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在患有和未患有创伤后应激障碍的退伍军人中,给予地塞米松后血浆皮质醇和淋巴细胞糖皮质激素受体的剂量反应变化。

Dose-response changes in plasma cortisol and lymphocyte glucocorticoid receptors following dexamethasone administration in combat veterans with and without posttraumatic stress disorder.

作者信息

Yehuda R, Boisoneau D, Lowy M T, Giller E L

机构信息

Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA.

出版信息

Arch Gen Psychiatry. 1995 Jul;52(7):583-93. doi: 10.1001/archpsyc.1995.03950190065010.

DOI:10.1001/archpsyc.1995.03950190065010
PMID:7598635
Abstract

BACKGROUND

Our previous studies have suggested that combat veterans with posttraumatic stress disorder (PTSD) have alterations in hypothalamic-pituitary-adrenal axis functioning that are different from the well-documented biological changes observed in major depressive disorder and following exposure to stress.

METHODS

In the present study, we examined cortisol and lymphocyte glucocorticoid receptor number before and after the administration of 0.50 and 0.25 mg of dexamethasone in 14 combat veterans with PTSD, 12 combat veterans without PTSD, and 14 nonpsychiatric healthy men. All subjects were medication free at the time of testing and none met diagnostic criteria for major depression or substance dependence.

RESULTS

Combat veterans with PTSD suppressed cortisol to a greater extent than did combat veterans without PTSD and normal controls in response to both doses of dexamethasone. Differences in cortisol suppression could not be attributed to substance dependence history or differences in dexamethasone bioavailability. Combat veterans with PTSD showed a larger number of baseline glucocorticoid receptors compared with normal men. Combat veterans without PTSD also had a larger number of baseline glucocorticoid receptors compared with normal men and in fact were comparable to combat veterans with PTSD on this measure. However, only veterans with PTSD showed a decrease in lymphocyte glucocorticoid receptor number following dexamethasone administration.

CONCLUSION

The data support the hypothesis of an enhanced negative feedback sensitivity of the hypothalamic-pituitary-adrenal axis in PTSD.

摘要

背景

我们之前的研究表明,患有创伤后应激障碍(PTSD)的退伍军人下丘脑-垂体-肾上腺轴功能存在改变,这与在重度抑郁症以及暴露于应激后所观察到的有充分记录的生物学变化不同。

方法

在本研究中,我们检测了14名患有PTSD的退伍军人、12名未患PTSD的退伍军人以及14名非精神科健康男性在给予0.50毫克和0.25毫克地塞米松前后的皮质醇和淋巴细胞糖皮质激素受体数量。所有受试者在测试时均未服用药物,且无人符合重度抑郁症或物质依赖的诊断标准。

结果

在对两种剂量的地塞米松作出反应时,患有PTSD的退伍军人比未患PTSD的退伍军人及正常对照组更能抑制皮质醇。皮质醇抑制的差异不能归因于物质依赖史或地塞米松生物利用度的差异。与正常男性相比,患有PTSD的退伍军人基线糖皮质激素受体数量更多。与正常男性相比,未患PTSD的退伍军人基线糖皮质激素受体数量也更多,事实上在这一指标上与患有PTSD的退伍军人相当。然而,只有患有PTSD的退伍军人在给予地塞米松后淋巴细胞糖皮质激素受体数量减少。

结论

数据支持PTSD患者下丘脑-垂体-肾上腺轴负反馈敏感性增强的假说。

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