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1
Decreased plasma fibrinolysis in patients with rheumatoid arthritis.类风湿关节炎患者血浆纤维蛋白溶解功能降低。
Ann Rheum Dis. 1984 Dec;43(6):774-7. doi: 10.1136/ard.43.6.774.
2
The effect of increasing fibrinolysis in patients with rheumatoid arthritis: a double blind study of stanozolol.增加类风湿关节炎患者纤维蛋白溶解作用的效果:司坦唑醇的双盲研究
Q J Med. 1986 Jan;58(225):19-27.
3
Fibrinolysis is down-regulated in mouse collagen-induced arthritis, but its normalization does not alleviate the course of disease.纤维蛋白溶解在胶原诱导的关节炎小鼠中受到抑制,但这种抑制的正常化并不能减轻疾病的进程。
Inflamm Res. 2011 Nov;60(11):1021-9. doi: 10.1007/s00011-011-0363-0. Epub 2011 Jul 24.
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The fibrinolytic system and its relation to inflammatory diseases.纤维蛋白溶解系统及其与炎症性疾病的关系。
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5
Effects of oral stanozolol used in the prevention of postoperative deep vein thrombosis on fibrinolytic activity.口服司坦唑醇预防术后深静脉血栓形成对纤溶活性的影响。
Thromb Haemost. 1985 Feb 18;53(1):141-2.
6
Prophylactic antithrombotic therapy with stanozolol in patients with familial antithrombin III deficiency.司坦唑醇对家族性抗凝血酶III缺乏症患者的预防性抗血栓治疗。
Br J Haematol. 1984 Jul;57(3):527-37. doi: 10.1111/j.1365-2141.1984.tb02927.x.
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On fibrinolysis in diabetes mellitus.关于糖尿病中的纤维蛋白溶解作用。
Acta Med Scand. 1975 Jul-Aug;198(1-2):101-6. doi: 10.1111/j.0954-6820.1975.tb19512.x.
8
Progress of fibrinolysis during tumor necrosis factor infusions in humans. Concomitant increase in tissue-type plasminogen activator, plasminogen activator inhibitor type-1, and fibrin(ogen) degradation products.人类肿瘤坏死因子输注期间纤维蛋白溶解的进展。组织型纤溶酶原激活物、1型纤溶酶原激活物抑制剂和纤维蛋白(原)降解产物同时增加。
Blood. 1990 Dec 1;76(11):2284-9.
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Prevention of fibrinolytic shut-down after major surgery by intramuscular stanozolol.肌注康力龙预防大手术后纤维蛋白溶解系统抑制。
Thromb Res. 1983 Aug 1;31(3):451-9. doi: 10.1016/0049-3848(83)90409-7.
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Elastase- and plasmin-mediated fibrinolysis in rheumatoid arthritis.类风湿关节炎中弹性蛋白酶和纤溶酶介导的纤维蛋白溶解作用
Int J Tissue React. 1994;16(2):89-93.

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A Novel Hypothetical Approach to Explain the Mechanisms of Pathogenicity of Rheumatic Arthritis.一种解释风湿性关节炎发病机制的新型假说方法。
Mediterr J Rheumatol. 2021 May 28;32(2):112-117. doi: 10.31138/mjr.32.2.112. eCollection 2021 Jun.
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Thrombin generation in rheumatoid arthritis: dependence on plasma factor composition.类风湿关节炎中的凝血酶生成:依赖于血浆因子组成。
Thromb Haemost. 2010 Aug;104(2):224-30. doi: 10.1160/TH10-02-0091. Epub 2010 Jun 30.
3
Proteolytic mechanisms of cartilage breakdown: a target for arthritis therapy?软骨破坏的蛋白水解机制:关节炎治疗的靶点?
Clin Mol Pathol. 1995 Aug;48(4):M167-77. doi: 10.1136/mp.48.4.m167.
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Biochemical and morphological alterations in lungs induced by experimental inhibition of fibrinolytic activity.
Mol Cell Biochem. 2002 Dec;241(1-2):9-19. doi: 10.1023/a:1020822801712.
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Tissue plasminogen activator, plasminogen activator inhibitor-1 and von Willebrand factor in rheumatoid arthritis.类风湿关节炎中的组织型纤溶酶原激活剂、纤溶酶原激活剂抑制剂-1和血管性血友病因子
Clin Rheumatol. 1993 Sep;12(3):318-24. doi: 10.1007/BF02231572.
6
Abnormal plasma fibrinolysis in patients with rheumatoid arthritis and impaired endothelial fibrinolytic response in those complicated by vasculitis.类风湿关节炎患者存在异常的血浆纤维蛋白溶解,而合并血管炎的患者存在内皮纤维蛋白溶解反应受损。
Ann Rheum Dis. 1993 Sep;52(9):643-9. doi: 10.1136/ard.52.9.643.
7
The differential effects of stanozolol on human skin and synovial fibroblasts in vitro: DNA synthesis and receptor binding.司坦唑醇对人皮肤和滑膜成纤维细胞的体外差异作用:DNA合成与受体结合
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Vascular damage and factor-VIII-related antigen in the rheumatic diseases.风湿性疾病中的血管损伤与因子VIII相关抗原
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9
The effect of the anabolic steroid, stanozolol, on the production of procollagenase by human synovial and skin fibroblasts in vitro.合成代谢类固醇司坦唑醇对人滑膜和成纤维细胞体外产生前胶原酶的影响。
Agents Actions. 1989 Nov;28(3-4):279-82. doi: 10.1007/BF01967415.
10
Plasminogen activators in synovial fluid and plasma from patients with arthritis.关节炎患者滑液和血浆中的纤溶酶原激活剂
Ann Rheum Dis. 1992 Aug;51(8):965-8. doi: 10.1136/ard.51.8.965.

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The production of arthritis in rabbits by an immunological reaction to fibrin.通过对纤维蛋白的免疫反应在兔子身上诱发关节炎。
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The mechanism of clot dissolution by plasmin.纤溶酶溶解血栓的机制。
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[Rapid physiological coagulation method in determination of fibrinogen].[快速生理凝血法测定纤维蛋白原]
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Correlation of clinical parameters of disease activity in rheumatoid arthritis with serum concentration of C-reactive protein and erythrocyte sedimentation rate.类风湿关节炎疾病活动临床参数与血清C反应蛋白浓度及红细胞沉降率的相关性
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Deposits of alpha 2M in the rheumatoid synovial membrane.类风湿性滑膜中α2M的沉积。
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Studies of the metabolism and distribution of fibrinogen in patients with rheumatoid arthritis.类风湿关节炎患者纤维蛋白原代谢与分布的研究
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Tissue repair in presence of locally applied inhibitors of fibrinolysis.在局部应用纤维蛋白溶解抑制剂的情况下进行组织修复。
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类风湿关节炎患者血浆纤维蛋白溶解功能降低。

Decreased plasma fibrinolysis in patients with rheumatoid arthritis.

作者信息

Belch J J, McArdle B, Madhok R, McLaughlin K, Capell H A, Forbes C D, Sturrock R D

出版信息

Ann Rheum Dis. 1984 Dec;43(6):774-7. doi: 10.1136/ard.43.6.774.

DOI:10.1136/ard.43.6.774
PMID:6084477
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1001534/
Abstract

We have investigated the fibrinolytic status of 56 patients with rheumatoid arthritis (RA). Plasma fibrinogen and plasminogen were significantly elevated. Levels of these two substrates, along with alpha 2 macroglobulin and antithrombin III correlated with disease activity. Plasminogen activator (PA) activity was decreased in patients with severe disease. Twelve patients were given stanozolol, a fibrinolytic enhancing agent, for two months as a test for endothelial production of plasminogen activator. This caused a significant increase in blood plasminogen and PA activity. Five patients received a two-week course of stanozolol with joint aspiration before and after. Joint plasminogen levels were increased. We suggest that inadequate fibrinolysis occurs in RA, and that this may contribute to some of the pathological features of the disease. It is possible to stimulate both blood and joint fibrinolysis by stanozolol. A more prolonged increase in plasminogen activator activity might decrease joint fibrin deposition, and stanozolol should be investigated as a therapeutic agent in RA.

摘要

我们研究了56例类风湿关节炎(RA)患者的纤溶状态。血浆纤维蛋白原和纤溶酶原显著升高。这两种底物的水平,以及α2巨球蛋白和抗凝血酶III与疾病活动相关。重症患者的纤溶酶原激活物(PA)活性降低。12例患者接受了两个月的司坦唑醇治疗,司坦唑醇是一种纤溶增强剂,以此检测内皮细胞纤溶酶原激活物的产生。这导致血液纤溶酶原和PA活性显著增加。5例患者在前后关节穿刺的同时接受了为期两周的司坦唑醇治疗。关节纤溶酶原水平升高。我们认为RA中存在纤溶不足,这可能导致了该疾病的一些病理特征。司坦唑醇可以刺激血液和关节的纤溶。纤溶酶原激活物活性的更持久增加可能会减少关节纤维蛋白沉积,司坦唑醇应作为RA的治疗药物进行研究。