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首页> 外文期刊>Biological psychiatry >Cross-Sectional and Longitudinal Associations of Chronic Posttraumatic Stress Disorder With Inflammatory and Endothelial Function Markers in Women
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Cross-Sectional and Longitudinal Associations of Chronic Posttraumatic Stress Disorder With Inflammatory and Endothelial Function Markers in Women

机译:慢性故障胁迫障碍与女性炎症和内皮功能标记的横截面和纵向关联

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摘要

Abstract Background Posttraumatic stress disorder (PTSD) may contribute to heightened cardiovascular disease risk by promoting a proinflammatory state and impaired endothelial function. Previous research has demonstrated associations of PTSD with inflammatory and endothelial function biomarkers, but most work has been cross-sectional and does not separate the effects of trauma exposure from those of PTSD. Methods We investigated associations of trauma exposure and chronic PTSD with biomarkers of inflammation (C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial function (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in 524 middle-aged women in the Nurses’ Health Study II. Using linear mixed models, we examined associations of trauma/PTSD status with biomarkers measured twice, 10 to 16 years apart, in cardiovascular disease–free women, considering either average levels over time (cross-sectional) or change in levels over time (longitudinal). Biomarker levels were log-transformed. Trauma/PTSD status (based on structured diagnostic interviews) was defined as no trauma at either blood draw ( n ?= 175), trauma at blood draw 1 but no PTSD at either draw ( n ?= 175), and PTSD that persisted beyond blood draw 1 (chronic PTSD; n ?= 174). The reference group was women without trauma. Results In models adjusted for known potential confounders, women with chronic PTSD had higher average C-reactive protein ( B ?= 0.27, p B ?= 0.07, p B ?= 0.04, p B ?= 0.05, p B ?= 0.003, p Conclusions Increased inflammation and impaired endothelial function may be pathways by which chronic PTSD increases cardiovascular disease risk.
机译:摘要背景后,通过促进促炎状态和内皮功能受损,可能有助于提高心血管疾病风险。以前的研究表明,PTSD与炎症和内皮功能生物标志物的关联,但大多数作品一直是横截面的,并没有将创伤暴露的影响与PTSD的作用分开。方法我们在524名中年女性中调查了炎症(C反应蛋白和肿瘤坏死因子α受体II)和内皮功能(细胞间粘附分子-1和血管细胞粘附分子-1)的生物标志物的疗法在护士的健康研究中。使用线性混合模型,我们将创伤/ PTSD状态的关联与两次,在血管疾病的妇女中测量的生物标志物,在心血管疾病的妇女中,考虑到平均水平随时间(横截面)或随时间的水平变化(纵向) )。生物标志物水平是对数转换的。 Trauma / PTSD状态(基于结构化诊断访谈)定义为血迹(N?= 175)的创伤,血迹1的创伤1,但在凹陷(n?= 175)中没有ptsd,并持续到以外的ptsd血液绘制1(慢性PTSD; N?= 174)。参考组是没有创伤的女性。导致针对已知潜在混淆的模型,慢性PTSD的女性具有较高的平均C反应蛋白(B?= 0.27,P <= 0.07,P B 2,PB≥0.05,P <= 0.003, P结论炎症增加和内皮功能受损可能是慢性受灾治愈性疾病风险的途径。

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