The Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta (Michopoulos, Rothbaum, Ressler); the Yerkes National Primate Research Center, Atlanta (Michopoulos); the Department of Psychiatry and Behavioral Sciences (Beurel, Gould, Dhabhar), the Department of Biochemistry and Molecular Biology (Beurel), and the Sylvester Comprehensive Cancer Center (Dhabhar), University of Miami Miller School of Medicine, Miami; the Department of Psychology, University of Miami, Coral Gables, Fla. (Dhabhar); the Department of Psychiatry, New York University School of Medicine, New York (Schultebraucks, Galatzer-Levy); Mclean Hospital, Harvard Medical School, Belmont, Mass. (Ressler); the Department of Psychiatry, Dell Medical School, and the Institute for Early Life Adversity Research, University of Texas at Austin (Nemeroff).
Am J Psychiatry. 2020 Jan 1;177(1):58-65. doi: 10.1176/appi.ajp.2019.19010039. Epub 2019 Jul 29.
Although several reports have documented heightened systemic inflammation in posttraumatic stress disorder (PTSD), few studies have assessed whether inflammatory markers serve as prospective biomarkers for PTSD risk. The present study aimed to characterize whether peripheral immune factors measured in blood samples collected in an emergency department immediately after trauma exposure would predict later chronic development of PTSD.
Participants (N=505) were recruited from a hospital emergency department and underwent a 1.5-hour assessment. Blood samples were drawn, on average, about 3 hours after trauma exposure. Follow-up assessments were conducted 1, 3, 6, and 12 months after trauma exposure. Latent growth mixture modeling was used to identify classes of PTSD symptom trajectories.
Three distinct classes of PTSD symptom trajectories were identified: chronic (N=28), resilient (N=160), and recovery (N=85). Multivariate analyses of covariance revealed a significant multivariate main effect of PTSD symptom trajectory class membership on proinflammatory cytokines. Univariate analyses showed a significant main effect of trajectory class membership on plasma concentrations of proinflammatory tumor necrosis factor α (TNFα) and interferon-γ (IFNγ). Concentrations of proinflammatory TNFα and IFNγ were significantly lower in individuals in the chronic PTSD class compared with those in the recovery and resilient classes. There were no significant differences in interleukin (IL) 1β and IL-6 concentrations by PTSD symptom trajectory class. Anti-inflammatory and other cytokines, as well as chemokines and growth factor concentrations, were not associated with development of chronic PTSD.
Overall, the study findings suggest that assessing the proinflammatory immune response to trauma exposure immediately after trauma exposure, in the emergency department, may help identify individuals most at risk for developing chronic PTSD in the aftermath of trauma.
尽管有几项报告记录了创伤后应激障碍（PTSD）患者的全身性炎症水平升高，但很少有研究评估炎症标志物是否可作为 PTSD 风险的前瞻性生物标志物。本研究旨在评估创伤后即刻采集的外周血免疫因子是否可预测 PTSD 的慢性发展。
参与者（N=505）从医院急诊室招募，并进行了 1.5 小时的评估。血液样本平均在创伤暴露后约 3 小时采集。在创伤暴露后 1、3、6 和 12 个月进行随访评估。采用潜在增长混合模型来确定 PTSD 症状轨迹的类别。
确定了 PTSD 症状轨迹的 3 个不同类别：慢性（N=28）、弹性（N=160）和恢复（N=85）。多变量协方差分析显示，PTSD 症状轨迹类别成员身份的多变量主要影响显著。单变量分析显示，轨迹类别成员身份对促炎性肿瘤坏死因子-α（TNFα）和干扰素-γ（IFNγ）的血浆浓度有显著的主效应。与恢复和弹性类别相比，慢性 PTSD 类别个体的促炎性 TNFα 和 IFNγ 浓度显著降低。PTSD 症状轨迹类别之间的白细胞介素（IL）1β和 IL-6 浓度无显著差异。抗炎和其他细胞因子以及趋化因子和生长因子浓度与慢性 PTSD 的发生无关。
总的来说，研究结果表明，在创伤后即刻于急诊室评估创伤后促炎免疫反应，可能有助于识别创伤后最易发生慢性 PTSD 的个体。
