The effect of alcohol on the liver hepatitis

In recent years, the number of liver lesions of alcoholic etiology has been steadily increasing in most industrialized countries, often exceeding viral lesions in frequency. Alcoholic liver lesions account for 30-40% of the overall structure of liver diseases.
In liver biopsy in a general therapeutic clinic, alcoholic hepatopathy ranks first. There is a strict correlation between mortality from liver cirrhosis (LC) and the level of alcohol consumption per capita. During autopsy, the frequency of detection of liver cirrhosis in patients with chronic alcoholism is 8%, while in "non-alcoholics" it is about 1%.
The body of women is more sensitive to the toxic effects of alcohol. The lower threshold of the daily dose, which, when consumed for more than 15 years, sharply increases the risk of developing alcoholic liver cirrhosis, is 20 g of pure ethyl alcohol for women and 60 g for men. Liver damage does not depend on the type of alcoholic beverages, but is determined only by the alcohol content in them. In addition to the dose of ethanol and the duration of its use, risk factors for alcoholic liver disease include the type of drunkenness (the constant type has a more pronounced damaging effect on the liver than the intermittent type), unbalanced nutrition, the age at which drunkenness began, and heredity.
With systematic use of alcohol in toxic doses, 5 stages of alcoholic liver damage develop sequentially or gradually: adaptive hepatomegaly (liver enlargement), alcoholic fatty steatosis, alcoholic hepatitis, alcoholic liver fibrosis, alcoholic cirrhosis. In 5-15% of cases, alcoholic liver disease ends with the development of hepatocellular cancer.

Adaptive alcoholic hepatomegaly

Adaptive hepatomegaly (liver enlargement) is caused by a disorder of protein metabolism in the liver. As a rule, liver enlargement is not accompanied by subjective sensations and changes in laboratory parameters. Morphological examination using light microscopy does not reveal pathological changes. Electron microscopy reveals mitochondrial hypertrophy and endoplasmic reticulum proliferation associated with activation of microsomal enzymes, which causes increased production of lipids and lipoproteins.

Fatty steatosis

Fatty steatosis is the most common morphological variant of alcoholic hepatopathy. It occurs in 60-75% of patients with chronic alcoholism. Alcohol abuse is the cause of fatty steatosis in 30-50%.
Patients with alcoholism cover up to 50% of their daily caloric intake with ethanol. Ethanol is utilized by consuming large amounts of nicotinamide adenine dinucleotide (NAD), which is also necessary for the final stage of fatty acid oxidation - the conversion of hydroxybutyric acid to acetoacetic acid, which leads to the accumulation of fatty acids in the liver. Alcohol promotes the activation of lipogenesis, the release of catecholamines, which cause the mobilization of fat from peripheral fat depots. In addition, the transport of lipids from the liver, the utilization of non-esterified fatty acids and triglycerides by muscle tissue are disrupted. The listed mechanisms naturally lead to the formation of fatty steatosis of the liver.
In 50% of drinkers, there are no complaints from the digestive organs. The rest of the drinkers experience a feeling of heaviness and discomfort in the right hypochondrium and epigastric region, bloating, fatigue, decreased performance, irritability. An objective examination most often reveals hepatomegaly (liver enlargement), sometimes significant. The consistency of the liver is dense-elastic or doughy, the edge is rounded, palpation causes moderate pain. Laboratory liver tests are unchanged in many patients.
A clinical diagnosis of alcoholic fatty steatosis is made when hepatomegaly (enlarged liver) is detected without significant compaction or deformation of the liver with normal or not sharply changed biochemical tests in a person who abuses alcohol.
A puncture biopsy of the liver is of decisive importance in the diagnosis of fatty steatosis. The diagnosis of fatty steatosis is justified only in cases where at least 50% of the liver cells contain fat droplets. Fat usually accumulates in the form of clearly visible vacuoles or droplets, which push the nucleus and organelles of the liver cell to the periphery.
With the complete exclusion of alcohol, fatsoi steatosis is completely reversible. Fat disappears from hepatocytes 2-4 weeks after stopping drinking alcohol.
Treatment of fatty steatosis consists of: prescribing a complete diet with sufficient protein, unsaturated fatty acids, vitamins, microelements, and some restriction of animal fats.

Alcoholic hepatitis

"Alcoholic hepatitis" is a term adopted in the International Classification of Liver Diseases (WHO, 1978) to denote acute degenerative and inflammatory liver lesions caused by alcohol and potentially capable of progression or regression.
Acute alcoholic hepatitis (AAH) (synonyms: alcoholic steatonecrosis, acute sclerosing hyaline necrosis, inflammatory steatosis of alcoholic liver, toxic hepatitis, etc.) is an acute degenerative and inflammatory liver lesion characterized morphologically by predominantly central lobular necrosis of hepatocytes, an inflammatory reaction with infiltration of the portal fields mainly by polynuclear leukocytes and the detection in the liver in some cases; alcoholic hyaline.
When examining large groups of alcoholics, acute alcoholic hepatitis is detected in 34% of drinkers. AAH develops in people who have been abusing alcohol for at least 5 years (usually 10 years or more), mainly in men aged 35-55 years. In the initial stage of the disease, the symptoms are scanty, dyspeptic phenomena are noted, an objective study reveals an enlarged liver, a biochemical study - mild hyperbilirubinemia, a moderate increase in aminotransferase activity.

The icteric form of OAG is the most common clinical variant of the disease. As a rule, there is pain in the liver area, varying in severity from abdominal discomfort to the picture of "acute abdomen", which sometimes gives reason to assume acute appendicitis, acute cholecystitis and serves as a reason for surgical intervention. In addition to abdominal pain, severe dyspeptic symptoms are often noted: nausea, vomiting, diarrhea, as well as an increase in body temperature, weight loss, in some cases ascites (an enlarged abdomen) develops. Laboratory indicators include leukocytosis with an increase in neutrophils, a band shift, an accelerated ESR, hyperbilirubinemia with a predominance of the direct fraction, hypertransaminasemia, a decrease in albumins and an increase in y-globulins in the blood serum. Skin itching, jaundice, discolored feces, dark urine are possible.

With complete abstinence from alcohol and treatment for about 6-8 weeks, clinical symptoms regress, but liver enlargement and minimal pain syndrome remain, as well as minor changes in blood tests.
The mortality rate from acute alcoholic hepatitis is 30-44%. In severe cases of acute alcoholic hepatitis, 60% of drinkers die during the first 2 weeks of the disease.
If a person continues to drink after treatment, then in about 65% of cases the disease develops into liver cirrhosis after 1 year, in the rest a little later (up to 3 years).

Alcoholic liver cirrhosis

Most liver cirrhosis is caused by alcohol. Liver cirrhosis develops in 30% of alcoholics approximately 10 years after the onset of alcohol abuse. The average age of people suffering from liver cirrhosis is 50 years.


The clinical picture is similar to alcoholic hepatitis, but the pain is more intense, an enlarged liver may be accompanied by an enlarged spleen. Drinkers are usually very exhausted. Against the background of decreased immunity and general health, other diseases join in.
If a person suffering from liver cirrhosis continues to drink alcohol, then 80% of them will die within 5 years. In 15% of cases, alcoholic cirrhosis transforms into cancer (the final stage of evolution).

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