Abstract

PEREZ-NERI, Iván et al. Role of manganese in the pathophysiology of hepatic encephalopathy: scoping review protocol. Arch. Neurocien. (Mex.) [online]. 2023, vol.28, n.1, pp.25-30.  Epub June 20, 2025. ISSN 2954-4122.  https://doi.org/10.31157/an.v28i1.354.

Introduction: Hepatic encephalopathy (HE) is a neuropsychiatric complication of liver disease and/ or portosystemic blood shunting, characterized by alterations in alertness, personality, cognition, and motor functions. Its severity can be classified into four grades from mild to coma. This disease may affect several brain regions, including the cingulate gyrus, insular cortex, and globus pallidus. The pathophysiology of HE is thought to be multifactorial, involving manganese accumulation in the brain, the damaging effect of ammonia on glial cells, etc. Previous studies describe the pathophysiology of HE or the effect of manganese on the central nervous system. However, there is no review addressing both topics from an integrative perspective through a systematic methodology. This scoping review aims to evaluate the role of manganese in HE. Methods: Published studies (all publication types) will be retrieved from Web of Science, Medline, Scopus, EBSCOhost, Ovid, and Google Scholar. Inclusion criteria: studies reporting manganese levels in any biological sample sample of patients with HE, any experimental model reporting the effect of manganese administration on neuroprotection in models of liver damage, or showing an effect on manganese levels in the liver and/or the brain. Exclusion criteria: studies reporting subjects exposed occupationally or environmentally to manganese, or written in languages different than Spanish or English that could not be appropriately translated, or whose full-text files could not be retrieved. Either clinical or preclinical studies will be analyzed separately but might be discussed together. Data summaries will be presented in graphs, figures, and tables. A narrative synthesis will be presented. This protocol complies with PRISMA-P.

Keywords : manganese; ammonia; oxidative stress; neurotransmitter; neuronal death.

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