Friedman Elliot M, Mroczek Daniel K, Christ Sharon L
Department of Human Development and Family Studies, Purdue University, 1202 West State Street, West Lafayette, IN 47907, USA.
Department of Psychology and Feinberg School of Medicine, Northwestern University, Evanston, IL, USA.
Ther Adv Chronic Dis. 2018 Oct 19;10:2040622318806848. doi: 10.1177/2040622318806848. eCollection 2019.
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.
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.
Multimorbidity ( 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.
These results show that inflammation, a nonspecific marker of multiple disease conditions, explains in part the degree to which multimorbidity is disabling.
本研究利用美国中年发展调查的纵向数据，在17 - 19年的随访期内，考察了全身性炎症在介导多种疾病与功能受限增加及功能受限发作之间联系中的作用。
参与者完成了慢性病和功能受限的问卷调查评估。检测血清中的白细胞介素-6、C反应蛋白和纤维蛋白原。采用结构方程模型预测与基线多种疾病状态相关的功能受限增加和发作情况；还确定了炎症的中介作用。
多种疾病（0 - 1种疾病）预示着更多的功能受限以及随着时间推移功能受限发作的几率更高。显著的间接效应表明，炎症部分介导了多种疾病与功能受限变化之间的联系，但不是功能受限的发作。
这些结果表明，炎症作为多种疾病状态的非特异性标志物，部分解释了多种疾病导致残疾的程度。
