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犬尿氨酸通路代谢物与双相情感障碍症状严重程度和临床特征的关联:概述。

The association of kynurenine pathway metabolites with symptom severity and clinical features of bipolar disorder: An overview.

机构信息

Department of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy.

Department of Psychiatry, Wrocław Medical University, Wrocław, Poland.

出版信息

Eur Psychiatry. 2022 Nov 11;65(1):e82. doi: 10.1192/j.eurpsy.2022.2340.

DOI:10.1192/j.eurpsy.2022.2340
PMID:36366795
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9724221/
Abstract

BACKGROUND

The balance between neurotoxic and neuroprotective effects of kynurenine pathway (KP) components has been recently proposed as a key element in the pathophysiology of bipolar disorder (BD) and related mood episodes. This comprehensive overview explored the link of KP with symptom severity and other clinical features of BD.

METHODS

We searched Medline, Embase, and PsycInfo electronic databases for studies assessing the association of peripheral and/or central concentrations of KP metabolites with putative clinical features, including symptom severity and other clinical domains in BD.

RESULTS

We included the findings of 13 observational studies investigating the possible variations of KP metabolites according to symptom severity, psychotic features, suicidal behaviors, and sleep disturbances in BD. Studies testing the relationship between KP metabolites and depression severity generated mixed and inconsistent findings. No statistically significant correlations with manic symptoms were found. Moreover, heterogeneous variations of the KP across different clinical domains were shown. Few available studies found (a) higher levels of cerebrospinal fluid kynurenic acid and lower of plasma quinolinic acid in BD with psychotic features, (b) lower central and peripheral picolinic acid levels in BD with suicide attempts, and (c) no significant correlations between KP metabolites and BD-related sleep disturbances.

CONCLUSIONS

An imbalance of KP metabolism toward the neurotoxic branches is likely to occur in people with BD, though evidence on variations according to specific clinical features of BD is less clear. Additional research is needed to clarify the role of KP in the etiopathogenesis of BD and related clinical features.

摘要

背景

色氨酸代谢途径 (KP) 成分的神经毒性和神经保护作用之间的平衡,最近被认为是双相障碍 (BD) 及相关心境发作的病理生理学的一个关键因素。本综述探讨了 KP 与 BD 的症状严重程度和其他临床特征的关系。

方法

我们检索了 Medline、Embase 和 PsycInfo 电子数据库,以评估外周和/或中枢 KP 代谢物与 BD 中假设的临床特征(包括症状严重程度和其他临床领域)之间的关联。

结果

我们纳入了 13 项观察性研究的结果,这些研究检测了 KP 代谢物根据 BD 中的症状严重程度、精神病特征、自杀行为和睡眠障碍的可能变化。测试 KP 代谢物与抑郁严重程度之间关系的研究得出了不一致的结果。与躁狂症状无统计学显著相关性。此外,还显示了 KP 在不同临床领域的异质性变化。少数可用的研究发现:(a) 有精神病特征的 BD 患者脑脊液中犬尿氨酸酸水平较高,血浆中喹啉酸水平较低;(b) 有自杀企图的 BD 患者中枢和外周吡啶甲酸水平较低;(c) KP 代谢物与 BD 相关的睡眠障碍之间无显著相关性。

结论

BD 患者的 KP 代谢可能向神经毒性分支失衡,但关于根据 BD 的特定临床特征的变化的证据尚不明确。需要进一步的研究来阐明 KP 在 BD 发病机制及相关临床特征中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a40c/9724221/42630400e309/S0924933822023409_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a40c/9724221/42630400e309/S0924933822023409_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a40c/9724221/42630400e309/S0924933822023409_fig1.jpg

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