地塞米松抑制试验(DST)反应对抑郁症患者临床病程的预测——DST的生理和临床结构效度

F Holsboer
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引用次数: 58

摘要

目前的调查强调了使用状态依赖性生物标志物作为抑郁症临床病程预测因子的基本原理。地塞米松治疗后皮质醇血浆水平提供了监测临床进展的工具。由于地塞米松抗性皮质醇在完全临床缓解之前逐渐恢复正常,因此该测量具有可能的预测潜力。此外,恢复到异常地塞米松反应是不符合预后的。虽然地塞米松试验有一定的优点,但在今后的研究中,应仔细考虑使试验结果无效的技术因素(如排除标准、地塞米松动力学)。皮质醇高分泌被认为是中枢去抑制的生理读出。在正常和异常DST应答者中应用促肾上腺皮质激素释放因子和促肾上腺皮质激素对这一假设进行了检验。数据支持假设在抑郁亚群中存在完整但过度活跃的垂体-肾上腺轴的概念的有效性。提出了一篇论文,将抑郁症的各种生物干扰置于两种极端观点之间。一种观点认为所有的生物紊乱都是一种特殊功能障碍的后遗症,例如皮质类固醇分泌的抑制解除。相反的观点认为,无数的生物干扰是秩序普遍丧失的标志,即熵的增加,其沉淀机制是未知的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Prediction of clinical course by dexamethasone suppression test (DST) response in depressed patients - physiological and clinical construct validity of the DST.

The present survey highlights the rationale for the use of state-dependent biological markers as predictors of clinical course in depression. Cortisol plasma levels after dexamethasone provide such a tool to monitor clinical progress. Since dexamethasone-resistant cortisol gradually returns to normalcy before a complete clinical remission is seen this measure has a possible predictive potential. Moreover, reversion to abnormal dexamethasone responses is prognostically infaust. Though the dexamethasone test has some merits, technical factors (e.g. exclusion criteria, dexamethasone-kinetics) which invalidate test results deserve careful consideration in future studies. Cortisol hypersecretion is considered as a physiological readout of a central disinhibition. This hypothesis is tested applying corticotropin-releasing factor and corticotropin in normal and abnormal DST responders. The data support the validity of the concept which assumes an intact but overactive pituitary-adrenal axis in a depressed subpopulation. A thesis is submitted which places the variety of biological disturbances in depression between two extreme viewpoints. One view considers all biological disturbances as sequelae to one particular dysfunction, e.g. disinhibition of corticosteroid secretion. The opposite view considers the myriad of biological disturbances as a sign of general loss of order, i.e. increased entropy, the precipitating mechanism of which is unknown.

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