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- Published on: 19 June 2018
- Published on: 19 June 2018Comment on: TNF-α and plasma albumin as biomarkers of disease activity in systemic lupus erythematosus
Dear editor,
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We read with interest the article of Idborg et al.1 who recently analyzed the role of several inflammatory mediators, and their usefulness as biomarkers in the measurement of activity of disease and the identification of clinical subphenotypes in systemic lupus erythematosus (SLE). Although interesting, these results may benefit of further discussion in light of systems medicine.
Authors concluded that the two main inflammatory mediators related with activity of SLE were TNF-α and p-albumin. However, previous studies have found that TNF-α and the TNF/IL-10 ratio were higher in patients with low activity of disease,2 and that TNF-α antagonists may induce SLE-like disease.3 These controversial data argues against a generalized model based on TNF-α as clinical activity biomarker, and advocate for the influence of other mediators in such a condition.
As shown by Idborg et al., IL-6, IL-10, IL-15, MCP-1, IP-10, MIP-1α, ESR, anti-dsDNA and U-albumin/creatinine were also positively correlated with activity of disease,1 suggesting that the exclusive role of TNF-α and p-albumin on activity of disease is unlikely. In fact, the pathological functions of these biomarkers are not isolate since they emerge from the interactions among them and between cells and tissues (i.e., systems medicine).4
In this sense, cytokine and autoantibody clusters (i.e., neutral, chemotactic/anti-phospholipid antibodies, and IFN-α/dsDNA) have been reported to be associat...Conflict of Interest:
None declared.