Hepatic encephalopathy (HE) is a neuropsychiatric complex syndrome, ranging from subtle behavioral abnormalities to deep coma and death. Hepatic encephalopathy emerges as the major complication of acute or chronic liver failure. Multiplicity of factors are involved in its pathophysiology, such as central and neuromuscular neurotransmission disorder, alterations in sleep patterns and cognition, changes in energy metabolism leading to cell injury, an oxidative/nitrosative state and a neuroinflammatory condition. Moreover, in acute HE, a condition of imminent threat of death is present due to a deleterious astrocyte swelling. In chronic HE, changes in calcium signaling, mitochondrial membrane potential and long term potential expression, N-methyl-D-aspartate-cGMP and peripheral benzodiazepine receptors alterations, and changes in the mRNA and protein expression and redistribution in the cerebral blood flow can be observed. The main molecule indicated as responsible for all these changes in HE is ammonia. There is no doubt that ammonia, a neurotoxic molecule, triggers or at least facilitates most of these changes. Ammonia plasma levels are increased two- to three-fold in patients with mild to moderate cirrhotic HE and up to ten-fold in patients with acute liver failure. Hepatic and inter-organ trafficking of ammonia and its metabolite, glutamine (GLN), lead to hyperammonemic conditions. Removal of hepatic ammonia is a differentiated work that includes the hepatocyte, through the urea cycle, converting ammonia into GLN via glutamine synthetase. Under pathological conditions, such as liver damage or liver blood by-pass, the ammonia plasma level starts to rise and the risk of HE developing is high. Knowledge of the pathophysiology of HE is rapidly expanding and identification of focally localized triggers has led the development of new possibilities for HE to be considered. This editorial will focus on issues where, to the best of our knowledge, more research is needed in order to clarify, at least partially, controversial topics.
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http://dx.doi.org/10.4254/wjh.v4.i3.50 | DOI Listing |
Aim And Background: This study aimed to evaluate the efficacy of silymarin in improving liver function and reducing liver stiffness in chronic liver disease (CLD) patients. Silymarin, a hepatoprotective agent, has shown potential benefits in non-alcoholic fatty liver disease (NAFLD) and liver fibrosis, but evidence in CLD with varied etiologies remains limited. This study addresses the gap by assessing its impact across diverse etiological subgroups.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Hepato-Neuro Laboratory, Centre Hospitalier de l'Université de Montréal (CRCHUM), Université de Montréal, 900, Rue Saint-Denis - Pavillon R, R08.422, Montréal (Québec), H2X 0A9, Canada.
Sarcopenia and hepatic encephalopathy (HE) are complications of chronic liver disease (CLD), which negatively impact clinical outcomes. Hyperammonemia is considered to be the central component in the pathogenesis of HE, however ammonia's toxic effects have also been shown to impinge on extracerebral organs including the muscle. Our aim was to investigate the effect of attenuating hyperammonemia with ornithine phenylacetate (OP) on muscle mass loss and associated molecular mechanisms in rats with CLD.
View Article and Find Full Text PDFEClinicalMedicine
February 2025
Faculty of Medicine, University of Queensland, Australia.
Background: Small Intestinal Bacterial Overgrowth (SIBO) has been implicated in the pathophysiology of chronic liver disease (CLD). We conducted a systematic review and meta-analysis to assess and compare the prevalence of SIBO among CLD patients (with and without with complications of end stage liver disease) and healthy controls.
Methods: Electronic databases were searched from inception up to July-2024 for case-control studies reporting SIBO in CLD.
World J Gastroenterol
January 2025
Department of Infectious Diseases, The First Affiliated Hospital of Fujian Medical University, Fuzhou 350004, Fujian Province, China.
In this article, we provide commentary on the recent article by Zhao . We focus on the shifts in the gut microbiota of patients with hepatitis B virus (HBV)-associated cirrhosis/portal hypertension (PH) following transjugular intrahepatic portosystemic shunt (TIPS) and the implications for understanding the mechanisms, diagnosis, and treatment. By comparing the gut microbiota composition and dynamic changes before and after TIPS in patients with and without hepatic encephalopathy, the authors found an increase in non-probiotic bacteria in those who developed hepatic encephalopathy post-TIPS, with species present only in the hepatic encephalopathy group.
View Article and Find Full Text PDFCurr Pharm Des
January 2025
State Key Laboratory of Bio-fibers and Eco-textiles, Qingdao University, Qingdao 266071, Shandong, China.
Background: Patients with hepatic encephalopathy (HE) have many triggers and a high mortality rate. The protective effect of existing therapeutic drugs on the liver is weak. We found that Danggui Shaoyao Powder can improve the symptoms of HE and may have a better liver protection effect.
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