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关节炎性滑液中硫酸化糖胺聚糖和蛋白聚糖片段的测量

Measurement of sulphated glycosaminoglycans and proteoglycan fragments in arthritic synovial fluid.

作者信息

Carroll G

机构信息

Department of Rheumatic Diseases, Royal Perth (Rehabilitation) Hospital, Shenton Park, Western Australia.

出版信息

Ann Rheum Dis. 1989 Jan;48(1):17-24. doi: 10.1136/ard.48.1.17.

Abstract

Immunoreactive proteoglycans (iPGs) and sulphated glycosaminoglycans (GAGs) were assayed in synovial fluid obtained from 22 patients with osteoarthritis (OA), 21 with rheumatoid arthritis (RA), 13 with gout, and five with Reiter's syndrome. A strong positive linear correlation was observed between concentrations of sulphated GAGs and iPGs in RA (r = 0.95) and gout (r = 0.94). A linear correlation was also observed in OA (r = 0.65). Patients with gout and Reiter's syndrome had significantly higher concentrations of sulphated GAGs and iPGs than patients with OA or RA. Patients with gout also had significantly higher total quantities of sulphated GAGs and iPGs in the knee joint cavity than patients with OA or RA. In all four diseases similar profiles were observed when comparisons were made between the total quantities and concentrations of sulphated GAGs and iPGs in synovial fluid. These results indicate that the observed differences in concentrations are not simply a function of dilution. The concentrations of sulphated GAGs and iPGs did not correlate closely with the type or number of inflammatory cells in the synovial fluid. Considerable variation was noted in the sulphated GAG/iPG ratios, suggesting that different mechanisms may be contributing to the release of proteoglycans in the diseases studied.

摘要

对22例骨关节炎(OA)患者、21例类风湿关节炎(RA)患者、13例痛风患者和5例赖特综合征患者的滑液进行了免疫反应性蛋白聚糖(iPGs)和硫酸化糖胺聚糖(GAGs)检测。在RA患者(r = 0.95)和痛风患者(r = 0.94)中,硫酸化GAGs和iPGs的浓度之间观察到强正线性相关性。在OA患者中也观察到线性相关性(r = 0.65)。痛风患者和赖特综合征患者的硫酸化GAGs和iPGs浓度显著高于OA或RA患者。痛风患者膝关节腔中硫酸化GAGs和iPGs的总量也显著高于OA或RA患者。在所有四种疾病中,当比较滑液中硫酸化GAGs和iPGs的总量与浓度时,观察到相似的分布情况。这些结果表明,观察到的浓度差异并非仅仅是稀释作用的结果。硫酸化GAGs和iPGs的浓度与滑液中炎症细胞的类型或数量没有密切相关性。硫酸化GAG/iPG比值存在相当大的差异,这表明在研究的疾病中,可能有不同的机制导致蛋白聚糖的释放。

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