de Kloet Carien, Vermetten Eric, Lentjes Eef, Geuze Elbert, van Pelt Johannes, Manuel Remy, Heijnen Cobi, Westenberg Herman
Department of Military Psychiatry, Central Military Hospital, Utrecht, The Netherlands.
Psychoneuroendocrinology. 2008 Apr;33(3):313-20. doi: 10.1016/j.psyneuen.2007.11.016. Epub 2008 Jan 22.
Neuroendocrine studies have shown profound alterations in HPA-axis regulation in posttraumatic stress disorder (PTSD). Based on baseline assessments and the response to dexamethasone, a hypothalamic overdrive with enhanced glucocorticoid feedback inhibition has been suggested. The dexamethasone-corticotrophin releasing hormone (DEX-CRH) test has shown to be a more sensitive test to assess HPA-axis dysregulation in major depression and therefore may provide a useful test tool to probe HPA-axis regulation in PTSD.
To evaluate the effect of PTSD on HPA-axis regulation, we compared the response to a DEX-CRH test between male veterans with PTSD (n=26) and male veterans, who had been exposed to similar traumatic events during their deployment, without PTSD (n=23). Patients and controls were matched on age, year and region of deployment. Additionally, we compared the response of PTSD patients with (n=13) and without co-morbid major depressive disorder (MDD) (n=13).
No significant differences were observed in ACTH and cortisol response to the DEX-CRH test between patients and controls. PTSD patients with co-morbid MDD showed a significantly lower ACTH response compared to patients without co-morbid MDD. The response to the DEX-CRH test did not correlate with PTSD or depressive symptoms.
The DEX-CRH test did not reveal HPA-axis abnormalities in PTSD patients as compared to trauma controls. PTSD patients with a co-morbid MDD showed an attenuated ACTH response compared to PTSD patients without co-morbid MDD, suggesting the presence of subgroups with different HPA-axis regulation within the PTSD group. Altered sensitivity of the CRH receptors at the pituitary or differences in AVP secretion might explain these differences in response.
神经内分泌学研究表明，创伤后应激障碍（PTSD）患者的下丘脑-垂体-肾上腺（HPA）轴调节存在显著改变。基于基线评估和对地塞米松的反应，有人提出存在下丘脑功能亢进并伴有增强的糖皮质激素反馈抑制。地塞米松-促肾上腺皮质激素释放激素（DEX-CRH）试验已被证明是评估重度抑郁症患者HPA轴失调的更敏感试验，因此可能为探究PTSD患者的HPA轴调节提供一个有用的检测工具。
为评估PTSD对HPA轴调节的影响，我们比较了患有PTSD的男性退伍军人（n = 26）和在部署期间遭受过类似创伤事件但未患PTSD的男性退伍军人（n = 23）对DEX-CRH试验的反应。患者和对照组在年龄、部署年份和地区方面进行了匹配。此外，我们比较了患有（n = 13）和未患有共病重度抑郁症（MDD）（n = 13）的PTSD患者的反应。
患者和对照组在对DEX-CRH试验的促肾上腺皮质激素（ACTH）和皮质醇反应方面未观察到显著差异。与未患有共病MDD的患者相比，患有共病MDD的PTSD患者的ACTH反应显著更低。对DEX-CRH试验的反应与PTSD或抑郁症状无关。
与创伤对照组相比，DEX-CRH试验未揭示PTSD患者存在HPA轴异常。与未患有共病MDD的PTSD患者相比，患有共病MDD的PTSD患者的ACTH反应减弱，这表明PTSD组内存在HPA轴调节不同的亚组。垂体中促肾上腺皮质激素释放激素（CRH）受体敏感性的改变或精氨酸加压素（AVP）分泌的差异可能解释了这些反应差异。
