Multimorbidity, inflammation, and disability: a longitudinal mediational analysis.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2018-10-19 eCollection Date: 2019-01-01 DOI:10.1177/2040622318806848
Elliot M Friedman, Daniel K Mroczek, Sharon L Christ
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引用次数: 0

Abstract

Background: Using longitudinal data from the Survey of Mid-Life Development in the United States, this study examined the role of systemic inflammation in mediating the link between multimorbidity and increases in and onset of functional limitations over a 17-19 year follow-up period.

Methods: Participants completed questionnaire assessments of chronic conditions and functional limitations. Interleukin-6, C-reactive protein, and fibrinogen were assayed in serum. Structural equation models were used to predict increases in and onset of functional limitations associated with baseline multimorbidity status; mediation by inflammation was also determined.

Results: Multimorbidity (versus 0-1 conditions) predicted more functional limitations and greater odds of onset of limitations over time. Significant indirect effects showed that inflammation partially mediated the link between multimorbidity and changes in, but not onset of, limitations.

Discussion: These results show that inflammation, a nonspecific marker of multiple disease conditions, explains in part the degree to which multimorbidity is disabling.

多发病、炎症和残疾:一项纵向中介分析
背景:本研究使用来自美国中年发展调查的纵向数据,在17-19年的随访期间,研究了全身性炎症在多重发病率和功能限制的增加和发生之间的联系中的作用。方法:参与者完成慢性病和功能限制的问卷评估。血清中检测白细胞介素-6、c反应蛋白、纤维蛋白原。结构方程模型用于预测与基线多重疾病状态相关的功能限制的增加和开始;还确定了炎症的调解作用。结果:多病(与0-1条件相比)预示着更多的功能限制和随着时间的推移发生限制的可能性更大。显著的间接效应表明,炎症部分介导了多发病和局限性变化之间的联系,但不是局限性的发生。讨论:这些结果表明,炎症是多种疾病的非特异性标志,在一定程度上解释了多种疾病致残的程度。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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