Abstract:Objective To detect the levels of tumor necrosis factor-α (TNF-α) in synovial fluid and blood serum of patients with gouty arthritis (GA) and explore its role in the development and progression of GA. Methods Sixty-seven GA patients in acute attack stage (AGA group) and 26 GA patients in remission period (RGA group) treated in the First Affiliated Hospital of Kunming Medical University from April 2016 to October 2017 were selected as the objects, another 35 healthy persons were served as control group at the same time. AGA patients were subdivided into severe AGA (SAGA) group(n=39) and mild AGA (MAGA) group (n=28) according to the degree of complaint pain scale of verbal rating scale (VAS) for AGA. The joint fluid and venous blood were extracted from GA patients and health persons respectively for the detections of erythrocyte sedimentation rate, blood uric acid and blood routine indexes, and enzyme linked immunosorbent assay (ELISA) was used to detect the levels of TNF-α, interleukin-1 (IL-1), IL-1β, IL-8, IL-10 and high-sensitivity C-reactive protein (hs-CRP). The correlations between TNF-α level and other experimental indexes were analyzed. Results The levels of TNF-α, blood uric acid, erythrocyte sedimentation rate, IL-1β, IL-8 and hs-CRP in serum and joint fluid significantly increased with the aggravation of the disease, but the level of IL-10 decreased with the aggravation of the disease(all P<0. 05). Serum TNF-α level in GA patients was positively correlated with the levels of IL-1β, IL-8 and hs-CRP (r=5.919, 0.607, 0.611 respectively, P<0.05) and was negatively correlated with IL-10 level (r=-0.633, P<0.05). TNF-α level in joint fluid of GA patients was positively correlated with the levels of blood uric acid, IL-1β, and hs-CRP (r=0.592, 0.618, 0.571, respectively, P<0.05) and was negatively correlated with the level of IL-10 (r=-0.609, P<0.05). Conclusion High level of TNF-α in serum and synovial fluid of GA patients may boost the expressions of inflammatory factors such as IL-1β, hs-CRP and so on, and promote the occurrence of inflammation.