Kellner Michael, Yehuda Rachel, Arlt Josef, Wiedemann Klaus
University Hospital Hamburg-Eppendorf, Department of Psychiatry and Psychotherapy, Hamburg, Germany.
Acta Psychiatr Scand. 2002 Feb;105(2):153-5; discussion 155-6. doi: 10.1034/j.1600-0447.2002.01012.x.
In chronic post-traumatic stress disorder (PTSD) lowered cortisol secretion and hypersuppression to dexamethasone has been described repeatedly. However, so far no longitudinal data on the natural course or on the effect of therapy are available.
We measured basal and post-dexamethasone morning salivary cortisol in a drug-free patient with chronic PTSD (DSM-IV) monthly for nearly 2 years and assessed PTSD and depressive symptoms.
Salivary cortisol decreased dramatically 3 months after the traumatic event and in the further course showed an inverse relation to fluctuating but gradually improving PTSD symptoms. Post-dexa-methasone cortisol was suppressed below the detection limit early after trauma and rose again more than 1 year post-trauma.
Both the potential renormalization of low cortisol levels in improving chronic PTSD and the putative vulnerability to develop PTSD in subjects with increased dexamethasone suppression need further research.
在慢性创伤后应激障碍（PTSD）中，皮质醇分泌降低以及对地塞米松的超抑制现象已被多次描述。然而，迄今为止，尚无关于自然病程或治疗效果的纵向数据。
我们对一名患有慢性PTSD（DSM-IV）的无药物治疗患者，连续近2年每月测量其基础及地塞米松给药后的晨间唾液皮质醇水平，并评估PTSD和抑郁症状。
创伤事件发生3个月后，唾液皮质醇显著下降，在后续病程中，其与波动但逐渐改善的PTSD症状呈负相关。创伤后早期，地塞米松给药后的皮质醇被抑制至检测限以下，创伤后1年多再次上升。
皮质醇水平降低在改善慢性PTSD中潜在的恢复正常情况，以及地塞米松抑制增强的受试者中发生PTSD的假定易感性，均需要进一步研究。
