The association between anxiety, traumatic stress, and obsessive-compulsive disorders and chronic inflammation: A systematic review and meta-analysis
The association between anxiety, traumatic stress, and obsessive-compulsive disorders and chronic inflammation: A systematic review and meta-analysis
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DOI：
10.1002/da.22790
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发表时间：
2018-11-01
影响因子：
7.4
通讯作者：
Mennin, Douglas S.
中科院分区：
文献类型：
--
作者：
Renna, Megan E.;O'Toole, Mia S.;Mennin, Douglas S.
背景方法焦虑的特点是长时间为真实的或感知的威胁做好准备。这可能表现为心理和生理激活，最终导致更大的健康不良风险。鉴于慢性炎症在慢性疾病中的影响作用，它可能在这种关系中发挥着不可或缺的作用。这项荟萃分析的目的是检查焦虑症、PTSD（创伤后应激障碍）或强迫症患者与健康对照者相比，通过炎症细胞因子和 C 反应蛋白测量的慢性炎症水平。还评估了几个调节变量，包括具体诊断和抑郁症合并症。对 76 篇全文文章进行了资格筛选，最终纳入了 41 项研究进行分析。结果 结论结果表明，健康对照 (HC) 和焦虑症患者在促炎细胞因子方面存在显着的总体差异（P = 0.013，Hedge's g = -0.39），这似乎主要是由白细胞介素 1 β（IL-1 β；P = 0.009，Hedge's g = -0.50）、IL-6（P < 0.001，Hedge's g = -0.50）、IL-6（P < 0.001，Hedge's g = -0.50）驱动的。 -0.93）和肿瘤坏死因子-α（P = 0.030，Hedge's g = -0.56）。调节分析揭示了诊断的调节作用（P = 0.050），因为只有患有 PTSD 的个体才表现出 HC 之间炎症的差异（P = 0.004，Hedge's g = -0.68）。这些数据证明了炎症失调与慢性、影响性和严重焦虑相关的诊断之间的关联，并提供了对焦虑（尤其是创伤后应激障碍）与某些炎症标志物相关方式的深入了解。在此过程中，这些发现可能为解开焦虑与基本健康过程之间的关系提供了第一步。
Background Methods Anxiety is characterized by prolonged preparation for real or perceived threat. This may manifest both as psychological and physiological activation, ultimately leading to greater risk for poor health. Chronic inflammation may play an integral role in this relationship, given the influential role that it has in chronic illness. The aim of this meta-analysis is to examine levels of chronic inflammation, measured by inflammatory cytokines and C-reactive protein, in people with anxiety disorders, PTSD (posttraumatic stress disorder), or obsessive-compulsive disorder compared to healthy controls. Several moderating variables, including specific diagnosis and depression comorbidity, were also assessed. Seventy six full-text articles were screened for eligibility with 41 studies ultimately included in analysis. Results ConclusionsResults demonstrated a significant overall difference between healthy controls (HCs) and people with anxiety disorders in pro-inflammatory cytokines (P = 0.013, Hedge's g = -0.39), which appears to be largely driven by interleukin-1 beta (IL-1 beta; P = 0.009, Hedge's g = -0.50), IL-6 (P < 0.001, Hedge's g = -0.93), and tumor necrosis factor-alpha (P = 0.030, Hedge's g = -0.56). Moderation analyses revealed a moderating effect of diagnosis (P = 0.050), as only individuals with PTSD demonstrated differences in inflammation between HCs (P = 0.004, Hedge's g = -0.68). These data demonstrate the association between inflammatory dysregulation and diagnoses associated with chronic, impactful, and severe anxiety and provides insight into the way that anxiety, and in particular PTSD, is related to certain inflammatory markers. In doing so, these findings may provide an initial step in disentangling the relationship between anxiety and basic health processes.