Cognitive Function of Alcoholic Compensated Liver Cirrhosis

Chuncheon Sacred Heart Hospital

Status: Completed

Conditions: Alcoholic Liver Disease

Treatments: Other: Cognitive function test

Study type: Observational

Funder types: Other

Identifiers

NCT04557774

COG

YR (Other Identifier)

Details and patient eligibility

About

Differences in cognitive function between patients with viral and alcoholic compensated liver cirrhosis

Full description

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.

Enrollment: 110 patients

Sex: All

Ages: 22 to 69 years old

Volunteers: Accepts Healthy Volunteers

Inclusion criteria

• Those who agreed to participate in this study and signed a written consent
• Those who have no evidence of neurological impairment

Exclusion criteria

• Those who have decompensated liver cirrhosis
• Those who have a high MELD score (≥20)
• Those who have OHE during admission
• Those who have parients' refusal

Trial design

110 participants in 1 patient group

Liver cirrhosis group

Description:

All included patients were asymptomatic at the baseline with no evidence of neurological impairment. Patients with a history of moderate alcohol drinking plus hepatitis B/C virus infection, medication for sedation, MELD (Model for End-stage Liver Disease) score of more than 20, OHE, seizure, head trauma, stroke, dementia, Parkinson's disease, or any kind of focal neurologic deficits were excluded. Any patients who were suspected of alcohol induced direct neurologic damages such as Wernicke's encephalopathy, alcohol induced spinal cord disease, or alcohol induced peripheral nerve disease were excluded. After evaluating the data including the laboratory findings, image findings, endoscopic findings, and medical records of all these patients, as well as liver biopsy findings for some patients, we sub-classified these 88 patients into two groups: alcoholic LC and viral LC. Finally, 80 patients (viral: 37; alcohol: 43) with compensated LC were prospectively considered in this study.

Treatment:

Other: Cognitive function test