Monoamine metabolites, corticotropin releasing factor and somatostatin as CSF markers in depressed patients.
Monoamine metabolites, corticotropin releasing factor and somatostatin as CSF markers in depressed patients.
复制标题
单胺代谢物、促肾上腺皮质激素释放因子和生长抑素作为抑郁症患者的脑脊液标志物。
DOI：
10.1016/0165-0327(88)90051-1
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发表时间：
1988
影响因子：
6.6
通讯作者：
Nemeroff,CB
中科院分区：
文献类型：
--
作者：
Widerlöv,E;Bissette,G;Nemeroff,CB
上午 9 点腰椎穿刺采集 10 名健康志愿者和 22 名重度抑郁症患者脑脊液样本，分析单胺代谢物、促肾上腺皮质激素释放因子（CRF）和生长抑素（SRIF）的含量。还分析了 TRH 激发试验（200 gmg）后的 TSH 血浆浓度和地塞米松（1 mg；DST）后的血浆皮质醇浓度。未观察到 CRF 或 SRIF 浓度与基础或地塞米松后皮质醇浓度之间的关系。 21 名抑郁症患者中有 14 名是 DST 非抑制剂，血浆皮质醇浓度截止点≥138 nmol/1。如果使用更保守的截止点 (> 290 nmol/1)，21 名患者中有 7 名显示出与严重程度相关的皮质醇非抑制。在 TSH 对 TRH 的反应方面，健康志愿者和抑郁症患者之间没有观察到显着差异。抑郁症患者脑脊液中CRF含量升高，SRIF含量降低。在健康志愿者中，CSF 和 MHPG 的 CSF 浓度之间观察到呈负相关（r= -0.72；P= 0.019）；未观察到 CRF 和 5-HIAA 或 HVA 浓度之间存在关系。在抑郁症患者中，CRF 和 5-HIAA 的 CSF 浓度之间以及 CRF 和 HVA 之间存在正相关（r = 0.59；P = 0.004）（r = 0.44；P = 0.042）。这些数据与去甲肾上腺素和血清素可能参与CRF分泌的调节的观点一致。然而，这些调节机制可能在重度抑郁症患者中发生改变，其中正常的去甲肾上腺素能抑制音被假定为 CRF 释放的血清素能刺激所取代。
CSF samples from ten healthy volunteers and 22 patients with major depression were collected by lumbar puncture at 9 a.m. and the content of monoamine metabolites, corticotropin releasing factor (CRF) and somatostatin (SRIF) was analyzed. Plasma concentrations of TSH following a TRH challenge test (200 gmg) and plasma cortisol following dexamethasone (1 mg; DST) were also analyzed.No relationships were observed between the CRF or SRIF concentrations and either basal or post-dexamethasone cortisol concentrations. Fourteen of 21 depressed patients were DST nonsuppressors using a plasma cortisol concentration cut off point ≧ 138 nmol/1. If a more conservative cut off point was used (> 290 nmol/1) seven out of 21 patients revealed a severity-related cortisol nonsuppression. No significant difference was observed between healthy volunteers and depressed patients with regard to TSH response to TRH. The CSF content of CRF was elevated and the content of SRIF reduced in the depressed patients. In the healthy volunteers an inverse relationship was observed between CSF concentrations of CRF and MHPG (r= -0.72;P= 0.019); no relationship was observed between the concentrations of CRF and 5-HIAA or HVA. In the depressed patients positive correlations were found between CSF concentrations of CRF and 5-HIAA (r= 0.59;P= 0.004) and between CRF and HVA (r= 0.44;P= 0.042). These data are concordant with the view that norepinephrine and serotonin may be involved in the regulation of CRF secretion. However, these regulatory mechanisms may be altered in patients with major depression, where a normal noradrenergic inhibitory tone is postulated to be replaced by a serotoninergic stimulation of CRF release.