Rifaximin in Chronic Liver Disease-induced Hepatic Encephalopathy: An In Vivo Longitudinal Study of Brain Metabolism on BDL Rats

Flatt, Emmanuelle; Cudalbu, Cristina; Braissant, Olivier; Mitrea, Stefan; Sessa, Dario; Gruetter, Rolf; Mclin, Valérie Anne

doi:10.1016/j.jceh.2017.01.072

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“…The characteristic 1 H-MRS pattern of type C HE, i.e., a gradual increase of Gln as a result of ammonia detoxification and a decrease in the main organic osmolytes as an osmoregulatory response (Rackayova et al, 2016;Flatt et al, 2017;Braissant et al, 2019;Rackayová et al, 2021;Mosso et al, 2022), was present in the rats investigated in the current study. 1 H-MRS in the hippocampus showed a significant increase of brain Gln (+178 ± 95%****), a decrease of Ins (−29 ± 14%**), trends of decrease for Tau, tCho, Glu, Asc, tCr (Cr + PCr), and GSH, and no difference for GABA, Lac, PE, tNAA (NAA + NAAG), and the macromolecules (Supplementary Figure S1).…”

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Diffusion of brain metabolites highlights altered brain microstructure in type C hepatic encephalopathy: a 9.4 T preliminary study

Mosso,

Briand,

Pierzchala

et al. 2024

Front. Neurosci.

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IntroductionType C hepatic encephalopathy (HE) is a decompensating event of chronic liver disease leading to severe motor and cognitive impairment. The progression of type C HE is associated with changes in brain metabolite concentrations measured by 1H magnetic resonance spectroscopy (MRS), most noticeably a strong increase in glutamine to detoxify brain ammonia. In addition, alterations of brain cellular architecture have been measured ex vivo by histology in a rat model of type C HE. The aim of this study was to assess the potential of diffusion-weighted MRS (dMRS) for probing these cellular shape alterations in vivo by monitoring the diffusion properties of the major brain metabolites.MethodsThe bile duct-ligated (BDL) rat model of type C HE was used. Five animals were scanned before surgery and 6- to 7-week post-BDL surgery, with each animal being used as its own control. 1H-MRS was performed in the hippocampus (SPECIAL, TE = 2.8 ms) and dMRS in a voxel encompassing the entire brain (DW-STEAM, TE = 15 ms, diffusion time = 120 ms, maximum b-value = 25 ms/μm2) on a 9.4 T scanner. The in vivo MRS acquisitions were further validated with histological measures (immunohistochemistry, Golgi-Cox, electron microscopy).ResultsThe characteristic 1H-MRS pattern of type C HE, i.e., a gradual increase of brain glutamine and a decrease of the main organic osmolytes, was observed in the hippocampus of BDL rats. Overall increased metabolite diffusivities (apparent diffusion coefficient and intra-stick diffusivity—Callaghan’s model, significant for glutamine, myo-inositol, and taurine) and decreased kurtosis coefficients were observed in BDL rats compared to control, highlighting the presence of osmotic stress and possibly of astrocytic and neuronal alterations. These results were consistent with the microstructure depicted by histology and represented by a decline in dendritic spines density in neurons, a shortening and decreased number of astrocytic processes, and extracellular edema.DiscussiondMRS enables non-invasive and longitudinal monitoring of the diffusion behavior of brain metabolites, reflecting in the present study the globally altered brain microstructure in BDL rats, as confirmed ex vivo by histology. These findings give new insights into metabolic and microstructural abnormalities associated with high brain glutamine and its consequences in type C HE.

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