| Literature DB >> 30302043 |
Rafael Ochoa-Sanchez1, Christopher F Rose1.
Abstract
Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome that occurs during chronic liver disease (CLD). While ammonia and other precipitating factors in liver disease including inflammation, bile acids, oxidative stress, and lactate play a role in the pathogenesis of HE, the exact mechanism that leads to HE is not fully understood. Notably, accumulating evidence points toward a synergic effect rather than independent actions among precipitating factors that contributes to the development and severity of HE in CLD. Hence, this review is aimed to briefly discuss the single and synergic interplay of pathological factors in the progression and severity of HE.Entities:
Keywords: AQP4, Aquaporin 4; BAs, Bile Acids; BBB, Blood-Brain Barrier; BDL, Bile Duct Ligation; CLD, Chronic Liver Disease; CSF, Cerebrospinal Fluid; GABA, Gamma-Aminobutyric Acid; GAMSAs, GABAA Receptor Modulating Steroid Antagonists; GFAP, Glial Fibrillary Acid Protein; GLAST, Glial Glutamate-Aspartate Transporter; GPR81, G-Protein-Coupled Receptor 81; GS, Glutamine Synthetase; HE, Hepatic Encephalopathy; ICP, Intracranial Pressure; ILs, Interleukins; MRI, Magnetic Resonance Imaging; NF-?B, Nuclear Factor Kappa B; NMDA, N-Methyl-d-Aspartate Glutamate Receptor; NO, Nitric Oxide; PCA, Portacaval Anastomosis; ROS, Reactive Oxygen Species; TJ, Tight Junction; TNF-a, Tumor Necrosis Alpha; ammonia; astrocyte swelling; bile acids; brain edema; cGMP, Cyclic Guanosine Monophosphate; cirrhosis; hepatic encephalopathy; inflammation; lactate; mGluR, Metabotropic Glutamate Receptor; neurotransmission; oxidative stress
Year: 2018 PMID： 30302043 PMCID： PMC6175755 DOI： 10.1016/j.jceh.2018.08.001
Source DB: PubMed Journal: J Clin Exp Hepatol ISSN： 0973-6883