Detection of Tumor Necrosis Factor-α and Receptors in the Serum and Synovial Fluid of Patients with Rheumatoid Arthritis and Osteoarthritis

類風濕性關節炎和退化性關節炎病患之血清和關節液腫瘤壞死因子及接受體之偵測

黃春明(Chung-Ming Huang) ； 陳季蘭(Chi-Lan Chen) ； 林彩秀(Tsai-Hsiu Lin) ； 王秀娟(Hsiu-Jain Wang)

《Mid-Taiwan Journal of Medicine》 4卷2期 (1999/06) Pp. 109-115

https://doi.org/10.6558/MTJM.1999.4(2).6

摘要

腫瘤壞死因子可誘發兩種游離性接受體（p55和p75）之產生，其在發炎性風濕病人身上濃度會有上升情形。本研究目的在於探討類風濕性關節炎、退化性關節炎及正常人其腫瘤壞死因子及接受體之差異及其臨床應用。我們使用酵素免疫吸收法測量類風濕性關節炎及退化性關節炎病人血清及關節液和正常人的血清之腫瘤壞死因子及其接受體p55、p75的濃度。結果顯示，血清之腫瘤壞死因子在類風濕性關節炎有20%患者可測到，然而退化性關節炎和正常人卻都偵測不出來。關節液之腫瘤壞死因子在類風濕性關節炎患者明顯高於退化性關節炎患者。p55腫瘤壞死因子接受體之血清濃度在類風濕性關節炎患者高於常人，然而在退化性關節炎患者和正常人在統計上則無明顯差異。類風濕性關節炎患者關節液中之p55卻較退化性關節炎患者來得高。而血清p75腫瘤壞死因子接受體在類風濕性關節炎和退化性關節炎病人皆比正常人高。在關節液方面，類風濕性關節炎則較退化性關節炎有明顯增高情形。另外，我們發現包括腫瘤壞死因子、p55、p75和疾病活動度，ESR及CRP數值相比皆沒有明顯之相關性存在。本研究顯示，腫瘤壞死因子和腫瘤壞死因子接受體在類風濕性關節炎患者扮演一調節角色，尤其是在關節內。另外，腫瘤壞死因子和腫瘤壞死因子接受體似乎和疾病活動度並沒有相關性存在。

關鍵字

疾病活動度 ； 類風濕性關節炎 ； 可溶性腫瘤壞死因子接受體 ； 甲型腫瘤壞死因子

並列摘要

Tumor necrosis factor (TNF) induces the production of two forms of soluble receptors (p55 and p75) that are present in human serum at concentrations that increase in inflammatory rheumatic disease. The purpose of this study was to evaluate the usefulness of TNF-α and soluble TNF receptor (sTNFR) for distinguishing between rheumatoid arthritis (RA), osteoarthritis (OA) and normal individuals. Serum and synovial fluid (SF) from patients with RA and OA, and serum from normal control subjects were analyzed for p55, p75 and TNF-α by enzyme-linked immunosorbent assays (ELISA). TNF-α was detectable in 20% of RA sera. However, it could not be measured in OA or control sera. Levels of TNF- were significantly higher in SF of RA group when compared with the OA group. Although p55 sTNFR concentrations in serum showed a significant increase in RA than in the controls, there was no difference between patients with OA and the controls. Measurement of p55 sTNFR in SF showed a significant difference between the RA and OA groups. Furthermore, p75 sTNFR in serum was markedly higher in RA and OA groups than in the controls. p75 in SF was significantly different between RA and OA patients. There was no significant correlation between p55, p75, TNF-α and disease activity, including clinical and laboratory parameters (erythrocyte sedimentation rate and C-reactive protein levels). In conclusion, our study demonstrates that TNF-α and sTNFR are up-regulated in patients with RA and produced locally in the joints. In addition, serum and SF levels of sTNFR and TNFdo not seem to be related to disease activity.

並列關鍵字

disease activity ； rheumatoid arthritis ； soluble tumor necrosis factor receptor ； tumor necrosis factor-α