Alcoholic liver damage is a group of acute and chronic liver diseases caused by systematic alcohol abuse. There are 4 types of alcoholic liver lesions: liver dystrophy, acute hepatitis, chronic hepatitis (fatty degeneration with hepatocyte necrosis and mesenchymal reaction) and cirrhosis.

The nature of the liver lesion does not always depend directly on the amount of alcohol consumed, but WHO does not recommend consuming more than 21 servings for men and 14 servings for women per week (one serving is 150 g of dry wine or 250 g of beer, or 30 g of 40% alcoholic beverage).

Fatty degeneration of the liver (fatty hepatosis).

Alcohol (ethanol) is metabolized mainly in hepatocytes by alcohol dehydrogenase to acetaldehyde, which in the Krebs cycle through acetyl-CoA is converted to CO2 and H2O with the formation of energy for the cell. If a person systematically takes a small amount of ethanol, then it is completely cleaved by alcohol dehydrogenase, but at the same time in the Krebs cycle, excess cholesterol, lactate, palm are synthesized from acetyl-CoA and other compounds that provide, on the one hand, high energy abilities of hepatocytes, and on the other, contributing to the early development of atherosclerosis. With systematic and excessive intake of alcohol, cholesterol and fatty acids are formed in high quantities. As a result of a decrease in the metabolism (metabolism) of fatty acids, triglycerides are formed, which are the source of the development of fatty hepatosis.

The enzyme alcohol dehydrogenase, which breaks down alcohol (ethanol) in different people, is produced in different quantities. In some, it is able to metabolize a significant amount of ethanol entering the body, while in others it is less. Its possibilities are still not unlimited, and therefore, when alcohol is abused, phosphorus compounds, O2 are consumed, toxic substances are formed and, along with fatty hepatosis , hepatocyte necrosis, a mesenchymal inflammatory reaction with the possible development of toxic hepatitis with a progressive course and with a possible outcome in liver cirrhosis .

With fatty degeneration of the liver, hepatomegaly, hypercholesterolemia, sometimes a slight change in GGTP and aminotransferases are detected. But the same changes can be with cirrhosis of the liver (CP).

Other causes of fatty liver hepatosis can be obesity, diabetes, parenteral nutrition.

Acute alcoholic hepatitis.

Jaundice, fever, symptoms of alcohol withdrawal (tremors, sweating, agitation), nausea, vomiting, pain in the upper abdomen are often observed. Most patients are inadequate, euphoric or, conversely, suppressed. Encephalopathy often develops , but its severity does not always depend on the severity of liver damage. Severe forms of encephalopathy can lead to hepatic coma.

Laboratory data: often hypercholesterolemia and beteliproproteinemia, increased activity of aminotransferases (up to 2-3 norms) and GGTP (more than 3-5 norms), increased serum uric acid level. Cholestatic syndrome, neutrophilic leukocytosis, anemia and an increase in ESR.

Often there is edematous ascites syndrome, which is an unfavorable prognosis.

Severe acute alcoholic hepatitis is characterized by encephalopathy, jaundice (bilirubin 100 μmol / L), edematous ascites and hemorrhagic syndromes. The risk of developing severe (fulminant) acute alcoholic hepatitis increases with paracetamol.

Chronic alcoholic active hepatitis (alcoholic CAH).

Clinical and biochemical manifestations are similar to other etiological forms of chronic active hepatitis (CAH). First of all, it is necessary to exclude other etilogical forms of chronic hepatitis. Without abstinence, as a rule, chronic alcoholic hepatitis progresses with an outcome in cirrhosis.

Alcoholic cirrhosis of the liver (ADC).

Teleangiectasias and Dupuytren’s contracture are the most common symptoms in ADC than in other etiological forms. Long-term use of alcohol can have a direct toxic effect on the gonads, leading them to atrophy and impotence; this process is accompanied by an increase in the level of estrogen in the blood, causing the formation of vascular “stars”, gynecomastia and palmar erythema. The alcohol etiology of liver cirrhosis is indicated by:

• Prolonged use of alcohol.
• The age of patients older than 40 years.
• Pseudo-cushingoid and pseudo-hyperthyroid status of the patient (puffy face, bulging eyes with injection of scleral vessels), a peculiar euphoric manner of behavior, enlargement of the parotid glands.
• Peripheral neuritis, myopathy, muscle atrophy, encephalopathy, cardiomyopathy, pancreatitis , gastritis, recurrent pneumonia.
• Neutrophilic leukocytosis, anemia, increased ESR, IgA, GGTP.
• Morphological changes: centrolobular accumulation of hyaline (Mallory’s body), neutrophilic reaction around hepatocytes, relative safety of portal tracts, pernicellular fibrosis.
• Refusal to take alcohol can lead to a remission of the pathological process or to its stabilization.

In the initial stage, there are few symptoms, but with palpation hepatomegaly is detected . In the expanded stage, dyspeptic disorders predominate due to concomitant alcoholic pancreatitis, gastritis, portal hypertension with ascites, and sometimes acute alcoholic hepatitis that has joined.

In the terminal stage of ADC, patients are depleted, severe hepatic cell failure with jaundice, hemorrhagic syndrome, refractory ascites develops, and peritonitis and other complications may join.

Treatment of patients with alcoholic liver damage.

• Abstinence is required for any form and stage of alcoholic liver damage.
• Detoxification measures are necessary in all forms: a) iv administration of 200-300ml of a 5-10% glucose solution with the addition of 10-20 ml of essentials (1 ampoule contains 1000 mg of essential phospholipids) or 4 ml of a 0.5% lipoic acid solution 4 ml of a 5% solution of pyridoxine, 4 ml of a 5% solution of thiamine (or 100-200 mg of cocarboxylase ), 5 ml of a 20% solution of piracetam , the course of treatment is 5 days; b) I / O hemodesis 200 ml 2-3 infusions per course; c) In the future, against the background of basic therapy, symptomatic treatment is carried out , including regarding complications of CP (portal hypertension, ascites, encephalopathy, etc.); d) often in patients with APT there is a deficiency of vitamins A, B, C, folic acid (it is advisable to administer the combined multivitamin drug parentrovit for 3 days). In the absence of this drug, vitamins are prescribed in injections ( vitamin B12 at 200 mcg / m) and inside – folic acid (200 mg 3 times a day).

Life forecast of patients with alcoholic liver damage!

In 15% of patients with alcoholism, after 10 years or more, Cirrhosis develops . It is difficult to predict the course of alcoholic Cirrhosis, but in the presence of jaundice, ascites, encephalopathy, weight loss, decreased serum albumin, the patient is threatened with life-threatening complications, especially bleeding from the dilated veins of the esophagus. Five – year survival with ADC as a whole is 50% for people who continue to drink – 30%, and for people who stop drinking alcohol -70%.