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. 2019 Dec 16;21(1):287.
doi: 10.1186/s13075-019-2029-1.

Performance of cytokine models in predicting SLE activity

Affiliations

Performance of cytokine models in predicting SLE activity

Nopparat Ruchakorn et al. Arthritis Res Ther. .

Abstract

Background: Identification of universal biomarkers to predict systemic lupus erythematosus (SLE) flares is challenging due to the heterogeneity of the disease. Several biomarkers have been reported. However, the data of validated biomarkers to use as a predictor for lupus flares show variation. This study aimed to identify the biomarkers that are sensitive and specific to predict lupus flares.

Methods: One hundred and twenty-four SLE patients enrolled in this study and were prospectively followed up. The evaluation of disease activity achieved by the SLE disease activity index (SLEDAI-2K) and clinical SLEDAI (modified SLEDAI). Patients with active SLE were categorized into renal or non-renal flares. Serum cytokines were measured by multiplex bead-based flow cytometry. The correlation and logistic regression analysis were performed.

Results: Levels of IFN-α, MCP-1, IL-6, IL-8, and IL-18 significantly increased in active SLE and correlated with clinical SLEDAI. Complement C3 showed a weakly negative relationship with IFN-α and IL-18. IL-18 showed the highest positive likelihood ratios for active SLE. Multiple logistic regression analysis showed that IL-6, IL-8, and IL-18 significantly increased odds ratio (OR) for active SLE at baseline while complement C3 and IL-18 increased OR for active SLE at 12 weeks. IL-18 and IL-6 yielded higher sensitivity and specificity than anti-dsDNA and C3 to predict active renal and active non-renal, respectively.

Conclusion: The heterogeneity of SLE pathogenesis leads to different signaling mechanisms and mediates through several cytokines. The monitoring of cytokines increases the sensitivity and specificity to determine SLE disease activity. IL-18 predicts the risk of active renal SLE while IL-6 and IL-8 predict the risk of active non-renal. The sensitivity and specificity of these cytokines are higher than the anti-dsDNA or C3. We propose to use the serum level of IL-18, IL-6, and IL-8 to monitor SLE disease activity in clinical practice.

Keywords: Biomarker; Cytokines; Disease activity; Interleukin; Systemic lupus erythematosus.

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Conflict of interest statement

The authors declare that they have no competing interests.

References

    1. Doria A, Ghirardello A, Iaccarino L, Zampieri S, Punzi L, Tarricone E, et al. Pregnancy, cytokines, and disease activity in systemic lupus erythematosus. Arthritis Rheum. 2004;51(6):989–995. doi: 10.1002/art.20837. - DOI - PubMed
    1. Herrmann M, Voll RE, Kalden JR. Etiopathogenesis of systemic lupus erythematosus. Immunol Today. 2000;21(9):424–426. doi: 10.1016/S0167-5699(00)01675-3. - DOI - PubMed
    1. Mejia-Vilet JM, Cordova-Sanchez BM, Arreola-Guerra JM, Morales-Buenrostro LE, Uribe-Uribe NO, Correa-Rotter R. Renal flare prediction and prognosis in lupus nephritis Hispanic patients. Lupus. 2016;25(3):315–324. doi: 10.1177/0961203315606985. - DOI - PubMed
    1. Fu Q, Chen X, Cui H, Guo Y, Chen J, Shen N, et al. Association of elevated transcript levels of interferon-inducible chemokines with disease activity and organ damage in systemic lupus erythematosus patients. Arthritis Res Ther. 2008;10(5):R112. doi: 10.1186/ar2510. - DOI - PMC - PubMed
    1. Jacob N, Stohl W. Cytokine disturbances in systemic lupus erythematosus. Arthritis Res Ther. 2011;13(4):228. doi: 10.1186/ar3349. - DOI - PMC - PubMed

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