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地塞米松抑制试验在抑郁症诊断中的应用

Dexamethasone suppression test in diagnosis of depressive illness.

作者信息

Hayes P E, Ettigi P

出版信息

Clin Pharm. 1983 Nov-Dec;2(6):538-45.

PMID:6140096
Abstract

Neuroendocrine abnormalities present in depressive illness and use of the dexamethasone suppression test (DST) in diagnosing depression are reviewed. The coexistence of neuroendocrine disturbances and depressive illness may be explained by a central nervous system neurochemical abnormality. Norepinephrine appears to inhibit hypothalamic corticotropin-releasing factor, thus decreasing ACTH secretion by the pituitary and, in turn, cortisol secretion by the adrenal glands. Thus, a deficiency in brain norepinephrine may lead to both depressive symptoms and increased adrenal cortisol production. Episodes of cortisol secretion are longer and more frequent in depressed patients, and the circadian rhythm of cortisol release is altered. Dexamethasone does not suppress plasma cortisol levels in depressed patients as compared with normal subjects. Abnormal DST results were obtained in 40-70% of inpatients and 20-50% of outpatients diagnosed as having unipolar primary depression or major depressive illness. The incidence of abnormal DST results in most nondepressed psychiatric patients is comparable with that in normal subjects. DST results do not distinguish between unipolar and bipolar depression but may differentiate primary from secondary depression. Depressed patients with abnormal DSTs responded positively to drug treatment. DST nonsuppressors responded more favorably to norepinephrine-reuptake blockers, while DST suppressors preferentially improved with serotonin-reuptake blockers. Normalization of DST response has been associated with clinical improvement. Certain drugs, a number of psychiatric conditions, and several major physical illnesses may alter DST response. The DST is a commonly used and practical tool in evaluating depressive illness; however, its diagnostic value in depressed outpatients and elderly depressed patients is not clear.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

本文综述了抑郁性疾病中存在的神经内分泌异常以及地塞米松抑制试验(DST)在抑郁症诊断中的应用。神经内分泌紊乱与抑郁性疾病的共存可能由中枢神经系统神经化学异常来解释。去甲肾上腺素似乎抑制下丘脑促肾上腺皮质激素释放因子,从而减少垂体促肾上腺皮质激素(ACTH)的分泌,进而减少肾上腺皮质醇的分泌。因此,脑内去甲肾上腺素缺乏可能导致抑郁症状和肾上腺皮质醇分泌增加。抑郁症患者皮质醇分泌的发作时间更长、更频繁,且皮质醇释放的昼夜节律发生改变。与正常受试者相比,抑郁症患者的地塞米松不能抑制血浆皮质醇水平。在被诊断为单相原发性抑郁症或重度抑郁性疾病的住院患者中,40%-70%的患者DST结果异常;在门诊患者中,这一比例为20%-50%。大多数非抑郁性精神疾病患者DST结果异常的发生率与正常受试者相当。DST结果不能区分单相和双相抑郁症,但可区分原发性抑郁症和继发性抑郁症。DST结果异常的抑郁症患者对药物治疗反应良好。DST不抑制者对去甲肾上腺素再摄取阻滞剂反应更佳,而DST抑制者优先使用血清素再摄取阻滞剂后病情改善。DST反应正常化与临床改善相关。某些药物、多种精神疾病和几种主要躯体疾病可能会改变DST反应。DST是评估抑郁性疾病常用且实用的工具;然而,其在门诊抑郁症患者和老年抑郁症患者中的诊断价值尚不清楚。(摘要截选至250词)

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