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Background: Takayasu arteritis (TA) is a rare autoimmune disease, which has varied clinical presentations with different disease progression1. There is growing need for clear biomarkers for TA2. At present, there is a wide range of research on cytokines, which vary greatly from patients to patients in TA3,4. It is important to scientifically explore the meaning behind different levels of cytokines and interpret their impact on outcomes and disease progression. Objectives: The research is to summarize subgroups characterized by cytokines in Takayasu arteritis and explore the differences in prognosis between subgroups. Methods: In this observational, longitudinal cohort study, serum cytokines (12 types) analyzed by flow cytometry were tested in 90 untreated TA cases. Disease duration, age of onset, elevated erythrocyte sedimentation rate (ESR), elevated c-reactive protein (CRP) and the levels of cytokines were analyzed by Twostep cluster analysis. Adverse events were defined as death, organ insufficiency and in-sent restenosis caused by the stenosis, occlusion and dilation of arteries due to TA. After the use of standard care therapy, relapse was defined as recurrence of active disease5. Refractory disease was defined as inability to attain disease remission despite the use of standard care therapy5. Kruskal-Wallis1-way (k samples) and Kaplan-Meier (Log-rank) were used to indicate the characterization and outcomes in subgroups. Results: In this study, 90 TA patients without treatment were divided into three subgroups, which were 34 (37.8%) in Cluster1, 10 (11.1%) in Cluster2 and 46 (51.1%) in Cluster3. The levels of CRP, ESR and IL-6 were significantly higher (20.18 8.33,41.05mg/L vs 1.52 0.68,3.37mg/L, pConclusion: The disease was more stable in Cluster3, which had the lower levels of CRP, ESR, IL-6. Additionally, there was a lower incidence of adverse events, relapse and refractory disease in Cluster3. Although the disease in Cluster2 wasn't as active as in Cluster1, the occurrence of outcomes was similar in the two subgroups. In clinical practice, elevated levels of cytokines should be noticed, which may predict different outcomes for patients. REFERENCES: 1 Quinn KA, Gribbons KB, Carette S, Cuthbertson D, Khalidi NA, Koening CL, et al. Patterns of clinical presentation in Takayasu's arteritis. Semin Arthritis Rheum. 2020;50(4):576-81. 2 Savioli B, Abdulahad WH, Brouwer E, Kallenberg CGM, de Souza AWS. Are cytokines and chemokines suitable biomarkers for Takayasu arteritis? Autoimmun Rev. 2017;16(10):1071-8. 3 Wen D, Feng L, Du X, Dong JZ, Ma CS. Biomarkers in Takayasu arteritis. Int J Cardiol. 2023;371:413-7. 4 Pan LL, Du J, Gao N, Liao H, Wan J, Ci WP, et al. IL-9-producing Th9 cells may participate in pathogenesis of Takayasu's arteritis. Clin Rheumatol. 2016;35(12):3031-6. 5 Hellmich B, Agueda A, Monti S, Buttgereit F, de Boysson H, Brouwer E, et al. 2018 Update of the EULAR recommendations for the management of large vessel vasculitis. Ann Rheum Dis. 2020;79(1):19-30. Acknowledgements: NIL. Disclosure of Interests: None declared.
Zhu et al. (Sat,) studied this question.