Department of Psychiatry, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.
Psychoneuroendocrinology. 2012 Mar;37(3):317-31. doi: 10.1016/j.psyneuen.2011.07.003. Epub 2011 Jul 29.
Hypothalamic-pituitary-adrenal (HPA)-axis dysregulation has inconsistently been associated with posttraumatic stress disorder (PTSD). Yet, trauma exposure rather than PTSD may be responsible for HPA-axis dysregulation. In two meta-analyses, we assessed the association of adulthood trauma exposure and HPA-axis functioning in healthy subjects with and without PTSD.
A literature search in Pubmed and PsychInfo, using keywords and MeSH terms such as cortisol, emotional trauma, and PTSD, was performed. Only studies that included mentally healthy trauma-exposed (TE) individuals as well as non-exposed (NE) healthy individuals and/or PTSD patients (PTSD) were selected. This resulted in 1511 studies of which ultimately, 37 studies (21 TE versus NE and 34 TE versus PTSD, N=2468) were included. Methodological quality of all studies was assessed according to specific quality criteria. Pooled effect sizes (Hedges's g) on cortisol levels were compared. For all analyses, random effect models were used.
Cortisol levels were neither significantly different between TE versus NE subjects (-0.029; 95%CI: -0.145; 0.088) nor between TE subjects versus PTSD patients (0.175; 95%CI: -0.012; -0.362). Subgroup analyses showed an increased cortisol suppression after the low dose dexamethasone suppression test (DST) in TE versus NE subjects (-0.509; 95%CI: -0.871; -0.148). This meta-analysis was limited by the fact that lifetime psychiatric illness and childhood trauma were not an exclusion criterion in all 37 studies.
Neither adulthood trauma exposure nor PTSD were associated with differences in HPA-axis functioning, although adulthood trauma may augment cortisol suppression after the DST. More evidence on other dynamic tests of HPA-axis functioning in PTSD and adulthood trauma exposure is needed.
下丘脑-垂体-肾上腺(HPA)轴失调与创伤后应激障碍(PTSD)不一致相关。然而,创伤暴露而不是 PTSD 可能是 HPA 轴失调的原因。在两项荟萃分析中,我们评估了成年期创伤暴露与 HPA 轴功能在 PTSD 和非 PTSD 的健康受试者中的关联。
在 Pubmed 和 PsychInfo 中使用关键词和 MeSH 术语(如皮质醇、情绪创伤和 PTSD)进行文献检索。仅选择包括心理健康的创伤暴露(TE)个体以及未暴露(NE)健康个体和/或 PTSD 患者(PTSD)的研究。这导致了 1511 项研究,最终包括 37 项研究(21 项 TE 与 NE 和 34 项 TE 与 PTSD,N=2468)。根据特定的质量标准评估所有研究的方法学质量。比较皮质醇水平的合并效应大小(Hedges's g)。对于所有分析,均使用随机效应模型。
TE 与 NE 受试者之间(-0.029;95%CI:-0.145;0.088)和 TE 与 PTSD 患者之间(0.175;95%CI:-0.012;-0.362)的皮质醇水平均无显著差异。亚组分析显示,TE 与 NE 受试者之间的低剂量地塞米松抑制试验(DST)后皮质醇抑制增加(-0.509;95%CI:-0.871;-0.148)。这项荟萃分析受到以下事实的限制,即并非所有 37 项研究都将终生精神疾病和儿童期创伤作为排除标准。
成年期创伤暴露或 PTSD 均与 HPA 轴功能差异无关,尽管成年期创伤可能会增强 DST 后的皮质醇抑制。需要更多关于 PTSD 和成年期创伤暴露的 HPA 轴功能其他动态测试的证据。