Glutamine as a pathogenic factor in hepatic encephalopathy

2001 ◽  
Vol 65 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Jan Albrecht ◽  
Monika Doli?ska
Keyword(s):  
Hepatic Encephalopathy ◽  
Pathogenic Factor

Elevation of autoantibodies to cerebral proteins in hepatic encephalopathy: Another pathogenic factor?

2021 ◽  
Author(s):  
Elina Manzhalii ◽  
Tetyana M Falalyeyeva ◽  
Valentyna O. Moyseyenko ◽  
Ralf Weiskirchen ◽  
Wolfgang Stremmel
Keyword(s):  
Hepatic Encephalopathy ◽  
Brain Dysfunction ◽  
Cell Swelling ◽  
Pathogenic Factor ◽  
Contributing Factors ◽  
Serum Autoantibody ◽  
Ammonia Accumulation ◽  
Immune Mediated ◽  
Experimental Rat Model ◽  
New Perspective

Background: The pathophysiology of hepatic encephalopathy is incompletely understood. It remains illusive how the contributing factors of neuronal ammonia accumulation, cell swelling and inflammation interact. Objective: Correlation of neuronal autoantibody levels to the degree of hepatic encephalopathy as first indication of immune mediated pathogenesis. Methods: We investigated serum autoantibody levels of representative brain proteins in patients with hepatic encephalopathy as well as in an experimental rat model with cirrhosis and hepatic encephalopathy after carbon tetrachloride exposure. They were examined in relation to presence of hepatic encephalopathy and the degree of neurological impaiment evaluated by quantitative scores. Results: In hepatic encephalopathy an increase of all of the examined antibodies was observed in serum. The grade of antibody elevation correlated to the degree of encephalopathy registered by quantitative evaluation of brain dysfunction. Conclusion: The degree of hepatic encephalopathy parallels neuronal autoantibody elevation. In case a causal relationship could finally be established, it adds to the understanding of hepatic encephalopathy and may open a new perspective for treatment of this handicaping condition by immunosuppressive strategies.

Hepatic Encephalopathy Can Impair Driving

2008 ◽  
Vol 38 (19) ◽  
pp. 28
Author(s):  
DAMIAN MCNAMARA
Keyword(s):  
Hepatic Encephalopathy

Risk Factors for Hepatic Encephalopathy after Transjugular Intrahepatic Portosystemic Shunt in Patients with Hepatocellular Carcinoma and Portal Hypertension

2015 ◽  
Vol 24 (3) ◽  
pp. 301-307 ◽  
Author(s):  
Jiannan Yao ◽  
Li Zuo ◽  
Guangyu An ◽  
Zhendong Yue ◽  
Hongwei Zhao ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatocellular Carcinoma ◽  
Portal Hypertension ◽  
Hepatic Encephalopathy ◽  
Pressure Gradient ◽  
Transjugular Intrahepatic Portosystemic Shunt ◽  
Meld Score ◽  
Portosystemic Shunt ◽  
Portal Flow ◽  
Intrahepatic Portosystemic Shunt

Aims: This study aimed at assessing the risk factors for hepatic encephalopathy (HE) after transjugular intrahepatic portosystemic shunt (TIPS) in patients with hepatocellular carcinoma (HCC) and portal hypertension. Method: Consecutive patients (n=279) with primary HCC who underwent TIPS between January 1997 and March 2012 at a single institution were retrospectively reviewed. Patients were followed up for 2 years. Pre-TIPS, peri-TIPS and post-TIPS clinical variables were reviewed using univariate and multivariate analyses to identify risk factors for HE after TIPS. Results: The overall incidence of HE was 41% (114/279). Multivariate analysis showed an increased odds for HE in patients with: >3 treatments with transcatheter arterial chemoembolization (TACE) and/or trans-arterial embolization (TAE) (odds ratio [OR], 4.078; 95% confidence interval [95%CI], 1.748-9.515); hepatopetal portal flow (OR, 2.362; 95%CI, 1.032-5.404); high portosystemic pressure gradient (OR, 1.198; 95%CI, 1.073-1.336) and high pre-TIPS MELD score (OR, 1.693; 95%CI, 1.390-2.062). Odds for HE were increased 1.693 fold for each 1-point increase in the MELD score, and 1.198 fold for each 1-mmHg decrease in the post-TIPS portosystemic pressure gradient. Conclusion: The identification of clinical variables associated with increased odds of HE may be useful for the selection of appropriate candidates for TIPS. Results suggest that an inappropriate decrease in the portosystemic pressure gradient might be associated with HE after TIPS. In addition, >3 treatments with TACE/TAE, hepatopetal portal flow, and high MELD score were also associated with increased odds of HE after TIPS. Key words:  –  –  – .

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