Alcoholic Liver Disease Clinical Trial
Official title:
Cognitive Function of Alcoholic Liver Disease Patients
Differences in cognitive function between patients with viral and alcoholic compensated liver cirrhosis
Hepatic encephalopathy (HE) is one of the important complications of liver cirrhosis (LC). HE
exhibits alterations in cognitive, psychomotor-intellectual, emotional, behavioral, or
fine-motor functions. Approximately 22-74 % of patients with non-fulminant HE have MHE with a
frequency proportional to the patient age and the severity of the liver disease. Patients
with MHE exhibit disability in most functional behaviors such as social connection,
alertness, emotional behavior, sleep, work, and leisure.
Alcohol consumption itself has a toxic effect on the brain. It has been documented that there
is a neuronal loss in the cerebral cortex, hypothalamus, hippocampus, septal region, and
cerebellum of an alcoholic brain.
The major causes of LC are hepatitis B/C viral infection and chronic alcohol consumption. The
most widely accepted theory of HE pathogenesis is that toxic substances derived from the gut
affect cerebral function after liver dysfunction or portosystemic shunting. This proposed
pathogenetic mechanism could apply to viral compensated LC. However, it is difficult to
explain the development of MHE in patients with alcoholic LC in this manner.
Therefore, patients with alcoholic LC may have different cognitive dysfunction as compared to
patients with viral LC.
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