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Stimulation of systemic low-grade inflammation by psychosocial stress.心理社会压力对全身低度炎症的刺激。
Psychosom Med. 2014 Apr;76(3):181-9. doi: 10.1097/PSY.0000000000000049.
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From stress to inflammation and major depressive disorder: a social signal transduction theory of depression.从压力到炎症再到重度抑郁症:一种抑郁症的社会信号转导理论。
Psychol Bull. 2014 May;140(3):774-815. doi: 10.1037/a0035302. Epub 2014 Jan 13.
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Review: the role of inflammation in depression.综述:炎症在抑郁症中的作用。
Psychiatr Danub. 2013 Sep;25 Suppl 2:S216-23.
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High-sensitivity C-reactive protein and risk of sepsis.高敏 C 反应蛋白与脓毒症风险。
PLoS One. 2013 Jul 23;8(7):e69232. doi: 10.1371/journal.pone.0069232. Print 2013.
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CRP, IL-6 and depression: a systematic review and meta-analysis of longitudinal studies.C 反应蛋白、白细胞介素 6 与抑郁:纵向研究的系统评价和荟萃分析。
J Affect Disord. 2013 Sep 25;150(3):736-44. doi: 10.1016/j.jad.2013.06.004. Epub 2013 Jul 17.
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Depression and cardiac disease: epidemiology, mechanisms, and diagnosis.抑郁症与心脏病:流行病学、机制及诊断
Cardiovasc Psychiatry Neurol. 2013;2013:695925. doi: 10.1155/2013/695925. Epub 2013 Apr 7.
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The 'perfect storm' and acute coronary syndrome onset: do psychosocial factors play a role?“完美风暴”与急性冠状动脉综合征发病:心理社会因素是否发挥作用?
Prog Cardiovasc Dis. 2013 May-Jun;55(6):601-10. doi: 10.1016/j.pcad.2013.03.003. Epub 2013 Apr 6.
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Late-life depression, mild cognitive impairment, and dementia.老年期抑郁症、轻度认知障碍和痴呆。
JAMA Neurol. 2013 Mar 1;70(3):374-82. doi: 10.1001/jamaneurol.2013.603.
9
Behavioral mechanisms, elevated depressive symptoms, and the risk for myocardial infarction or death in individuals with coronary heart disease: the REGARDS (Reason for Geographic and Racial Differences in Stroke) study.行为机制、抑郁症状升高与冠心病患者心肌梗死或死亡风险:REGARDS(中风地域和种族差异原因)研究。
J Am Coll Cardiol. 2013 Feb 12;61(6):622-30. doi: 10.1016/j.jacc.2012.09.058. Epub 2013 Jan 2.
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Depressive symptoms as an independent risk factor for mortality in elderly persons: results of a national longitudinal study.抑郁症状是老年人死亡的独立危险因素:一项全国性纵向研究的结果。
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心理社会压力作为脓毒症的一个风险因素:一项基于人群的队列研究。

Psychosocial stress as a risk factor for sepsis: a population-based cohort study.

作者信息

Ojard Connor, Donnelly John P, Safford Monika M, Griffin Russell, Wang Henry E

机构信息

From the Departments of Emergency Medicine (H.E.W, J.P.D.), Epidemiology (J.P.D.), Medicine, and Emergency Medicine (H.E.W.), and Division of Preventive Medicine (M.M.S., J.P.D.), University of Alabama School of Medicine (C.O.), Birmingham, Alabama; and Department of Epidemiology (R.G.), University of Alabama at Birmingham, Birmingham, Alabama.

出版信息

Psychosom Med. 2015 Jan;77(1):93-100. doi: 10.1097/PSY.0000000000000120.

DOI:10.1097/PSY.0000000000000120
PMID:25469683
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4293326/
Abstract

OBJECTIVE

To characterize the relationship between stress and future risk of sepsis. We also evaluated the role of depression in this relationship.

METHODS

We used population-based data on 30,183 participants in the Reasons for Geographic and Racial Differences in Stroke cohort, characterizing stress using the Perceived Stress Scale (PSS) and depressive symptoms using the Center for Epidemiologic Studies Depression Scale (CES-D). We identified incident sepsis events as hospitalizations for a serious infection with the presence of at least two systemic inflammatory response syndrome criteria. We assessed associations between PSS and incidence of sepsis for 1 and 10 years of follow-up, adjusting for demographics and chronic medical conditions and assessing the role of health behaviors and CES-D in these relationships.

RESULTS

In 2003 to 2012, 1500 participants experienced an episode of sepsis. Mean PSS and CES-D scores were 3.2 (2.9) and 1.2 (2.1). PSS was associated with increased 1-year adjusted incidence of sepsis (hazard ratio [HR] = 1.21 per PSS standard deviation, 95% confidence interval = 1.06-1.38); multivariable adjustment for health behaviors and CES-D did not change this association (1.20, 1.03-1.39). PSS was also associated with increased 10-year adjusted incidence of sepsis (HR = 1.07 per PSS standard deviation; 95% confidence interval = 1.02-1.13). Multivariable adjustment showed that health behaviors did not affect this long-term association, whereas the addition of CES-D reduced the association between PSS and sepsis during 10-year follow-up (HR = 1.04, 0.98-1.11).

CONCLUSIONS

Increased stress was associated with higher 1-year adjusted incidence of sepsis, even after accounting for depressive symptoms. The association between stress and 10-year adjusted incidence of sepsis was also significant, but this association was reduced when adjusting for depressive symptoms. Reduction of stress may limit short-term sepsis risk.

摘要

目的

明确应激与未来脓毒症风险之间的关系。我们还评估了抑郁在这种关系中的作用。

方法

我们使用了基于人群的数据,这些数据来自卒中队列中30183名参与者的地理和种族差异原因研究,使用感知应激量表(PSS)来描述应激情况,使用流行病学研究中心抑郁量表(CES-D)来描述抑郁症状。我们将脓毒症事件定义为因严重感染住院且至少符合两条全身炎症反应综合征标准。我们评估了随访1年和10年时PSS与脓毒症发病率之间的关联,对人口统计学和慢性疾病进行了校正,并评估了健康行为和CES-D在这些关系中的作用。

结果

在2002012年期间,1500名参与者经历了脓毒症发作。PSS和CES-D的平均得分分别为3.2(2.9)和1.2(2.1)。PSS与校正后的1年脓毒症发病率增加相关(风险比[HR]=每PSS标准差1.21,95%置信区间=1.061.38);对健康行为和CES-D进行多变量校正并未改变这种关联(1.20,1.031.39)。PSS还与校正后的10年脓毒症发病率增加相关(HR=每PSS标准差1.07;95%置信区间=1.021.13)。多变量校正显示,健康行为并未影响这种长期关联,而加入CES-D后降低了10年随访期间PSS与脓毒症之间的关联(HR=1.04,0.98~1.11)。

结论

即使在考虑抑郁症状后,应激增加仍与校正后的1年脓毒症发病率较高相关。应激与校正后的10年脓毒症发病率之间的关联也很显著,但在校正抑郁症状后这种关联减弱。减轻应激可能会限制短期脓毒症风险。