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Background: Systemic lupus erythematous (SLE) is an autoimmune disease characterized by deregulation of cytokine production. Interferon (IFN) is a proinflamatory cytokine considered as a key molecule in the SLE etiopathogenesis, being responsible of the differentiation of dendritic cells from monocytes, and indirectly of IL10 upregulation. Objectives: We aimed to analyze the association between inflammatory cytoquine levels (IFN-a2, IFN-b, IFN-g and IL10) and SLE clinical activity for a follow-up period of 12 months in SLE patients. Methods: A longitudinal, observational prospective study with evaluations at baseline and follow-up visits every 3 months (for 1 year) in SLE patients (SLICC 2012 criteria) was performed. In all cases complete laboratory test, clinical evaluation and SLEDAI score was carried out. We analyzed inflammatory cytokines serum levels by colorimetric methods. Results: 45 SLE patients (86.7% female) participated in the study, with a mean age at diagnosis of 32.8 (16.2) years and a mean time of disease evolution of 17.9 (11.4) years. The 28.9% of patients showed SLEDAI>6 at the basal visit. The 66.7% of patients were under glucocorticoid treatment, 44.4% under immunosupressants (methotrexate, azatioprine, belimumab or mycophenolate) and 66.7% under antimalarials. SLEDAI and inflammatory cytoquine levels during follow-up is shown in Table 1. Regarding to clinical activity biomarkers, we observed an association between high levels of antidsDNA and elevated IFN-beta (P=0.005) and IFN-gamma (P=0.038), and low levels of C3 and an increment in IL-10 (P=0.006). Patients under antimalarials treatment during follow-up exhibit low levels of IL-10 (P=0.012). No influence of age at diagnosis, time of evolution, vitamin D levels, corticoids and tobacco use in cytoquine levels was observed. Conclusion: We observed an association between IL-10, IFN-alpha2, IFN-beta and IFN-gamma levels with clinical activity, independently of the time of follow-up. IL-10 levels may also be influenced by antimalarial treatment. REFERENCES: NIL. Acknowledgements: NIL. Disclosure of Interests: None declared.
García et al. (Sat,) studied this question.