History of Hepatic Encephalopathy

2020 ◽  
Vol 24 (2) ◽  
pp. xiii-xvii
Author(s):  
Vinod K. Rustgi
2020 ◽  
Author(s):  
Sammy Saab ◽  
Matthew Zhao ◽  
Ishan Asokan ◽  
Jung Jun Yum ◽  
Edward Wolfgang Lee

2016 ◽  
Vol 38 (5) ◽  
pp. 1081-1089.e4 ◽  
Author(s):  
Christian A. Bannister ◽  
James G. Orr ◽  
Alan V. Reynolds ◽  
Mark Hudson ◽  
Peter Conway ◽  
...  

2017 ◽  
Vol 112 ◽  
pp. S567
Author(s):  
Alex N. Zimmet ◽  
George Stukenborg ◽  
Blake Niccum ◽  
Gold Adkins ◽  
Jennifer Wang ◽  
...  

2016 ◽  
Vol 6 ◽  
pp. S53-S54
Author(s):  
Deepa Shrestha ◽  
Radha K. Dhiman ◽  
Sandeep Grover ◽  
Sunil Taneja ◽  
Ajay Duseja ◽  
...  

2017 ◽  
Vol 7 ◽  
pp. S47 ◽  
Author(s):  
Deepa Shrestha ◽  
Sandeep Grover ◽  
Sahaj Rathi ◽  
Ajay Duseja ◽  
Yogesh Kumar Chawla ◽  
...  

2008 ◽  
Vol 20 (6) ◽  
pp. 807-811 ◽  
Author(s):  
Gregory K. Wilkerson ◽  
Monali M. Bera ◽  
Timothy N. Holt ◽  
Robert J. Callan ◽  
Karamjeet Pandher

Two juvenile, intact, female mixed-breed goats from a common sire were presented for periodic neurologic deficits, seizures, and a generalized loss of body condition that occurred over a 4–6-week period. On physical examination, both goats were thin, obtunded, blind, and ataxic. Laboratory diagnostics revealed increased serum bile acids (95 μmol/l; reference interval: 0–50 μmol/l) in one of the goats. Both goats exhibited progressive physical and mental deterioration, and were eventually euthanized. Upon necropsy, no significant macroscopic lesions were noted. Microscopic examination, however, demonstrated hepatocellular atrophy and anomalies in the hepatic microvasculature, including duplication of hepatic arteries, small-to-indistinct portal veins, and oval cell hyperplasia. In addition, spongiform change was microscopically identified throughout the parenchyma of the brain, most notably within the white matter and along the junction of gray and white matter. The diagnosis of congenital portal vein hypoperfusion (suggestive of a portosystemic shunt) with resultant hepatic encephalopathy was proposed in each case based on the characteristic microscopic lesions in conjunction with the signalment and history of the goats. The observation that the affected kids were sired by the same buck suggests a hereditary basis for the condition in these animals as well.


2021 ◽  
Vol 15 ◽  
Author(s):  
Óscar López-Franco ◽  
Jean-Pascal Morin ◽  
Albertina Cortés-Sol ◽  
Tania Molina-Jiménez ◽  
Diana I. Del Moral ◽  
...  

Hepatic encephalopathy (HE) is one of the most disabling metabolic diseases. It consists of a complication of liver disease through the action of neurotoxins, such as excessive production of ammonia from liver, resulting in impaired brain function. Its prevalence and incidence are not well known, although it has been established that up to 40% of cirrhotic patients may develop HE. Patients with HE episodes display a wide range of neurological disturbances, from subclinical alterations to coma. Recent evidence suggests that the resolution of hepatic encephalopathy does not fully restore cognitive functioning in cirrhotic patients. Therefore, the aim of this review was to evaluate the evidence supporting the presence of lingering cognitive deficits in patients with a history of HE compared to patients without HE history and how liver transplant affects such outcome in these patients. We performed two distinct meta-analysis of continuous outcomes. In both cases the results were pooled using random-effects models. Our results indicate that cirrhotic patients with a history of HE show clear cognitive deficits compared control cirrhotic patients (Std. Mean Difference (in SDs) = −0.72 [CI 95%: −0.94, −0.50]) and that these differences are not fully restored after liver transplant (Std. Mean Difference (in SDs) = −0.72 [CI 95%: −0.94, −0.50]).


2016 ◽  
Vol 5 (2) ◽  
pp. 193-198 ◽  
Author(s):  
Emi Yoshimura ◽  
Tatsuki Ichikawa ◽  
Hisamitsu Miyaaki ◽  
Naota Taura ◽  
Satoshi Miuma ◽  
...  

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