Sleep Disturbances are a Significant Predictor of Chikungunya Arthritis Flare Severity.

Sleep Disturbances are a Significant Predictor of Chikungunya Arthritis Flare Severity.
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睡眠障碍是chikungunya关节炎耀斑严重程度的重要预测指标。

DOI:
10.33696/immunology.3.098
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发表时间:
2021
期刊:
Journal of cellular immunology
影响因子:
--
通讯作者:
Chang AY
Chang AY
中科院分区:
其他
文献类型:
--
作者:
Tritsch SR;Amdur R;Encinales L;Cadena A;Fierbaugh P;Avendaño G;Gomez CAH;Suchowiecki K;Mendoza-Torres E;Rosales W;Jimenez D;Hernandez CAP;Hernandez AS;Silvera PB;Crespo YG;Jimenez ADC;Zapata JCM;Mores CN;Firestein GS;Simon G;Chang AY

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这项研究的主要目的是探索与基孔肯雅病毒(CHIKV)感染相关的睡眠和爆发性疼痛之间的联系。次要目的是研究细胞因子和调节性T细胞(Treg)是否对这种关系产生影响。使用在哥伦比亚巴兰基利亚收集的数据进行了一项横断面研究,该研究招募了有基孔肯雅病毒感染史的慢性关节炎和非慢性关节炎患者。通过适用于CHIKV关节炎的风湿性关节炎临床试验结果测量(OMERACT)发作问卷的版本测量发作严重性,包括疼痛、体力活动困难、疲劳、僵硬和由于关节炎导致的维持社交活动困难的度量,这些度量有助于发作严重性。此外,还测量了四项睡眠障碍项目、五项炎性细胞因子水平、四项抗炎性细胞因子水平和六项Treg水平。然后,多变量线性回归模型被用来测试耀斑疼痛对睡眠障碍的直接和间接影响,并确定这种关系是否是由细胞因子或TdR介导的。最后,SAS CALIS程序被用来测试路径模型,显示可能的因果关系的影响与中介和混淆。分析表明,睡眠障碍与CHIKV关节炎发作疼痛呈正相关,并且在调整人口统计学变量,细胞因子和T细胞水平后,它是发作严重程度的重要预测因子。此外,T细胞和细胞因子都不介导CHIKV关节炎中的疼痛/睡眠关系。睡眠障碍与关节炎发作疼痛和严重程度之间存在强烈的关联;然而,这种关系不是由细胞因子或T细胞介导的。由于这项研究无法确定因果关系,因此需要进一步研究以确定睡眠障碍和CHIKV关节炎发作之间关系的机制。
The primary objective of this research was to explore the link between sleep and flare pain associated with chikungunya virus (CHIKV) infection. The secondary objective was to investigate if cytokines and T regulatory (Treg) cells have an influence on this relationship. A cross-sectional study was performed using data collected in Barranquilla, Colombia, which enrolled patients with and without chronic arthritis with a history of chikungunya infection. Flare severity was measured by a version of the Outcome Measures in Rheumatoid Arthritis Clinical Trials (OMERACT) flare questionnaire adapted for CHIKV arthritis, including metrics for pain, difficulty with physical activity, fatigue, stiffness and difficulty maintaining social activities due to arthritis that contribute to flare severity. In addition, four sleep disturbance items, five inflammatory cytokine levels, four anti-inflammatory cytokine levels, and six Treg levels were measured. Then, multivariable linear regression models were used to test the direct and indirect effects of flare-pain on sleep disturbance, and to determine whether this relationship was mediated by cytokines or Tregs. Finally, the SAS CALIS procedure was used to test path models showing possible causal effects with mediators and confounds. The analysis showed that sleep disturbance is positively correlated with CHIKV arthritis flare pain, and that it is a significant predictor of flare severity after adjusting for demographic variables, cytokine, and T cell levels. Further, neither T cells nor cytokines mediate the pain/sleep relationship in CHIKV arthritis. There is a strong association between sleep disturbance and arthritis flare pain and severity; however, this relationship is not mediated by cytokines or T cells. Since this study is unable to determine causation, further research is needed to determine the mechanism underlying the relationship between sleep disturbances and CHIKV arthritis flares.