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SAT0424 Serum Tweak as a Biomarker for Disease Activity of Systemic Lupus Erythematosus
  1. S.-K. Kim,
  2. J.-Y. Choe
  1. Catholic University of Daegu School of Medicine, Daegu, Korea, Republic Of


Background Biomarkers related with disease susceptibility, diagnosis, and organ involvement in systemic lupus erythematosus (SLE) has been found to be closely related with the presence of antibodies to dsDNA, C1q, and monocyte chemotactic protein-1 (MCP-1). Recently, the variable cytokines and chemokines including interferon γ-induced protein-10 (IP-10), TNF-like weak inducer of apoptosis (TWEAK), and MCP-1 have been suggested as potent effectors or indicators for disease activity and/or renal involvement in SLE.

Objectives This study investigated to identify optimal serum and urine biomarkers related with disease activity in female patients with SLE.

Methods Seventy SLE patients and sixty-one healthy controls were consecutively enrolled. IP-10, TWEAK, and MCP-1 in both serum and urine were measured using enzyme-linked immunosorbent assay. Statistical analysis was performed by Mann-Whitney U test, Spearman correlation analysis, multivariate regression analysis, and logistic regression analysis.

Results Both serum and urine TWEAK, IP-10, and MCP-1 levels in either low and high SLEDAI groups of SLE were markedly higher than those in healthy controls. Serum TWEAK levels was positively associated with serum IP and serum MCP-1 levels (p<0.001 of both). There were significant differences of serum TWEAK levels, SLEDAI score, and urine protein/creatinine between non-renal and renal involvement of SLE (p=0.034, p<0.001, and p<0.001, respectively). Serum TWEAK levels was found to be a crucial determinant to high SLEDAI activity and renal involvement (p=0.044, OR =1.006, 95% CIs 1.000 - 1.011 and p=0.046, OR =1.005, 95% CIs 1.000 - 1.019, respectively).

Conclusions This study demonstrated that serum TWEAK levels might be a potent biomarker to reflect disease activity and renal involvement in SLE patients.


  1. Liu CC, et al. Best Pract Res Clin Rheumatol 2009;23:507-23.

  2. Narumi S, et al. Cytokine 2000;12:1561-5.

  3. Schwartz N, et al. J Autoimmun 2006;27:242-50.

Disclosure of Interest None declared

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