Amsterdam J D, Maislin G, Winokur A, Berwish N, Kling M, Gold P
Department of Psychiatry, School of Medicine, University of Pennsylvania, Philadelphia 19104.
J Affect Disord. 1988 May-Jun;14(3):213-22. doi: 10.1016/0165-0327(88)90037-7.
A substantial body of data suggests that excessive cortisol secretion in depression may result from a dysregulation at several sites within the hypothalamic-pituitary-adrenocortical (HPA) axis. These alterations in regulatory mechanisms are thought to be the result of a hypothalamic 'overdrive' of corticotropin-releasing hormone (CRH). Previous studies have demonstrated a diminished adrenocorticotropin (ACTH) secretory response, as well as a heightened adrenocortical responsiveness after ovine-CRH administration in depressed patients. In the present investigation, we examined pituitary and adrenocortical responsiveness after an ovine-CRH stimulation test before and during clinical recovery in seven depressed patients. Cumulative ACTH responses increased significantly during clinical recovery (P = 0.014). Paradoxically, maximum and peak cortisol responses increased after recovery, suggesting that heightened adrenocortical responsiveness to ACTH during depression may take longer to 'normalize' than abnormal pituitary responsiveness to ovine-CRH stimulation.
大量数据表明，抑郁症患者皮质醇分泌过多可能是由于下丘脑 - 垂体 - 肾上腺皮质（HPA）轴内多个部位的调节异常所致。这些调节机制的改变被认为是促肾上腺皮质激素释放激素（CRH）下丘脑“过度驱动”的结果。先前的研究表明，抑郁症患者静脉注射羊CRH后，促肾上腺皮质激素（ACTH）分泌反应减弱，而肾上腺皮质反应性增强。在本研究中，我们检测了7例抑郁症患者临床康复前及康复过程中静脉注射羊CRH刺激试验后垂体和肾上腺皮质的反应性。临床康复期间，累积ACTH反应显著增加（P = 0.014）。矛盾的是，康复后皮质醇的最大和峰值反应增加，这表明抑郁症期间肾上腺皮质对ACTH反应性增强可能比垂体对羊CRH刺激的异常反应性“恢复正常”所需的时间更长。
