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[类风湿关节炎:治疗现状]

[Rheumatoid arthritis: current status of therapy].

作者信息

El Bahri Dalila Mrabet, Meddeb Nihel, Sellami Slaheddine

机构信息

Service de Rhumatologie, Hôpital La Rabta, Tunis, Tunisie.

出版信息

Tunis Med. 2007 Jan;85(1):1-8.

PMID:17424701
Abstract

Rheumatoid Arthritis (RA) is a frequent chronic inflammatory disease characterized by distal, bilateral and symmetrical lesions, leading to joint distortions and articular destructions. RA can also cause severe extra-articular manifestations associated with a poor prognosis. Recent advances in the field of immunopathology of RA have oriented treatment targeting the pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF alpha), interleukin (IL) and IL6. These biotherapies are considered as an important therapeutic progress in the treatment of RA acting at the level of cellular processes responsible for rheumatoid disease. These new therapies are active not only in controlling the disease inflammatory processes but also to stop the radiological course of RA. These new therapies are however efficient as long as prescribed, their interruption being rapidly followed by a flare-up of RA. Multiple adverse events attributed to anti-TNF-alpha have been described especially severe opportunistic infections and tuberculosis. B cells playing a critical role in sustaining the chronic inflammatory process in RA, targeted depleting B cells therapies have been developed in refractory forms of RA giving promising results. However, before any biotherapy prescription especially of anti-TNF-alpha, an initial screening should be achieved to exclude patients with history of untreated tuberculosis, solid cancers, malignant hemopathies or demyelinating disorders. It is also essential to assure a strict follow-up in patients under biotherapy to detect adverse events that can be sometimes severe. Thus, the ratio benefit/risk must be evaluated before any biotherapy prescription.

摘要

类风湿关节炎(RA)是一种常见的慢性炎症性疾病,其特征为远端、双侧及对称性病变,可导致关节畸形和关节破坏。RA还可引起严重的关节外表现,预后较差。RA免疫病理学领域的最新进展使治疗方向转向针对促炎细胞因子,如肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)和IL-6。这些生物疗法被认为是RA治疗中的一项重要治疗进展,作用于类风湿疾病相关的细胞过程层面。这些新疗法不仅在控制疾病炎症过程方面有效,而且能阻止RA的放射学进程。然而,这些新疗法仅在按规定使用时有效,一旦中断,RA很快就会复发。已描述了多种归因于抗TNF-α的不良事件,尤其是严重的机会性感染和结核病。B细胞在维持RA慢性炎症过程中起关键作用,针对难治性RA形式开发的靶向清除B细胞疗法已取得了有前景的结果。然而,在开具任何生物疗法处方尤其是抗TNF-α处方之前,应进行初步筛查,以排除有未治疗结核病、实体癌、恶性血液病或脱髓鞘疾病病史的患者。对接受生物疗法的患者进行严格随访以检测有时可能很严重的不良事件也至关重要。因此,在开具任何生物疗法处方之前,必须评估效益/风险比。

相似文献

1
[Rheumatoid arthritis: current status of therapy].[类风湿关节炎:治疗现状]
Tunis Med. 2007 Jan;85(1):1-8.
2
[New drugs and treatment strategies for rheumatoid arthritis].[类风湿关节炎的新药及治疗策略]
Recenti Prog Med. 2003 Sep;94(9):361-79.
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Lack of adverse effect of anti-tumor necrosis factor-α biologics in treatment of rheumatoid arthritis: 5 years follow-up.抗肿瘤坏死因子-α生物制剂治疗类风湿关节炎无不良影响:5 年随访。
Int J Rheum Dis. 2012 Jun;15(3):330-5. doi: 10.1111/j.1756-185X.2012.01715.x. Epub 2012 Feb 13.
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Does tumor necrosis factor alpha inhibition promote or prevent heart failure in patients with rheumatoid arthritis?肿瘤坏死因子α抑制对类风湿关节炎患者心力衰竭具有促进作用还是预防作用?
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Treatment, management, and monitoring of established rheumatoid arthritis.已确诊类风湿性关节炎的治疗、管理及监测
J Fam Pract. 2007 Oct;56(10 Suppl Rapid):S1-7; quiz S8.
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[Biotherapies for the treatment of asthma: are they the treatment of the future?].[用于治疗哮喘的生物疗法:它们是未来的治疗方法吗?]
Rev Mal Respir. 2006 Sep;23(4 Pt 2):10S44-10S48.
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[Paradigm shift in the treatment of rheumatoid arthritis by biologics].[生物制剂治疗类风湿关节炎的范式转变]
Rinsho Byori. 2008 Apr;56(4):309-15.
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Cancer risk in patients with rheumatoid arthritis treated with anti-tumor necrosis factor alpha therapies: does the risk change with the time since start of treatment?接受抗肿瘤坏死因子α治疗的类风湿关节炎患者的癌症风险:风险会随着治疗开始后的时间而改变吗?
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Tumor necrosis factor inhibition: a part of the solution or a part of the problem of heart failure in rheumatoid arthritis?肿瘤坏死因子抑制:类风湿关节炎中心力衰竭问题解决方案的一部分还是问题的一部分?
Arthritis Rheum. 2008 Mar;58(3):637-40. doi: 10.1002/art.23280.
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[Anti-TNF-alpha therapy as a new option in treatment of rheumatoid arthritis?].[抗肿瘤坏死因子-α疗法作为类风湿关节炎治疗的新选择?]
Wien Med Wochenschr. 1999;149(19-20):554-7.

引用本文的文献

1
Pathogenesis and Function of Interleukin-35 in Rheumatoid Arthritis.白细胞介素-35在类风湿关节炎中的发病机制及作用
Front Pharmacol. 2021 May 13;12:655114. doi: 10.3389/fphar.2021.655114. eCollection 2021.
2
Distinct terminal and cell body mechanisms in the nociceptor mediate hyperalgesic priming.伤害感受器中不同的终末和胞体机制介导痛觉过敏致敏。
J Neurosci. 2015 Apr 15;35(15):6107-16. doi: 10.1523/JNEUROSCI.5085-14.2015.
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Transient decrease in nociceptor GRK2 expression produces long-term enhancement in inflammatory pain.
伤害感受器 GRK2 表达的短暂下降可产生炎症性疼痛的长期增强。
Neuroscience. 2012 Oct 11;222:392-403. doi: 10.1016/j.neuroscience.2012.07.004. Epub 2012 Jul 13.