increased in inflamed colonic tissues. However, the association between plasma LRG level and disease activity in RA patients remains obscure. This study aimed to investigate whether the plasma LRG level is elevated in patients with RA and its correlation with disease activity and other parameters.

Methods: Our study included 69 patients with RA and 48 age- and sex- matched healthy controls. Plasma samples were obtained from patients with RA during active and inactive disease status and from controls. We assessed the clinical characteristics and laboratory parameters including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and disease activity score 28 (DAS28). Plasma concentrations of tumor necrosis factor-a (TNF-a) and LRG were determined by enzyme-linked immunosorbent assay (ELISA).

Results: Plasma LRG concentrations were significantly elevated in RA patients compared with healthy control (30.8 ± 14.4 ng/mL vs 22.2 ± 6.1 ng/mL, p < 0.001). In patients with RA, plasma LRG levels were found to be correlated with DAS28, ESR, and CRP (g = 0.671, p < 0.001; g = 0.612, p < 0.001; and g = 0.601, p < 0.001, respectively), but not with plasma TNF-a levels. Plasma LRG levels in patients with an active disease status (DAS28 >= 2.6) were significantly higher than in patients with a remission status (DAS28 < 2.6) (36.45 ± 14.36 ng/mL vs 24.63 ± 8.81 ng/mL, p < 0.001).

Conclusion: Patients with RA had higher plasma LRG levels than healthy subjects, and plasma LRG concentrations were well correlated with disease activity measures. Our findings suggest that plasma LRG could play a role in the inflammatory process independently of the TNF- a, and that it may be a novel biomarker for reflecting inflammatory activity in RA patients.