Subclinical disease activity in systemic lupus erythematosus: immunoinflammatory markers do not normalize in clinical remission

Thomas Wais, Walter Fierz, Thomas Stoll, Peter M Villiger
Journal of Rheumatology 2003, 30 (10): 2133-9

OBJECTIVE: To correlate various laboratory measures in systemic lupus erythematosus (SLE) with the British Isles Lupus Assessment Group (BILAG) disease activity index, to search for organ-specific laboratory patterns and to compare with a control population.

METHODS: A cohort of 57 Caucasian outpatients fulfilling the American College of Rheumatology criteria for SLE and a control population of 17 patients admitted for coronarography were examined. Disease activity was assessed with BILAG index. Plasma samples were investigated for sCD44, interleukin 6 (IL-6), IL-10, IL-12, tumor necrosis factor-a (TNF-a), soluble TNF receptor-55 (sTNFR-55), sTNFR-75, IL-1-receptor antagonist, soluble intercellular adhesion molecule (sICAM), soluble vascular cell adhesion molecule (sVCAM), E-selectin, and neopterin as well as for C3, C4, dsDNA, and other conventional indicators.

RESULTS: Thirty-nine patients had inactive disease (total BILAG score < or = 5), 18 patients had active SLE. Surprisingly, except for C-reactive protein (p < 0.001), no statistically significant difference of the laboratory indicators was found between patients with active and those with inactive SLE. However, there was a significant difference between SLE patients and controls for sTNFR-75 (p < 0.008). We found significant correlations between laboratory markers and some BILAG organ system scores, such as between IL-1ra and the musculoskeletal score (p < 0.003) and between sTNFR-55/sTNFR-75 and renal BILAG (p < 0.001, p < 0.004, respectively). Significant nonparametric correlations were revealed between C3 and C4 (p < 0.0001), and between sTNFR-75 and dsDNA, neopterin, sVCAM, sICAM and sTNFR-55 concentrations (p < 0.0001 for all), and between sTNFR-75 and IL-1ra (p < 0.006).

CONCLUSION: Patients with SLE in clinical remission show ongoing systemic immunoinflammatory activity measured with a variety of cytokines, adhesion molecules, and other inflammatory markers. This indicates that laboratory measures may provide qualitatively different additional information to validated disease activity indexes such as the BILAG. Different laboratory markers correlate with disease activity in different organ systems. This suggests differences in pathogenic mechanisms in SLE depending on the organ system involved.


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