Hepatic Encephalopathy: Insights Into the Impact of Metabolic Precipitates

IF 2.3 4区 医学 Q2 DEVELOPMENTAL BIOLOGY
Udit Kumar Dash, Aparna Tripathi, Debashree Mazumdar, Dusmanta Podh, Santosh Singh
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引用次数: 0

Abstract

Hepatic failure is a severe condition marked by the progressive or sudden loss of liver function, broadly categorized into acute liver failure (ALF), which develops within days to weeks, and chronic liver failure (CLF), which evolves over months or years. Both forms can lead to serious complications such as jaundice, impaired detoxification, portal hypertension, ascites, multi-organ dysfunction, and coagulation disorders. A significant neuropsychiatric consequence of liver failure is hepatic encephalopathy (HE), a spectrum of cognitive, motor, and behavioral abnormalities. Although elevated ammonia levels have long been implicated as a central factor in the pathogenesis of HE, emerging evidence suggests that other metabolic toxins also play critical roles. These include manganese (Mn), altered glucose metabolism, short-chain fatty acids (SCFAs), mercaptans, and gamma-aminobutyric acid (GABA). This review aims to explore the multifactorial metabolic landscape contributing to HE, highlighting the potential synergistic effects and mechanistic roles of these blood-borne precipitates. Understanding these diverse metabolic contributors may pave the way for more comprehensive diagnostic and therapeutic approaches beyond the traditional focus on ammonia.

肝性脑病:代谢沉淀的影响
肝功能衰竭是一种以进行性或突发性肝功能丧失为特征的严重疾病,大致分为急性肝功能衰竭(ALF)和慢性肝功能衰竭(CLF),前者在数天至数周内发生,后者在数月或数年内发生。两种形式均可导致严重的并发症,如黄疸、解毒功能受损、门脉高压、腹水、多器官功能障碍和凝血障碍。肝衰竭的一个重要神经精神后果是肝性脑病(HE),这是一系列认知、运动和行为异常。尽管氨水平升高一直被认为是HE发病的核心因素,但新出现的证据表明,其他代谢毒素也起着关键作用。这些包括锰(Mn)、改变的葡萄糖代谢、短链脂肪酸(SCFAs)、硫醇和γ -氨基丁酸(GABA)。本文旨在探讨促进HE的多因子代谢景观,强调这些血源性沉淀的潜在协同作用和机制作用。了解这些不同的代谢贡献者可能会为更全面的诊断和治疗方法铺平道路,而不是传统的关注氨。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Developmental Neurobiology
Developmental Neurobiology 生物-发育生物学
CiteScore
6.50
自引率
0.00%
发文量
45
审稿时长
4-8 weeks
期刊介绍: Developmental Neurobiology (previously the Journal of Neurobiology ) publishes original research articles on development, regeneration, repair and plasticity of the nervous system and on the ontogeny of behavior. High quality contributions in these areas are solicited, with an emphasis on experimental as opposed to purely descriptive work. The Journal also will consider manuscripts reporting novel approaches and techniques for the study of the development of the nervous system as well as occasional special issues on topics of significant current interest. We welcome suggestions on possible topics from our readers.
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