How Are Alcohol and Cirrhosis Connected?

Alcoholic cirrhosis is caused by chronic heavy drinking. It is the end stage of alcoholic liver. The occurrence of alcoholic cirrhosis is related to the drinking style, sex, genetic factors, nutritional status and whether he was infected with hepatitis virus. A large amount of drinking at a time is more harmful than a small amount of drinking at a time, and daily drinking is more harmful than intermittent drinking. Women who drink alcohol are more likely to develop alcoholic liver disease than men.

Basic Information

English name
alcoholiccirrhosis
Visiting department
Internal medicine
Multiple groups
Drinking women
Common causes
Long-term heavy drinking

Clinical manifestations of alcoholic cirrhosis

Symptoms usually occur around the age of 50, with a male-to-female ratio of about 2: 1, and they usually die around the age of 60. It is often asymptomatic in the early stages, and weight loss, loss of appetite, abdominal pain, fatigue, burnout, dark urine, bleeding gums, and nosebleeds may occur later. Gray complexion, poor nutrition, telangiectasia, spider mole, liver palm, non-inflammatory swelling of the parotid gland, palm contracture, male breast development, testicular atrophy, and female distribution of pubic hair, and primary peritonitis caused by anaerobic bacteria , Hepatic encephalopathy and so on.

Alcoholic cirrhosis

Laboratory inspection
(1) Hemoglobin, platelet, and white blood cell counts are reduced.
(2) Severe abnormalities in the compensatory phase of liver function experiments , decreased serum protein, increased globulin, and A / G inversion during decompensated phase. Prothrombin time prolongs and prothrombin activity decreases. Transaminase and bilirubin increased. Total cholesterol and cholesterol lipids decrease, and blood ammonia can increase. Disorders of amino acid metabolism, imbalance of branch / aromatic ratio. Urea nitrogen and creatinine increased. Electrolyte disorders: low sodium, low potassium.
(3) Etiology test is negative for HBV-M or HCV-M or HDV-M.
(4) Fibrosis examination The serum type III procollagen amino terminal peptide (PNP) value increased, prolyl hydroxylase (PHO) increased, monoamine oxidase (MAO) increased, and serum lamin (LM) increased.
(5) Ascites examination Ascites is drawn for routine inspection, adenosine deaminase (ADA) measurement, bacterial culture and cytology examination. In order to increase the positive rate of culture, ascites culture should be performed by the bedside, using blood culture bottles for aerobic and anaerobic bacteria cultures.
2. Imaging examination
(1) X-ray examination of barium of esophagus and gastric fundus shows that esophageal gastric fundus veins show worm-like or earthworm-like varices.
(2) B-type and color Doppler ultrasound in the early stage of alcoholic cirrhosis, the regenerative nodules formed by the pseudolobules of the liver are small, and the surrounding fiber bundles are narrow and neat. The intrahepatic echo is densely enhanced and slightly thicker, which is not easy to distinguish from other chronic liver diseases. As the course of the disease progresses, hepatocytes are destroyed, liver cells regenerate, and fibrous tissues proliferate. Ultrasound section images can show numerous circular or circular hypoechoic nodules that are diffusely distributed throughout the liver. Nodules are more cirrhotic than hepatitis They are small and uniform, most of which are between 0.2cm and 0.5cm. The fibrous tissue is surrounded by a nodular strong echo around the nodules. The liver capsule is thickened and the echo is enhanced, but the jagged changes common in liver cirrhosis after hepatitis do not appear, and the liver volume is often reduced.
(3) CT examination showed abnormal proportions of each lobe of the liver, decreased density, nodular-like changes, widened hilum, enlarged spleen, and ascites.
3. Endoscopy
Can determine the presence of esophageal gastric varices, the positive rate is higher than barium meal, X-ray examination, can still understand the extent of varicose veins, and evaluate the risk of bleeding. Varicose veins of the esophagus and gastric fundus are the most reliable indicators for the diagnosis of portal hypertension. In cases of upper gastrointestinal bleeding, emergency gastroscopy can identify the bleeding site and cause, and perform hemostatic treatment.
4. Liver biopsy
A liver biopsy can confirm the diagnosis.
5. Laparoscopy
Can directly observe the abdominal organs and tissues such as liver and spleen, and can take biopsy under direct vision, which is valuable for those who have difficulty in diagnosis.
6. Portal vein pressure measurement
Hepatic vein wedge pressure and free pressure were measured via jugular vein intubation. The difference between the two was the hepatic vein pressure gradient (HVPG), which reflected portal pressure. Normally less than 5mmHg, more than 10mmHg is portal hypertension.

Alcoholic cirrhosis treatment

There is no specific treatment for this disease. The key lies in abstaining from alcohol and early diagnosis. Targeting at the cause and strengthening general treatment to alleviate the disease and extend its compensatory period. Patients with decompensated period are mainly symptomatic treatment to improve liver function and rescue complications. For patients with portal hypertension, various effective measures to prevent upper gastrointestinal bleeding should be taken, including choosing good indications and timing for surgical treatment.

Alcoholic cirrhosis prevention

1. Choose a healthy and civilized lifestyle.
2. Control the amount of alcohol consumed and try to drink low alcohol or non-alcoholic beverages as much as possible.
3. After drinking alcohol, supplement high-protein, high-fiber diet in time, especially vitamin B family, vitamin A, C, K, and folic acid.

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