目的 检测类风湿关节炎（RA）患者血清和关节液白细胞介素17A（IL-17A）的变化，探讨其与临床炎症指标、疾病活动性的关系。 方法 2011年6月－2012年6月采用酶联免疫吸附试验检测30例活动性RA患者和20例健康对照血清IL-17A水平，其中18例有膝关节积液RA患者同时检测配对血清和关节液IL-17A水平。 结果 RA组患者血清IL-17A水平显著高于健康对照组[（40.651 ± 16.402）、（23.799 ± 10.693） pg/mL，P＜0.05]。RA患者关节液IL-17A水平明显高于其血清中水平[（63.555 ± 23.405）、（43.727 ± 17.212） pg/mL，P＜0.05]。RA患者血清IL-17A水平只与疾病活动性评分（DAS28）呈正相关（r=0.498，P=0.020），而RA患者关节液IL-17A水平与DAS28和血清C反应蛋白有相关性（r=0.515，P=0.029；r=0.498，P=0.035）。 结论 RA患者血清和关节液IL-17A水平与疾病活动性显著相关，提示IL-17A可作为衡量疾病活动和关节损伤的标志之一。
ObjectiveTo discuss the changes of joint fluid and blood-related indexes in patients with gouty arthritis and rheumatoid arthritis, and to analyze the clinical significance of these changes. MethodsSeventy-five patients with gouty arthritis and 68 with rheumatoid arthritis treated between January and December 2014 were included in our study. Their joint fluid-related indicators including white blood cell count (WBC), total protein (TP), albumin (ALB), glucose (GLU), and uric acid (UA), and their blood indicators including immunoglobulin G (IgG), immunoglobulin M (IgM), immunoglobulin A (IgA), C3 and C4, rheumatoid factor (RF), anti-streptolysin O (ASO), and c-reactive protein (CRP) were detected. ResultsFor joint fluid-related indicators, TP and ALB levels were not significantly different between the two groups (P > 0.05), while WBC, GLU, UA, RF and ASO between the two groups were significantly different (P < 0.05); For blood indexes, C4 was not significantly different between the two groups (P > 0.05), but IgG, IgM, IgA, CRP, C3, UA, RF and ASO were significantly different between the two groups (P < 0.05). The detection rate of ASO from the joint fluid was significantly higher than that detected from the blood in both the two groups (P < 0.05), while UA level was not significantly different between the joint fluid and the blood (P > 0.05). In patients with rheumatoid arthritis, RF detection rate was not significantly different between the joint fluid and the blood (P > 0.05), but it was significantly different for patients with gouty arthritis (P < 0.05). The positive rate of ASO in the blood and joint fluid of patients with gouty arthritis was respectively 38.7% and 44.0%, and it was 75.0% and 73.5% for patients with rheumatoid arthritis. UA positive rate in the blood and joint fluid of patients with gouty arthritis was 92.0% and 80.0% respectively, while it was 38.2% and 32.4% for patients with rheumatoid arthritis. RF positive rate was 33.3% and 40.0% in the blood and joint fluid of patients with gouty arthritis, while the rate was 86.8% and 91.2% for patients with rheumatoid arthritis. ConclusionThe joint fluid and blood indicators are in change in patients with gouty arthritis and rheumatoid arthritis, which has a certain clinical value in disease diagnosis and curative effect observation.
Objective To analyze the differences in the effects of different mechanical stimuli on cells, cytokines, and proteins in synovial fluid of osteoarthritis joints, and to elucidate the indirect mechanism by which mechanical signals remodel the synovial fluid microenvironment through tissue cells. Methods Systematically integrate recent literature, focusing on the regulatory effects of different mechanical stimuli on the physicochemical properties of synovial fluid. Analyze the dynamic process by which mechanical stimuli regulate secretory and metabolic activities through tissue cells, thereby altering the physicochemical properties of cytokines and proteins. Results Appropriate mechanical stimuli activate mechanical signals in chondrocytes, macrophages, and synovial cells, thereby influencing cellular metabolic activities, including inhibiting the release of pro-inflammatory factors and promoting the secretion of anti-inflammatory factors, and regulating the expression of matrix and inflammation-related proteins such as cartilage oligomeric matrix protein, peptidoglycan recognition protein 4, and matrix metalloproteinases. Conclusion Mechanical stimuli act on tissue cells, indirectly reshaping the synovial fluid microenvironment through metabolic activities, thereby regulating the pathological process of osteoarthritis.