女性慢性创伤后应激障碍与炎症和内皮功能标志物的横断面和纵向关联。
Cross-Sectional and Longitudinal Associations of Chronic Posttraumatic Stress Disorder With Inflammatory and Endothelial Function Markers in Women.
机构信息
Center for Behavioral Cardiovascular Health, Columbia University Medical Center, New York, New York; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Department of Biostatistics, Columbia University Mailman School of Public Health, New York, New York.
出版信息
Biol Psychiatry. 2017 Dec 15;82(12):875-884. doi: 10.1016/j.biopsych.2017.06.020. Epub 2017 Jun 27.
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 < .05), tumor necrosis factor alpha receptor II (B = 0.07, p < .01), and intercellular adhesion molecule-1 (B = 0.04, p < .05) levels. Women with trauma but without PTSD had higher average tumor necrosis factor alpha receptor II levels (B = 0.05, p < .05). In addition, women with chronic PTSD had a greater increase in vascular cell adhesion molecule-1 over time (B = 0.003, p < .05).
CONCLUSIONS
Increased inflammation and impaired endothelial function may be pathways by which chronic PTSD increases cardiovascular disease risk.
背景
创伤后应激障碍（PTSD）可能通过促进促炎状态和内皮功能障碍来增加心血管疾病的风险。先前的研究表明 PTSD 与炎症和内皮功能生物标志物之间存在关联，但大多数研究都是横断面的，并没有将创伤暴露的影响与 PTSD 的影响区分开来。
方法
我们在护士健康研究 II 中调查了创伤暴露和慢性 PTSD 与炎症生物标志物（C 反应蛋白和肿瘤坏死因子受体 II）和内皮功能生物标志物（细胞间黏附分子-1 和血管细胞黏附分子-1）之间的关联，研究对象为 524 名中年女性，她们均无心血管疾病。使用线性混合模型，我们在无心血管疾病的女性中，考虑到随时间的平均水平（横断面）或随时间的水平变化（纵向），对两次测量的生物标志物与创伤/PTSD 状态之间的关联进行了研究。生物标志物水平进行了对数转换。根据结构诊断访谈确定的创伤/PTSD 状态定义为两次采血均无创伤（n=175）、采血 1 时有创伤但两次采血均无 PTSD（n=175）和 PTSD 持续到采血 1 后（慢性 PTSD；n=174）。参考组为无创伤的女性。
结果
在调整了已知潜在混杂因素的模型中，患有慢性 PTSD 的女性的平均 C 反应蛋白（B=0.27，p<0.05）、肿瘤坏死因子受体 II（B=0.07，p<0.01）和细胞间黏附分子-1（B=0.04，p<0.05）水平较高。有创伤但无 PTSD 的女性的平均肿瘤坏死因子受体 II 水平较高（B=0.05，p<0.05）。此外，患有慢性 PTSD 的女性的血管细胞黏附分子-1随时间的增加幅度更大（B=0.003，p<0.05）。
结论
炎症增加和内皮功能障碍可能是慢性 PTSD 增加心血管疾病风险的途径。
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