摘要
背景:类风湿关节炎 (RA)患者患心力衰竭 (HF) 的风险升高被部分认为是由于慢性低级系统性炎症造成的。作为强有力的炎症抑制因子,生物制剂有望影响RA患者HF的发展。不幸的是,HF在RA患者和非RA-HF研究病例报告表明,这些药物可能增加RA患者患HF的几率。目的:本综述我们要通过升高的细胞因子、免疫细胞改变和生物制剂影响RA患者的心肌功能来洞察的分子机制。临床前数据,综述了评估HF发展的生物制剂的影响的临床研究。结果:临床前研究表明,调查因子(TNF-α、IL–1、IL-6)对心肌功能有双向作用。在HF和RA的免疫细胞变化的共同机制已在临床前研究中观察得到。患HF的非RA患者英夫利昔单抗高剂量被认为是有害的。绝大多数回顾性研究表明TNF-α抑制剂不增加RA患者疾病HF发展的风险。然而,随机对照试验没有做,而TNF-α抑制剂是患心衰NYHA III / IV的RA患者的禁忌且基于非RA- HF研究,患HF NYHA I / II的 RA患者应慎用。由于HF罕见的不良事件,利妥昔单抗是患心衰NYHA IV的RA患者的禁忌。结论:细胞因子似乎对RA患者HF的发展的有双向作用。根据已发表的证据, TNFα抑制剂大幅度提高RA人口疾病发展的风险是不可能的。然而他们是患心衰NYHA III / IV的RA患者的禁忌且患HF NYHA I / II的 RA患者应慎用。禁忌的RA患者心衰NYHA III / IV和应用HF NYHA I / II在RA患者慎用。阿那白滞素,tocilizumab,利妥昔单抗和阿贝西普的影响需要在今后继续研究。
关键词: 生物制剂,B细胞,慢性炎症,细胞因子,心力衰竭,风湿性关节炎,T细胞。
Current Medicinal Chemistry
Title:Biological Therapies: Effects of Proinflammatory Pathways and their Inhibition on the Myocardium of Rheumatoid Athritis Patients
Volume: 22 Issue: 16
Author(s): Florian Obermair and Herwig Pieringer
Affiliation:
关键词: 生物制剂,B细胞,慢性炎症,细胞因子,心力衰竭,风湿性关节炎,T细胞。
摘要: Background: The elevated risk of heart failure (HF) in rheumatoid arthritis (RA) is considered to be partly caused by the chronic low-grade systemic inflammation. As potent suppressors of inflammation, biologics were expected to influence HF development in RA. Unfortunately, case reports of HF in RA patients and non-RA HF studies have suggested that these drugs may even increase HF rates in RA. Aim: With this review we want to provide insight into the molecular mechanisms by which elevated cytokines, immune cell alterations and biologics influence myocardial function in RA patients. Beside preclinical data, clinical studies that assess the influence of biologics on HF development are reviewed. Results: Preclinical studies suggest a bidirectional role of the investigated cytokines (TNF-alpha, IL- 1, IL-6) on myocardial function. Common mechanisms of immune cell alterations in HF and RA have been observed in preclinical studies. High doses of infliximab in non-RA patients with HF were found to be harmful. The vast majority of retrospective studies suggest that TNF-alpha inhibitors do not increase the risk of HF development in RA patients. Nevertheless randomized controlled trials are missing and TNF-alpha inhibitors are contraindicated in RA patients with HF NYHA III/IV and should be used with caution in RA patients with HF NYHA I/II based on non-RA HF studies. Due to rare adverse events of HF, rituximab is contraindicated in RA patients with HF NYHA IV. Conclusion: Cytokines seem to have a bidirectional influence on HF development in RA. According to the published evidence it is unlikely that TNFalpha inhibitors substantially increase the risk of HF development in an RA population. Nevertheless they are contraindicated in RA patients with HF NYHA III/IV and should be used with caution in RA patients with HF NYHA I/II. The influence of anakinra, tocilizumab, rituximab and abatacept needs to be investigated in future studies.
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Cite this article as:
Florian Obermair and Herwig Pieringer , Biological Therapies: Effects of Proinflammatory Pathways and their Inhibition on the Myocardium of Rheumatoid Athritis Patients, Current Medicinal Chemistry 2015; 22 (16) . https://dx.doi.org/10.2174/0929867322666150209160918
DOI https://dx.doi.org/10.2174/0929867322666150209160918 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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