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Fatigue in inflammatory rheumatic diseases: current knowledge and areas for future research
Nature Reviews Rheumatology ( IF 29.4 ) Pub Date : 2021-10-01 , DOI: 10.1038/s41584-021-00692-1
Kristen Davies 1, 2 , Emma Dures 3, 4 , Wan-Fai Ng 1, 2
Affiliation  

Fatigue is a complex phenomenon and an important health concern for many people with chronic inflammatory rheumatic diseases, such as rheumatoid arthritis, psoriatic arthritis, primary Sjögren syndrome and systemic lupus erythematosus. Although some clinical trials have shown the benefits of cognitive behavioural therapy in fatigue management, the effect of this approach is relatively modest, and no curative treatment has been identified. The pathogenesis of fatigue remains unclear. Despite many challenges and limitations, a growing body of research points to roles for the immune system, the central and autonomic nervous systems and the neuroendocrine system in the induction and maintenance of fatigue in chronic diseases. New insights indicate that sleep, genetic susceptibility, metabolic disturbances and other biological and physiological mechanisms contribute to fatigue. Furthermore, understanding of the relationships between psychosocial factors and fatigue is increasing. However, the interrelationships between these diverse mechanisms and fatigue remain poorly defined. In this Review, we outline various biological, physiological and psychosocial determinants of fatigue in inflammatory rheumatic diseases, and propose mechanistic and conceptual models of fatigue to summarize current understanding, stimulate debate and develop further research ideas.



中文翻译:

炎症性风湿病的疲劳:当前知识和未来研究领域

疲劳是一种复杂的现象,对于许多患有慢性炎症性风湿病(例如类风湿性关节炎、银屑病关节炎、原发性干燥综合征和系统性红斑狼疮)的人来说,疲劳是一个重要的健康问题。尽管一些临床试验显示了认知行为疗法在疲劳管理中的益处,但这种方法的效果相对有限,并且尚未确定治愈方法。疲劳的发病机制仍不清楚。尽管存在许多挑战和局限性,但越来越多的研究指出免疫系统、中枢神经系统和自主神经系统以及神经内分泌系统在诱发和维持慢性病疲劳方面的作用。新的见解表明睡眠、遗传易感性、代谢紊乱和其他生物和生理机制会导致疲劳。此外,对社会心理因素与疲劳之间关系的了解也在增加。然而,这些不同机制与疲劳之间的相互关系仍然不清楚。在这篇综述中,我们概述了炎症性风湿病疲劳的各种生物学、生理学和心理社会决定因素,并提出了疲劳的机制和概念模型,以总结当前的理解、激发争论并发展进一步的研究思路。

更新日期:2021-10-01
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