Abstract #2983

Treatments in chronic liver disease induced hepatic encephalopathy: a longitudinal in vivo 1H MRS study of brain metabolism using rifaximin

Emmanuelle Flatt¹, Cristina Cudalbu², Olivier Braissant³, Stefanita Mitrea², Valérie McLin⁴, Dario Sessa⁴, and Rolf Gruetter⁵

¹Laboratory for Functional and Metabolic Imaging, Center for Biomedical Imaging, Ecole polytechnique Fédérale de Lausanne, Lausanne, Switzerland, ²Center for Biomedical Imaging(CIBM), Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland, ³Service of Biomedicine, University Hospital of Lausanne, Lausanne, Switzerland, ⁴Swiss Center for Liver Disease in Children, Department of Pediatrics, University Hospitals Geneva, Geneva, Switzerland, ⁵Laboratory for Functional and Metabolic Imaging (LIFMET) & Center for Biomedical Imaging (CIBM), Ecole polytechnique Fédérale de Lausanne, Lausanne, Switzerland

Hepatic encephalopathy (HE) is a severe complication of chronic liver disease (CLD). Treatments for HE have focused on reducing plasma ammonia levels implicated in HE pathogenesis. The antibiotic rifaximin reduces the production of gut ammonia which is considered to be the main toxin in CLD-induced HE. Rifaximin is commonly used in the treatment of HE and has been shown to reduce the frequency of HE episodes, but the molecular mechanisms behind this effect are unknown. We assessed, in vivo and longitudinally, the effect of rifaximin on brain metabolites in bile duct ligated rats using high-field proton Magnetic Resonance Spectroscopy.

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