Plotsky P M, Owens M J, Nemeroff C B
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, USA.
Psychiatr Clin North Am. 1998 Jun;21(2):293-307. doi: 10.1016/s0193-953x(05)70006-x.
Among the more consistent observations in patients with major depression is dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis presenting as elevation of basal cortisol, dexamethasone-mediated negative feedback resistance, increased cerebrospinal fluid levels of corticotropin-releasing factor (CRF), and a blunted adrenocorticotropic hormone (ACTH) response to challenge with exogenous CRF. These features appear to be state, rather than trait markers, and are normalized upon successful treatment. These pathophysiologic adaptations may arise from defects in central drive to the neuroendocrine hypothalamus, disruption of normal adrenocortical hormone receptor function or a modification of HPA axis function at any level. Functional assessment of the HPA axis is thought to provide a window into central nervous system operation that may be of diagnostic value in this and other affective disorders regardless of whether CRF and glucocorticoids are directly involved in the origin of major depression or merely exacerbate the consequences of other primary defects.
在重度抑郁症患者中较为一致的观察结果包括下丘脑 - 垂体 - 肾上腺（HPA）轴功能障碍，表现为基础皮质醇升高、地塞米松介导的负反馈抵抗、脑脊液中促肾上腺皮质激素释放因子（CRF）水平升高以及外源性CRF刺激后促肾上腺皮质激素（ACTH）反应迟钝。这些特征似乎是状态而非特质标志物，并且在成功治疗后会恢复正常。这些病理生理适应性变化可能源于神经内分泌下丘脑的中枢驱动缺陷、正常肾上腺皮质激素受体功能的破坏或HPA轴在任何水平的功能改变。HPA轴的功能评估被认为是了解中枢神经系统运作的一个窗口，这在这种及其他情感障碍中可能具有诊断价值，无论CRF和糖皮质激素是否直接参与重度抑郁症的发病机制，还是仅仅加剧其他原发性缺陷的后果。
