Yehuda R, Southwick S M, Krystal J H, Bremner D, Charney D S, Mason J W
Department of Psychiatry, Yale University School of Medicine, New Haven, Conn.
Am J Psychiatry. 1993 Jan;150(1):83-6. doi: 10.1176/ajp.150.1.83.
The authors investigated the possibility of enhanced negative feedback sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis in posttraumatic stress disorder (PTSD) by using a low dose of dexamethasone.
Baseline blood samples were obtained at 8:00 a.m., and 0.5 mg of dexamethasone was administered to 21 male patients with PTSD and 12 normal age-comparable men at 11:00 p.m. Cortisol and dexamethasone levels were measured 9 and 17 hours after dexamethasone administration.
After correction for differences in dexamethasone levels, the PTSD patients showed greater suppression of cortisol in response to dexamethasone than did the normal subjects. This was true even in patients meeting concurrent diagnostic criteria for major depression.
The data support earlier studies showing that HPA abnormalities in PTSD are different from those seen in depression and suggest that the low-dose dexamethasone suppression test may be a potentially useful tool for differentiating the two syndromes and further exploring differences in their pathophysiology.
作者通过使用低剂量地塞米松研究创伤后应激障碍（PTSD）患者下丘脑-垂体-肾上腺（HPA）轴负反馈敏感性增强的可能性。
上午8点采集基线血样，晚上11点给21名男性PTSD患者和12名年龄匹配的正常男性服用0.5毫克地塞米松。在地塞米松给药后9小时和17小时测量皮质醇和地塞米松水平。
校正地塞米松水平差异后，PTSD患者对地塞米松的反应中皮质醇抑制程度比正常受试者更大。即使在符合重度抑郁症并发诊断标准的患者中也是如此。
数据支持早期研究，即PTSD中的HPA异常与抑郁症中的不同，并表明低剂量地塞米松抑制试验可能是区分这两种综合征以及进一步探索其病理生理学差异的潜在有用工具。
