Inflammatory markers in systemic lupus erythematosus

While systemic lupus erythematosus (SLE) is an autoantibody and immune complex disease by nature, most of its organ manifestations are in fact inflammatory. SLE activity scores thus heavily rely on assessing inflammation in the various organs. This focus on clinical items demonstrates that routine laboratory markers of inflammation are still limited in their impact. The erythrocyte sedimentation rate (ESR) is used, but represents a rather crude overall measure. Anemia and diminished serum albumin play a role in estimating inflammatory activity, but both are reflecting more than one mechanism, and the association with inflammation is complex. C-reactive protein (CRP) is a better marker for infections than for SLE activity, where there is only a limited association, and procalcitonin (PCT) is also mainly used for detecting severe bacterial infection. Of the cytokines directly induced by immune complexes, type I interferons, interleukin-18 (IL-18) and tumor necrosis factor (TNF) are correlated with inflammatory disease activity. Still, precise and timely measurement is an issue, which is why they are not currently used for routine purposes. While somewhat more robust in the assays, IL-18 binding protein (IL-18BP) and soluble TNF-receptor 2 (TNF-R2), which are related to the respective cytokines, have not yet made it into clinical routine. The same is true for several chemokines that are increased with activity and relatively easy to measure, but still experimental parameters. In the urine, proteinuria leads and is essential for assessing kidney involvement, but may also result from damage. Similar to the situation in serum and plasma, several cytokines and chemokines perform reasonably well in scientific studies, but are not routine parameters. Cellular elements in the urine are more difficult to assess in the routine laboratory, where sufficient routine is not always available. Therefore, the analysis of urinary T cells may have potential for better monitoring renal inflammation.