DETERMINATION OF CYTOKINES IN SYNOVIAL-FLUIDS - CORRELATION WITH DIAGNOSIS AND HISTOMORPHOLOGICAL CHARACTERISTICS OF SYNOVIAL TISSUE
DETERMINATION OF CYTOKINES IN SYNOVIAL-FLUIDS - CORRELATION WITH DIAGNOSIS AND HISTOMORPHOLOGICAL CHARACTERISTICS OF SYNOVIAL TISSUE
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DOI：
10.1136/ard.51.6.731
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发表时间：
1992-06-01
影响因子：
27.4
通讯作者：
PAWELEC, G
中科院分区：
文献类型：
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作者：
KAHLE, P;SAAL, JG;PAWELEC, G
在一项旨在研究滑膜液中细胞因子水平与类风湿关节炎（RA）病理相关性的研究中，对27例类风湿关节炎患者、16例其他关节炎患者、23例骨关节炎患者、13例创伤患者和18例尸检无炎性疾病且未知关节疾病的患者（中位死亡后27小时）进行了肿瘤坏死因子- α、白细胞介素- 1- β和干扰素- γ的免疫分析。白细胞介素1- β的结果清楚地表明，与骨关节炎、创伤或尸检患者相比，RA和其他关节炎患者的细胞因子水平更高。然而，骨关节炎患者和尸检患者的干扰素- γ水平明显高于RA患者，而尸检患者的肿瘤坏死因子- α水平也高于RA患者。该研究还将滑膜炎的组织形态学模式和局部炎症活动性指标与滑膜液细胞因子水平联系起来，例如，白细胞介素1- β滴度与溃疡肉芽肿性滑膜炎（本身与RA相关）呈正相关，干扰素γ滴度与溃疡肉芽肿性滑膜炎呈负相关。综上所述，这些结果扩展并加强了一些数据，表明滑膜液中白细胞介素1- β水平的增加可能在RA的关节破坏中起作用，但没有证据表明肿瘤坏死因子- α或干扰素- γ水平的增加影响疾病病理。
In a study aimed at correlating cytokine levels in synovial fluid with the pathology of rheumatoid arthritis (RA), tumour necrosis factor-alpha, interleukin 1-beta and interferon-gamma were immunoassayed in 27 patients with RA, 16 patients with other arthritides, 23 with osteoarthritis, 13 patients with trauma, and 18 patients at necropsy without inflammatory disease and not known to have had joint disease (median 27 hours after death). The results for interleukin 1-beta clearly show higher cytokine levels in patients with RA and other arthritides than in patients with osteoarthritis, trauma, or the patients at necropsy. Interferon-gamma levels in patients with osteoarthritis and the patients at necropsy, however, were significantly greater than in patients with RA, and tumour necrosis factor-alpha levels were also greater in the patients at necropsy compared with patients with RA. This study also correlated histomorphological patterns of synovitis and indicators of local inflammatory activity with synovial fluid cytokine levels, showing, for example, a positive association of interleukin 1-beta titre and a negative association of interferon-gamma titre with ulcerogranulomatous synovitis (itself associated with RA). Taken together, these results extend and strengthen data suggesting a possible part played by increased synovial fluid levels of interleukin 1-beta in joint destruction in RA, but provide no evidence for increases in levels of tumour necrosis factor-alpha or interferon-gamma affecting the disease pathology.