The roles of comorbidity and trauma exposure and its timing in shaping HPA axis patterns in depression.
The roles of comorbidity and trauma exposure and its timing in shaping HPA axis patterns in depression.
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DOI：
10.1016/j.psyneuen.2020.104776
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发表时间：
2020-10
影响因子：
3.7
通讯作者：
Abelson JL
中科院分区：
文献类型：
--
作者：
Mayer SE;Peckins M;Kuhlman KR;Rajaram N;Lopez-Duran NL;Young EA;Abelson JL
许多研究已经证明了重度抑郁症（MDD）患者的下丘脑-垂体-肾上腺（HPA）轴异常，但不一致的是，该系统在疾病中的作用尚不清楚。跨研究的比较因共病（创伤后应激障碍，焦虑症），创伤暴露和创伤时间（儿童与成人）的变化而复杂化。在这里，我们研究了这些因素对抑郁症HPA谱的影响。我们招募了5组受试者：MDD（n = 14），成人创伤后MDD + PTSD共病（MDD+ PTSD-成人; n = 12），儿童创伤后MDD + PTSD共病（MDD+ PTSD-儿童; n = 18），共病MDD +社交焦虑障碍（MDD+SAD; n = 12），以及与患者性别和年龄匹配的非抑郁对照参与者（合并总数n = 36）。HPA轴功能评估使用三个挑战：通过特里尔社会应激试验（TSST）的应激反应，通过地塞米松抑制试验（DST）的反馈灵敏度，和中央驱动通过甲吡酮挑战（MET）。我们比较了患者组和他们各自的非抑郁对照组之间的激素反应。MDD+ PTSD-儿童显示基线时皮质醇水平较低，基线时和整个TSST期间促肾上腺皮质激素（ACTH）水平降低。在HPA轴对TSST的反应方面，仅MDD、MDD+ PTSD-成人和MDD+SAD与非抑郁对照组无差异。对照儿童期创伤严重程度，MDD+ PTSD-儿童组基线水平降低不再显著，MDD+ PTSD-成人组基线皮质醇水平显著降低。DST和MET未检测到诊断组效应。儿童期虐待亚型与TSST和MET的独特HPA轴反应相关。合并症和创伤暴露，以及他们的时间和类型，有助于不一致的抑郁症文献，必须包括在努力澄清HPA轴在MDD中的作用。
Much work has documented hypothalamic pituitary adrenal (HPA) axis abnormalities in major depressive disorder (MDD), but inconsistencies leave this system’s role in the illness unclear. Comparisons across studies are complicated by variation in co-morbidity (Posttraumatic Stress Disorder-PTSD, anxiety disorders), exposure to trauma, and timing of trauma (child vs. adult). Here, we examined the impact of these factors on HPA profiles in depression. We recruited 5 groups of participants: MDD (n = 14), comorbid MDD + PTSD following adulthood trauma (MDD+PTSD-Adult; n = 12), comorbid MDD + PTSD following childhood trauma (MDD+PTSD-Child; n = 18), comorbid MDD + social anxiety disorder (MDD+SAD; n = 12), and non-depressed control participants who were sex and age matched to patients (combined total n = 36). HPA axis function was assessed using three challenges: stress reactivity via the Trier Social Stress Test (TSST), feedback sensitivity via a dexamethasone suppression test (DST), and central drive via a metyrapone challenge (MET). We compared hormonal responses between patient groups and their respective non-depressed controls. MDD+PTSD-Child showed low cortisol levels at baseline, and reduced adrenocorticotropic hormone (ACTH) levels at baseline and throughout the TSST. MDD-only, MDD+PTSD-Adult, and MDD+SAD did not differ from non-depressed controls in HPA axis responses to the TSST. Controlling for childhood trauma severity, the reduced baseline levels in MDD+PTSD-Child were no longer significant and significantly reduced baseline cortisol levels emerged for MDD+PTSD-Adult. No diagnostic group effects were detected with DST and MET. Childhood maltreatment subtypes were associated with unique HPA axis responses to TSST and MET. Comorbidity and trauma exposure, as well as their timing and type, contribute to inconsistencies in the depression literature and must be included in efforts to clarify the role of the HPA-axis in MDD.
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