To death leads to toxic damage to the liver with alcohol. Why does alcoholic liver disease appear and how is it treated?

Long-term alcohol abuse inevitably leads to liver damage, which can manifest as:

fatty hepatosis (liver steatosis or fatty degeneration);

alcoholic hepatitis;

cirrhosis of the liver;

adenocarcinoma of the liver.

It is believed that drinking 80 g of alcohol per day for a year is sufficient for the development of chronic liver disease in men. In women, alcoholic liver disease occurs after drinking 20 g of alcohol daily for a year. Cirrhosis of the liver affects about 15% of chronic alcoholics, and its development requires an average of 10 years of alcohol abuse.

The rate of occurrence of alcoholic liver damage and the dynamics of their progression are significantly affected by the polymorphism of genes encoding the formation of enzymes that break down ethanol; obesity; the effect of hepatotoxic substances (for example, paracetamol); and infection with the hepatitis C virus.

Frequent alcoholic liver damage is explained by the fact that 90-95% of the ethanol entering the body is metabolized in the liver into acetaldehyde and acetate, and only 5-10% of ethanol is excreted unchanged from the body. The main enzymes that break down ethanol in the liver are: cytosolic HAD + -dependent alcohol dehydrogenase; microsomal HADPH-dependent ethanol-oxidizing system and catalase. In chronic alcoholics, the activity of the last two enzyme systems increases significantly, and if in healthy individuals 7-10 g of ethanol is broken down in the liver per hour, then in patients with alcoholism, the rate of alcohol degradation is higher.

Development mechanisms hepatic steatosis with alcohol abuse, the following: firstly, under the influence of ethanol, the release of hormones that stimulate lipolysis (adrenaline and ACTH) into the blood increases. As a result, the flow of free fatty acids into hepatocytes increases. Secondly, under the action of ethanol in hepatocytes, the synthesis of free fatty acids increases and the processes of their β-oxidation are suppressed; the formation of triglycerides increases and the processes of release of lipoproteins into the blood are disrupted. First, fats are deposited centrilobularly, then dystrophic changes in hepatocytes progress. Fatty degeneration of the liver is a reversible damage to hepatocytes, and their structure is completely restored if alcohol is given up. As a rule, liver steatosis is not accompanied by any clinical manifestations. It should also be noted that liver steatosis is observed in other forms of pathology: obesity, decompensated diabetes mellitus, severe protein starvation and prolonged use of glucocorticosteroids.

Alcoholic hepatitis characterized by central necrosis of hepatocytes, infiltration of the inflammatory focus by neutrophils and the development of fibrosis. The following pathogenetic mechanisms lead to the development of alcoholic hepatitis:

ethanol disrupts the processes of tissue respiration of hepatocytes, promotes an increase in the formation of ROS in mitochondria, causes a decrease in the content of intracellular reduced glutathione, and damages mitochondrial DNA. As a result, the integrity of the inner membrane of hepatocyte mitochondria is violated, they swell, and some of them are destroyed. The result of these events is a decrease in the formation of ATP and the development of "oxidative" stress in hepatocytes, which leads to the death of these cells as a result of necrosis;

with prolonged alcohol abuse, the permeability of the intestinal mucosa increases significantly. This contributes to an increase in the severity of bacterial translocation from the intestinal lumen to the vascular bed, and under the action of endotoxin in hepatocytes, the production of pro-inflammatory cytokines increases - TNF-α, IL-1, IL-6, IL-8. On the one hand, these cytokines contribute to the development of inflammation, on the other hand, they cause the death of hepatocytes as a result of necrosis or apoptosis. So, TNF- can activate the enzyme sphingomyelinase. At the same time, the content of ceramides increases in hepatocytes, which inhibit the transfer of electrons in the respiratory chain of mitochondria. ROS that accumulate at high concentrations cause oxidative damage to hepatocytes, and these cells die as a result of necrosis. TNF-α can also cause apoptosis of hepatocytes: after the interaction of this cytokine with the corresponding receptor, caspase 8 is activated on the membrane of hepatocytes. It cleaves the Bid protein, and as a result, cytochrome c-oxidase enters the cytoplasm from mitochondria, activating proapoptotic caspase 3.

Under physiological conditions, the interaction of TNF-α with its receptor on the hepatocyte membrane can lead to redox-dependent activation of the transcription factors NF-kB and AP-1. Their interaction with the corresponding DNA regions causes the expression of genes encoding the formation of Bcl family proteins that prevent cell apoptosis and antioxidant enzymes. This increases the resistance of hepatocytes to the action of damaging factors. However, in conditions of deficiency of the most important antioxidants, in particular, reduced glutathione, this mechanism does not work in chronic alcoholism.

In alcoholic hepatitis, laboratory signs of damage to hepatocytes are detected (see below).

Alcoholic cirrhosis of the liver is a natural result of the development of chronic hepatitis. Histologically, alcoholic cirrhosis of the liver is characterized by the presence of foci of hepatocyte necrosis in the pericentral zones, deposition of hyaline (Mallory bodies) in hepatocytes, and fibrosis of the liver parenchyma. The proliferation of connective tissue is due to an imbalance between the formation and degradation of the components of the extracellular matrix. Collagen fibers are formed mainly by stellate cells and fibroblasts under the action of cytokines: transforming growth factor-, platelet growth factor and fibroblast growth factor, which are produced by activated hepatocytes, leukocyte blood cells, endotheliocytes, etc. With the growth of connective tissue, portal venous blood flow is disturbed, which promotes the appearance of foci of regeneration of hepatocytes and portosystemic shunting of blood. Pro-inflammatory cytokines activate the induced isoform of NO-synthase in the endotheliocytes of the blood vessels of the liver. This leads to an NO-dependent decrease in their tone and an even greater disruption of hepatic blood flow. Alcoholic liver cirrhosis is manifested by signs of liver failure, hepatorenal syndrome and portal hypertension.

Against the background of cirrhosis, adenocarcinoma of the liver may develop due to the accumulation of damage to the genetic apparatus of hepatocytes and disturbances in their cell cycle.

Pathophysiological Rationale for the Use of Clinical Laboratory Tests to Evaluate Liver Damage

Hepatocytes contain a large number of enzymes, the increase in the activity of which or the appearance in the blood serum is associated with damage to liver cells. Therefore, these enzymes are called indicator. Some of these enzymes are located in the cytoplasm of hepatocytes (AlAT, AsAT aminotransferases, LDH lactate dehydrogenase), the other part is in mitochondria (MDH malate dehydrogenase and GlDH glutamate dehydrogenase), endoplasmic reticulum (hydroxylases, acylases, glucuronyltransferases), ribosomes (cholinesterase), lysosomes (hydrolases) . Some enzymes are associated with hepatocyte membranes. So, -glutamyl transpeptidase (-GTP), 5'-nucleotidase (5'-NT), alkaline phosphatase (AP) and leucine aminopeptidase (LAP) are associated with the canalicular membrane of hepatocytes, that is, that part of it that faces the bile capillary.

Let us consider the most important reasons for the appearance in the blood serum or an increase in the activity of the main indicator enzymes.

Increased activity of aminotransferases . Under physiological conditions, AST and ALT are widely represented in the cells of various organs and tissues. AST is present in the cells of the liver, myocardium, skeletal muscles, kidneys, brain, pancreas, lungs, as well as in erythrocytes and leukocytes. The highest amounts of ALT are found in hepatocytes. The release of AST and ALT into the blood is observed when the cell membranes of hepatocytes are damaged. In this case, damage to liver cells can be both reversible and irreversible. The degree of hyperfermentemia allows only indirectly to make an assumption about the severity of damage to hepatocytes. Most often, an increase in the activity of AST, and especially ALAT, occurs in the following forms of liver pathology: acute and chronic hepatitis of an infectious and non-infectious nature, alcoholic liver damage, fatty liver of various etiologies, as well as liver damage with hemochromatosis, Wilson-Konovalov disease and deficiency  1 -antitrypsin. However, it should be remembered that, since ALT and AST are not strictly specific for hepatocytes, there may be other reasons for the increase in the activity of these aminotransferases that do not depend on liver damage: hereditary metabolic defects in muscles, acquired muscle diseases, excessive exercise and sprue (celiac disease). Some drugs (synthetic penicillins, ciprofloxacin, nitrofurans, isoniazid, some antifungal, anticonvulsant and non-steroidal anti-inflammatory drugs, as well as HMG-CoA reductase inhibitors, steroid anabolics, chloroform and others) with prolonged use can lead to an increase in the activity of ALT and AST.

There are some features of changes in the activity of aminotransferases in various liver diseases. For example, in alcoholic liver damage, the ratio between the activity of AST and ALT, as a rule, is 2 or more. This is explained by the fact that with alcohol abuse (acute or chronic) due to the developing deficiency of pyrodoxal-5-phosphate, ALT activity decreases. If the ratio of AST/ALAT activity is less than 1, one should think about viral hepatitis or extrahepatic obstruction of the biliary tract, which is due to a sharp increase in the release of ALAT from hepatocytes into the blood.

Increased activity of LDH. Since this enzyme is contained in the cytoplasm not only of hepatocytes, but also of myocardial, skeletal muscle, lung, and blood cells, an increase in the activity of the LDH 5 isoenzyme indicates hepatocellular diseases.

Increased activity of MDH and GlDH indicates damage to the mitochondria of hepatocytes. Detection of increased GDH activity in the blood serum may be one of the early signs of alcoholic liver damage. This is due to the fact that ethanol, being metabolized in liver mitochondria, contributes to their swelling, disruption of the integrity of the inner mitochondrial membrane, inhibition of tissue respiration, increased generation of ROS and ROS, and, ultimately, destruction of mitochondria.

Increased alkaline phosphatase activity may be physiological or pathological. Under physiological conditions, an increase in the activity of alkaline phosphatase in the blood serum is found in women during the third trimester of pregnancy due to the penetration of placental alkaline phosphatase into the bloodstream. Sometimes an increase in the activity of alkaline phosphatase occurs in people with I or III blood groups after excessive consumption of fatty foods, which is associated with the entry of intestinal alkaline phosphatase into the blood. The activity of alkaline phosphatase due to intensive growth increases in adolescents, as well as in women aged 40-65 years, which is explained by the release of this enzyme from bone tissue against the background of incipient osteoporosis.

A pathological increase in the activity of alkaline phosphatase in the blood serum can be due to both various pathologies of bone tissue and liver diseases. In the latter case, as a rule, there is an increase in the activity of other indicator enzymes. An increase in ALP activity is caused by diseases of the liver and biliary tract, accompanied by cholestasis (obstruction of the biliary tract, primary biliary cirrhosis of the liver, sclerosing chalangitis, cholestasis caused by taking certain drugs), as well as infiltrative liver diseases (sarcoidosis, granulomatous diseases, metastases of malignant tumors in liver). The increase in ALP activity in these cases is due to a violation of its connection with the canalicular membrane of hepatocytes and the entry of ALP into the bloodstream.

Increasing activity  -GTP. An increase in the activity of this enzyme indicates the presence of hepatobiliary diseases, but this test is not specific enough. An increase in -glutamyl-transpeptidase activity indicates cholestasis, as well as possible alcoholic liver damage (acute or chronic). An increase in the activity of -GTP in intrahepatic cholestasis is explained by an increase in the number of lipoproteins - carriers of this enzyme. The activity of -GTP can also increase with pancreatic damage, myocardial infarction, renal failure, chronic obstructive pulmonary disease, diabetes mellitus, and when taking certain medications. Barbiturates, anticoagulants, steroid anabolics, estrogen-containing drugs, and others have the ability to induce the activity of -GTP.

The following table can be used to assess the nature of liver damage.

Alcoholic liver disease is one of the urgent problems of hepatology due to its widespread prevalence in all countries of the world. Alcohol use is a cause of alcoholic liver disease and occurs in people who drink heavily or are dependent on alcohol.

There are two terms "alcoholism" and "alcoholic liver disease". The first is used to refer to a person's condition characterized by mental and physiological dependence on alcohol. These patients are patients of psychiatrists-narcologists. In people with alcoholic liver disease, a pronounced dependence on alcohol is rarely observed, and a severe hangover syndrome rarely occurs, which allows such people to drink alcohol for a long time. Alcoholic liver disease affects more often representatives of certain social groups, in which alcohol intake is an attribute of professional activity or emotional stress relief.

With alcohol abuse, almost all organs of the body suffer, but the liver is more affected, due to the fact that it plays a central role in the metabolism (metabolism) of alcohol, which turns into acetaldehyde, which has a direct toxic damaging effect on liver cells (hepatocytes).

Genetic, hereditary factors are involved in the risk of developing alcoholic liver disease. So, from parents suffering from chronic alcoholism, children can inherit a low level of enzymes that utilize ethanol, and then the problem of alcoholism becomes relevant for them already at the age of 15-20. One of the luminaries of Russian medicine, A.A. Ostroumov, demonstrating a young man with liver pathology, claimed that “the father “drank away” his son’s liver.”

Liver damage from alcohol depends on the amount of alcohol consumed and duration. Most researchers agree that a dangerous daily dose of alcohol is more than 40 - 80 ml of pure ethanol per day for at least 5 years. A dose of more than 80 g per day for 10-12 years is considered extremely dangerous, alcoholic liver disease easily occurs at such values. This amount of ethanol is contained in 100-200 ml of vodka 40%, in 400-800 ml of dry wine 10%, 800-1600 ml of beer 5%. These data are given in relation to men, the dose of women is 20% ethanol per day.

Alcoholic liver disease is formed only in 20% of those who constantly abuse alcohol, which is influenced by other risk factors - nutrition, gender. It is known that in women with the use of smaller doses of alcohol and for a shorter period of time, even after giving up alcohol, the disease can progress. Alcohol disrupts the processes of digestion, the appearance of dyspeptic phenomena indicates the involvement of the pancreas, intestines in the process, a lack of protein, vitamins, and minerals develops. Nutritional deficiencies contribute to the progression of alcoholic liver disease, and even good nutrition does not prevent alcoholic liver disease. General malnutrition, lack of nutrients, contribute to the development of liver damage in people who use alcohol, aggravate the course of the disease and have an adverse effect on other organs and body systems.

Stages of the disease

Alcoholic liver disease goes through four stages:

fatty degeneration (steatosis) of the liver,
alcoholic hepatitis (steatohepatitis),
cirrhosis of the liver,
hepatic carcinoma (hepatoma).

The metabolism of alcohol, the mechanisms of the damaging effect of toxic products of its metabolism on liver cells, especially the most important structural component of cell membranes - phospholipids, the replacement of liver cells with connective (non-functioning) tissue - progressive fibrosis of liver cells - are a complex long-term biochemical process. Each stage of this process determines the stage of liver damage and is a dynamic criterion for diagnostic observation of the patient.

Stage of fatty degeneration of the liver (steatosis)

This stage may be asymptomatic. But clinical observations show that patients often complain of intestinal discomfort for several years: bloating, periodic diarrhea, loss of appetite, mood, nausea, which is already an early sign of alcoholic damage to the pancreas. With an objective examination, it is possible to note an increase in the liver, an increase in liver parameters.

Alcoholic hepatitis (steatohepatitis)

The most common in clinical practice is the icteric form (jaundice of the sclera and skin), jaundice is not accompanied by itching of the skin. In addition, patients experience pain and heaviness in the right hypochondrium, nausea, vomiting, weakness, loss of appetite, diarrhea, and rarely fever. But in 5-10% of cases, jaundice can be prolonged and accompanied by skin itching, discolored feces, less often temperature reaction and pain in the right hypochondrium - a cholestatic form of alcoholic liver disease. In laboratory studies, liver tests, tests of stagnation of bile in the liver (cholestasis) are sharply violated.

Fulminant alcoholic hepatitis has a rapidly progressive course with jaundice, mental disorders (encephalopathy), liver failure and often ends in death in a hepatic coma. Also, however, as cirrhosis and hepatic carcinoma. So it does not make sense to consider these stages within the framework of this article.

Diagnosis of alcoholic liver disease

Diagnosis of alcoholism is based on a clinical examination, special tests to identify post-intoxication alcohol syndrome and a list of physical signs of chronic alcohol intoxication.

Diagnosis of alcoholic liver disease and its stage is based on a thorough history taking, clinical, laboratory and instrumental examinations.

To recognize alcoholic liver damage, it is very important to know how long and in what quantities alcohol was taken by the patient. Often patients hide their alcohol abuse, so it is very important to talk to family and friends and get tested.

To identify hidden alcohol addiction, special tests are used, the most common is the CAGE questionnaire. The answer "yes" to two or more questions is considered a positive test and indicates a hidden alcohol dependence in a particular patient.

There is a test developed by the World Health Organization, "Identification of Alcohol Use Disorders", with a positive answer to test questions of 8 or more, the test is considered positive.

Identifying Alcohol Use Disorders

Clinical manifestations of alcoholic liver damage are very poor: weakness, heaviness in the right hypochondrium, intestinal discomfort - bloating, loosening of the stool after eating fatty and plentiful food, nausea. Most patients do not present active complaints, and during examination or ultrasound, it is sometimes possible to accidentally detect an increase in the liver, icterus of the sclera and skin is less common and manifests itself in more severe cases.

Laboratory studies, among which, first of all, attention is drawn to the indicators of biochemical blood tests:

ALT and AST and AST/ALT ratio (1.5:2),
gamma-glutamyl transpeptidase, which exceeds transaminases and has a diagnostic value of its decrease in alcohol withdrawal,
a relatively new marker of alcohol intoxication is transferrin, the concentration of which increases with the use of more than 60 g or more of ethanol daily,
increase in bilirubin and its fractions,
decreased albumin (a protein synthesized by the liver),
in a clinical blood test - a decrease in hemoglobin, leukocytes, platelets.

Instrumental research methods:

Ultrasound examination of the liver, gallbladder, pancreas and spleen,
endoscopic examination - esophagogastroduodenoscopy,
Elastometry, which allows to clarify the severity of liver fibrosis - a marker of disease progression.

With alcoholic liver disease, patients may feel quite satisfactory, even with deviations in laboratory tests and indicators of instrumental research methods. Often they turn to doctors already with severe complications - bleeding from varicose veins of the esophagus and stomach, hepatic encephalopathy, severe jaundice, fluid retention in the abdominal cavity, etc., requiring hospital treatment.

Alcohol has a systemic effect on various organs and systems of the body, which patients often do not notice - this is an effect on the cardiovascular system, central nervous system, musculoskeletal and other systems, but liver damage is increasing.

Treatment of the disease

Should Alcoholic Liver Damage Be Treated? Yes.

Creating conditions for recovery

The first and indispensable condition for the successful treatment of alcoholic liver damage is a complete refusal to take alcohol, without which the progression of the disease is inevitable.

Fulfillment of this requirement at the stage of steatosis and hepatitis makes it possible to reverse the development of alcoholic liver damage.

Nutrition is an important and necessary component of the treatment of alcoholic liver damage. The energy value of adequate nutrition should be at least 2000 calories per day with a protein content of 1 g per 1 kg of body weight with a sufficient amount of vitamins, minerals, mainly foods and vitamin-mineral complexes. It is possible to recommend the food of the table 5.

Medical treatment

Alcoholic liver disease is effectively treated with drug therapy, drugs with different mechanisms of action are used and are combined into a group of hepatoprotectors.

Essential phospholipids

Essentiale forte, Essentiale-N, Floravit - drugs restore the cellular structure of liver cells, various enzyme systems, normalize the metabolism of proteins and fats in the liver, have a detoxifying effect and prevent the formation of fibrous tissue in the liver, stopping the progression of the process. These drugs are prescribed in capsules, 1-2 capsules 3 times a day with meals for 3 months. In - subsequent repeated courses.

Silymarin

Dry extract from the fruits of milk thistle - for example, Karsil, Legalon, Silimar, Gepabene contain flavonoids that have a hepatoprotective and bile-forming effect, stimulating enzyme structures that restore liver cell membranes. The course is 4 weeks, 70-140 mg 2 times a day before meals or during meals. According to indications repeated courses.

Ademetionine

Heptral is a natural substance that is formed from the amino acid methionine and has a hepatoprotective, detoxifying effect. It can be administered intravenously by drip or intramuscular injection of 400 mg with a solvent and in saline in a course of 10-20 days. Heptral can be taken orally in tablets. The form of administration of the drug and the duration is determined by the doctor.

Ursodeoxycholic acid

Ursofalk, Ursosan, etc. - normalizes the activity of aminotransferases (ALT, AST), reduces the formation of fibrosis in the liver. Preparations in capsules, calculated on body weight or individually by a doctor, are prescribed for a long time up to several years.

Herbal combined hepatoprotective preparations Lif-52, Hepatofalk, etc.

Lipoic acid (Thiagamma, Thiotacid, etc.) has a hepatoprotective and detoxifying effect, normalizes various types of metabolism in the liver (energy, carbohydrate, fat, protein, cholesterol). A course of 1 month is prescribed, taking 600 mg orally 1 time per day before breakfast.

Corticosteroids

They are prescribed in severe cases of acute alcoholic hepatitis in a hospital setting.

Alcoholic liver disease. Forecast

It all depends on the rate of progression of fibrosis in the liver cells and, consequently, the formation of cirrhosis of the liver.

The impact on the prognosis is exerted by the cessation of alcohol consumption after the diagnosis of the disease is established.

The most unfavorable are acute alcoholic hepatitis and cholestatic hepatitis (with jaundice).

Aggravate the prognosis may be joined by viral infections of hepatitis B and C.

Every day, our liver is tested in connection with the use of low-quality food, fatty and fried foods, fast foods, convenience foods. Because of this, the liver ceases to perform its functions of cleansing the blood and the whole body to the fullest. Alcohol is particularly harmful to this organ. Even the ancient Greeks noted the connection between frequent alcohol consumption and liver diseases. We can safely distinguish three main liver diseases that occur against the background of alcohol abuse: hepatosis, cirrhosis.

Symptoms of alcohol abuse

All symptoms of alcoholic lesions of the gland depend on the duration and amount of alcohol abuse. Signs begin to manifest themselves, as a rule, after several years of a systematic wrong lifestyle. The first symptoms of the disease are:

If alcoholic liver damage is actively progressing, there may be such symptoms that are characteristic of hepatitis and cirrhosis:

Often, all symptoms are accompanied by internal bleeding, which is characterized by a dark color of feces mixed with blood. As a result of alcoholic liver damage, the patient may complain of frequent vomiting and bleeding from the nose. There are disturbances in the work of the central nervous system: a decrease in attention, loss of coordination and awareness of oneself in society. As soon as the symptoms begin to manifest themselves, you should immediately seek help from a hepatologist doctor.

Alcohol metabolism

A healthy body is able to remove 4 mg of alcohol per kilogram of human weight in about an hour. If alcoholic beverages have been consumed in large quantities for several years, the excretion process slows down. Very actively alcohol is absorbed in the gastrointestinal tract. It is this system of the body that begins to suffer first after alcohol damage. If the consumption of alcohol is accompanied by a meal, the absorption decreases and the alcohol begins to be excreted from the body more quickly. Food slows down all these absorption processes. Also, after eating, the concentration of alcohol in the blood does not reach the marginal values, which cannot be said about an empty stomach.

Alcohol in a matter of minutes enters the circulatory system. Especially in the bloodstream of the brain and liver. Very bad alcohol is able to dissolve in fats. The bulk of alcohol undergoes the process of oxidation in the liver. Some of the ethanol is oxidized in the stomach and intestines before passing through the liver.

In the liver, ethanol is oxidized and decomposed to acetaldehyde. The metabolism of alcohol in an organ such as the liver has three stages. First, oxidation to acetaldehyde occurs. Then the resulting substance undergoes the process of oxidation to acetic acid. This acid then enters the bloodstream where it is oxidized to carbon dioxide. All these processes very quickly lead to fatty degeneration of the liver. In a healthy person, when drinking alcohol, all oxidative processes occur in the liver, without the release of acetaldehyde into the circulatory system.

Stages of alcoholic liver damage

Alcoholic liver damage occurs as a result of several factors. First, acetaldehyde changes the structure of membranes, cells and walls of the liver. This promotes the flow of fat from other tissues into this organ. In addition, a large amount of proteins accumulate in hepatocytes. As a result, the blood supply to the cells is reduced.

After all the almost irreversible changes in the structure of the liver when exposed to an alcoholic beverage, a gradual alcoholic disease occurs. First of all, the patient is faced with alcoholic hepatomegaly. Under the influence of alcohol, the liver increases in size. In chronic alcoholism, this condition is observed in 30% of patients. Thus, the body tries to compensate for its size with an increase in the amount of alcohol consumed (doses increase - the liver enlarges). Patients have no special complaints. Sometimes there is pain in the area of this organ. Only when diagnosing with the help of ultrasound, specialists observe an increase in the organ. And in the study of blood, an increase in the number of certain enzymes is traced.

Since hepatomegaly is mostly asymptomatic, a disease such as fatty liver as a result of alcohol damage is inevitable. This disease is observed in every second person suffering from alcohol dependence. Ethanol interferes with the oxidation of fatty acids, which simply turn into fats. They are deposited on the walls of the liver. Alcohol also removes fat deposits from adipose tissue, one hundred increases its amount in the blood. As a result, the amount of fat in the muscles decreases. Muscular dystrophy occurs.

In the case of fatty hepatosis, the following symptoms are observed:

Some patients have dystrophic changes in the liver. All this is accompanied by jaundice and a sharp increase in body temperature. And some patients do not feel any discomfort and, as a result, resist treatment. In the process of diagnosis, some compaction of the organ and an increase are noticeable. If you stop drinking any alcoholic beverage at this stage, all pathogenic changes in the gland can go through the reverse process.

The third stage of alcoholic damage to the gland is characteristic. As a result of this disease, there is an increase in connective tissue in the liver. Symptoms of this disease:

Such a diagnosis can only be established by performing a liver biopsy. If the patient then continues to drink alcohol even in a minimal amount, the disease will definitely develop into cirrhosis of the liver.

Alcoholic hepatitis occurs when alcohol is abused for at least five years. The disease is acute and chronic. In an acute course, a strong inflammation of the gland occurs, as a result of which the central lobules of the organ are destroyed. This disease generally develops gradually. But, if there is abuse in large doses, and especially with hard drinking, acute alcoholic hepatitis occurs abruptly and immediately. The symptoms are nausea and vomiting. The eyes and skin become yellow.

With a severe course of the disease, jaundice occurs first. Patients begin to lose weight dramatically. It may be accompanied by an increase in body temperature and constant sharp pains in the right hypochondrium. Experts say that with alcoholic hepatitis, the central nervous system and heart suffer greatly. Another option for the course of hepatitis is a violation of the outflow of bile. You can recognize it by observing itching of the skin, dark urine, discoloration of feces.

In an advanced case, a large amount of fluid begins to accumulate in the abdominal cavity, and kidney failure occurs. Everything is accompanied by internal hemorrhages. And if no measures are taken to eliminate the symptoms and save the patient, alcoholic hepatitis is fatal. If you stop drinking alcohol, every fourth patient recovers.

In the case of chronic hepatitis of this organ, all the same symptoms are observed. The difference is that in most cases, chronic alcoholic damage to the gland turns into cirrhosis. And even with the refusal of alcohol, recovery does not occur.

Alcoholic cirrhosis of the liver is observed in chronic alcoholics with an experience of 15-20 years. In this case, symptoms such as pain, weakness, apathy, nausea occur only during periods of drinking. In the case of abstinence from them, the patient feels normal. Most of the gland cells die, and its tissues are replaced by connective tissue. Because of this, the organon stops working fully. This form of cirrhosis is expressed in vitamin deficiency. With this disease, liver damage is accompanied by other destruction and dysfunctions of the patient's body systems.

Manifestations of cirrhosis from the central nervous system:

Patients complain of pain in the limbs. They result from hardening of the tendons. Outwardly, this is manifested in the impossibility to completely unbend the fingers. They are close to the palm. With such alcoholic liver damage, pancreatitis and diabetes mellitus develop. Everything is accompanied by alcoholic gastritis of the stomach.

The main complication of this disease is considered to be a malignant overgrowth of the gland - cancer. Pain, heaviness, weakness, loss of appetite are observed. It is even difficult for the patient to get out of bed. When passing the most minimal distance, shortness of breath and dizziness occur. The liver increases to its maximum size and thickens (petrification of the organ).

Methods of treatment of alcoholic liver damage

Treatment of alcoholic damage is necessarily accompanied by a complete rejection of alcoholic beverages. Only in this case it is possible to carry out therapy to restore the normal functioning of the liver. Treatment is mainly symptomatic, that is, it is aimed at eliminating individual symptoms of the disease. Such drugs should strengthen the body, remove toxins and toxins, relieve inflammation in the liver and other body systems. At the same time, bed rest is strictly observed.

To get rid of intoxication, it is necessary to inject glucose intravenously. Among the most effective sobrents in the case of alcoholic liver damage, Smecta and Atoxil are noted. Treatment of such diseases involves the removal of stagnant bile in the liver. For this purpose:

Allochol;
Cholestil;
Tanacehol.

To relieve pain, an effective drug is No-shpa. It is also possible to replace it with Baraglin. Often, all alcoholic lesions of this organ are accompanied by swelling of the lower extremities. For this, treatment involves the use of diuretics. But, with cirrhosis, they are used with extreme caution and only under the supervision of a doctor.

To restore liver function, hepatoprotectors are required. They promote the regeneration of gland cells. There are the following types of these drugs:

Milk thistle products;
Preparations, the main component of which is ademetionine;
Based on substances of animal origin;
Preparations with essential phospholipids.

These include:

Hepatosan	The drug is based on substances of animal origin. Treatment with the drug is to improve metabolic processes in the liver. Promotes the elimination of toxins. Take two capsules twice a day, half an hour before meals.
Chepaguard	The drug accelerates the regeneration of liver cells. Restores all protective functions of the body. Reduces cholesterol levels. Take one capsule three times a day with meals.
Phosphogliv	It has an immunomodulating effect and an antiviral effect. Relieves inflammation of the liver and other organs as a result of alcohol damage. One or two capsules should be taken three times a day, depending on the complexity of the course of the disease.
Essentiale	Restores liver cells, the structure of its shell. Prevents the formation of connective tissue in the gland. They are used both as a treatment for liver damage and for prevention. The dosage is prescribed by the doctor.
Essliver	The tool normalizes metabolism and the process of biosynthesis of phospholipids. Promotes structural regeneration of the liver in case of its alcoholic damage.

Treatment also consists in prescribing vitamin therapy. The use of folic acid, thiamine is recommended. The level of potassium, calcium and glucose in the body is corrected. Be sure to follow a therapeutic diet. Its principles are aimed at reducing the amount of protein and fat in the body. It is very important to observe fractional nutrition - eat 5-6 times a day in small portions. You should limit your salt intake. From the diet of the patient are completely excluded:

Margarine, lard, fatty meats;
Fried and smoked dishes;
Spicy food, spices and condiments;
Carbonated drinks.

If it is not possible to refuse to eat bread, you should eat only white and with bran. The diet should consist of such cereals: buckwheat, wheat, oatmeal, rice. The most acceptable fruits and vegetables in the treatment of alcoholic lesions of the gland: cauliflower, carrots, beets, zucchini, tomatoes, watermelon, grapes, prunes, strawberries, apples.

If the patient suffers from frequent diarrhea, all vegetables and fruits should be introduced into the diet in the form of juices. The most effective are blueberry and pomegranate juice. But radishes, garlic, onions, radishes, sorrel should be excluded for the period of the diet. They act irritatingly on the mucous membrane of the stomach and intestines. With alcoholic liver damage, the diet is observed for a long period of time. It is important to maintain some of its principles even after a complete cure.

In the case of cirrhosis, regeneration of the gland is not observed. So, experts prescribe only maintenance therapy. This is quite enough for a small area of liver death. They may also resort to surgery. Such treatment takes place by cutting off part of the gland. If more than 50% of the organ is damaged, a transplant is required.

The liver is a powerful organ with an impressive ability to regenerate. However, alcoholic beverages can disrupt the function of this organ and completely destroy it in just a few years. Against the background of regular long-term use of alcohol, alcoholic liver disease appears and begins to develop rapidly. Often it ends with cirrhosis and death of a person.

What does an alcoholic need to know about alcoholism?

Corticosteroids may be prescribed. Their use is justified in the case of patients with an acute form of alcoholic hepatitis, not accompanied by gastrointestinal bleeding and infectious complications.

A course of treatment is prescribed using ursodeoxycholic acid and methylprednisolone. Under the influence of ursodeoxycholic acid, a stabilizing effect on the membranes of hepatocytes will be exerted. This will help improve laboratory parameters.

Essential phospholipids may be used. These drugs restore the structure of cell membranes. When they are used, molecular transport is normalized, the activity of systems is stimulated, and the processes of cell division and differentiation are restored. The drugs exhibit antifibrotic and antioxidant properties. Simultaneously with the injections of Essentiale, as a rule, a parallel administration of the drug in the form of capsules is prescribed.

Ademetionine may be prescribed. It is administered by jet or drip, in the morning. After completing the course of injections, the drug is continued in the form of tablets. Among other things, it has an antidepressant effect.

In the later stages of alcoholic liver disease, measures are taken to treat Dupuytren's contracture. It can be conservative and surgical, depending on the severity of the disease.

Any medications are taken only as prescribed by a doctor and under his control. If the disease has developed into cirrhosis, treatment will be aimed at preventing the occurrence and eliminating its complications. Complications are also diagnosed in patients with alcoholic hepatitis. For the treatment of complications, medications and surgical techniques are used.

Surgical treatment of alcoholic liver disease

Patients with a severe stage of the disease are prescribed liver transplantation. First of all, you need to find a donor and refrain from drinking alcohol for at least six months. On average, the operation allows to prolong the life of patients with the last stages of alcoholic liver disease by 5 years, who would die in the shortest possible time without transplantation. The use of alcohol during illness in the case of a successful transplant is out of the question.

Thus, when detecting liver diseases that have developed against the background of regular alcohol abuse, it is necessary, first of all, to give up alcoholic beverages, undergo the prescribed diagnostic measures and follow the further recommendations of the doctor. Do not abuse alcohol and be healthy!

Thanks for the feedback

Comments

Megan92 () 2 weeks ago

Has anyone managed to save her husband from alcoholism? Mine drinks without drying up, I don’t know what to do ((I thought of getting a divorce, but I don’t want to leave the child without a father, and I feel sorry for my husband, he’s a great person when he doesn’t drink

Daria () 2 weeks ago

I have already tried so many things and only after reading this article, I managed to wean my husband from alcohol, now he doesn’t drink at all, even on holidays.

Megan92 () 13 days ago

Daria () 12 days ago

Megan92, so I wrote in my first comment) I will duplicate it just in case - link to article.

Sonya 10 days ago

Isn't this a divorce? Why sell online?

Yulek26 (Tver) 10 days ago

Sonya, what country do you live in? They sell on the Internet, because shops and pharmacies set their markup brutal. In addition, payment is only after receipt, that is, they first looked, checked and only then paid. And now everything is sold on the Internet - from clothes to TVs and furniture.

Editorial response 10 days ago

Sonya, hello. This drug for the treatment of alcohol dependence is indeed not sold through the pharmacy chain and retail stores in order to avoid overpricing. Currently, you can only order official website. Be healthy!

- This is a structural degeneration and impaired liver function, due to the systematic long-term use of alcohol. In patients with alcoholic liver disease, there is a decrease in appetite, dull pain in the right hypochondrium, nausea, diarrhea, jaundice; in the late stage, cirrhosis and hepatic encephalopathy develop. The diagnosis is facilitated by ultrasound, dopplerography, scintigraphy, liver biopsy, and the study of biochemical blood samples. Treatment involves giving up alcohol, taking medications (hepatoprotectors, antioxidants, sedatives), and if necessary, liver transplantation.

General information

Alcoholic liver disease develops in persons who abuse alcohol-containing drinks for a long time (more than 10-12 years) in average daily doses (in terms of pure ethanol) of 40-80 grams for men and more than 20 grams for women. Manifestations of alcoholic liver disease are fatty degeneration (steatosis, fatty tissue degeneration), cirrhosis (replacement of liver tissue with connective - fibrous), alcoholic hepatitis.

The risk of alcohol disease in men is almost three times higher, since alcohol abuse occurs in a ratio of 4 to 11 among women and men. However, the development of alcohol disease in women occurs faster and with less alcohol. This is due to the gender characteristics of absorption, catabolism and excretion of alcohol. Due to the increase in the consumption of strong alcoholic beverages in the world, alcoholic liver disease is a serious social and medical problem, which is being addressed by specialists in the field of modern gastroenterology and narcology.

The reasons

Pathogenesis

The bulk of ethyl alcohol entering the body (85%) is exposed to the action of the enzyme alcohol dehydrogenase and acetate dehydrogenase. These enzymes are produced in the liver and stomach. The rate of alcohol breakdown depends on genetic characteristics. With regular prolonged use of alcohol, its catabolism accelerates, and there is an accumulation of toxic products formed during the breakdown of ethanol. These products have a toxic effect on the liver tissue, causing inflammation, fatty or fibrous degeneration of the liver parenchyma cells.

Symptoms

The first stage of alcoholic liver disease, which occurs in almost 90 percent of cases of regular alcohol abuse for more than 10 years, is fatty liver disease. Most often, it is asymptomatic, sometimes patients report decreased appetite and periodic dull pain in the right hypochondrium, possibly nausea. Approximately 15% of patients have jaundice.

Acute alcoholic hepatitis can also occur without pronounced clinical symptoms, or have a severe fulminant course, leading to death. However, the most common signs of alcoholic hepatitis are pain (dull pain in the right hypochondrium), dyspeptic disorder (nausea, vomiting, diarrhea), weakness, loss of appetite and weight loss. Also a frequent symptom is hepatic jaundice (the skin has an ocher tint). In half of the cases, acute alcoholic hepatitis is accompanied by hyperthermia.

Chronic alcoholic hepatitis proceeds for a long time with periods of exacerbations and remissions. Periodically, moderate pain occurs, nausea, belching, heartburn, diarrhea, alternating with constipation, may appear. Jaundice is sometimes noted.

With the progression of alcoholic disease, the symptoms of hepatitis are joined by signs characteristic of developing liver cirrhosis: palmar erythema (reddening of the palms), telangiectasias (spider veins) on the face and body, "drum sticks" syndrome (characteristic thickening of the distal phalanges of the fingers), "watch glasses" (pathological change in the shape and consistency of nails); "heads of a jellyfish" (dilated veins of the anterior abdominal wall around the navel). In men, gynecomastia and hypogonadism (enlargement of the mammary glands and reduction of the testicles) are sometimes noted.

With the further development of alcoholic cirrhosis, patients have a characteristic increase in the parotid glands. Another characteristic manifestation of alcoholic liver disease in the terminal stage is Dupuytren's contractures: initially, a dense connective tissue nodule (sometimes painful) is found on the palm above the tendons of the IV-V fingers. In the future, it grows with involvement in the process of the joints of the hand. Patients complain of difficulty in bending the ring finger and little finger. In the future, their complete immobilization may occur.

Complications

Alcoholic liver disease often leads to the development of gastrointestinal bleeding, hepatic encephalopathy (toxic substances that accumulate in the body as a result of a decrease in functional activity are deposited in the brain tissues), and impaired kidney function. Alcoholics are at risk for developing liver cancer.

Diagnostics

In the diagnosis of alcoholic liver disease, a significant role is played by the collection of anamnesis and the identification of a patient's prolonged alcohol abuse. During the consultation, a hepatologist or gastroenterologist carefully finds out how long, with what regularity and in what quantities the patient drinks alcohol.

In laboratory studies, a general blood test shows macrocytosis (the toxic effect of alcohol on the bone marrow), leukocytosis, and accelerated ESR. Megablastic and iron deficiency anemia may be present. A reduced platelet count is associated with inhibition of bone marrow function, and is also detected as a symptom of hypersplenism with increased pressure in the vena cava system in cirrhosis.

In a biochemical blood test, an increase in the activity of AST and ALT (hepatic transferases) is noted. Also note the high content of bilirubin. Immunological analysis reveals an increase in the level of immunoglobulin A. When alcohol is consumed in an average daily dose of more than 60 g of pure ethanol in the blood serum, an increase in carbohydrate-depleted transferrin is noted. Sometimes there may be an increase in the amount of serum iron.

A thorough history taking is essential for the diagnosis of alcoholic liver disease. It is important to consider the frequency, amount and type of alcoholic beverages consumed. In connection with the increased risk of developing liver cancer in patients with suspected alcoholic disease, the content of alpha-fetoprotein in the blood is determined. At its concentration of more than 400 ng / ml, the presence of cancer is suggested. Also, patients have a violation of fat metabolism - the content of triglycerides in the blood increases.

Instrumental techniques that help diagnose alcohol disease include ultrasound of the abdominal cavity and liver, dopplerography, CT, MRI of the liver, radionuclear testing and liver tissue biopsy.

When performing ultrasound of the liver, signs of changes in size and shape, fatty degeneration of the liver (characteristic hyperechogenicity of liver tissues) are clearly visible. Doppler ultrasound reveals portal hypertension and increased pressure in the hepatic vein system. Computed and magnetic resonance imaging well visualizes the liver tissue and its vascular system. Radionuclide scanning reveals diffuse changes in the hepatic lobules, and the rate of hepatic secretion and bile production can also be determined. For the final confirmation of alcoholic disease, a liver biopsy is performed for histological analysis.

Treatment of alcoholic liver disease

A prerequisite is the complete and final renunciation of alcohol. This measure causes an improvement in the condition, and in the early stages of steatosis can lead to a cure. Also, patients with alcoholic liver disease are prescribed a diet. Be sure to eat with sufficient calories, a balanced content of proteins, vitamins and minerals, since people who abuse alcohol often suffer from hypovitaminosis and protein deficiency. Patients are recommended to take multivitamin complexes. With severe anorexia - parenteral nutrition or with a probe.

Drug therapy includes detoxification measures (infusion therapy with glucose solutions, pyridoxine, cocarboxylase). Essential phospholipids are used to regenerate liver tissue. They restore the structure and functionality of cell membranes and stimulate the activity of enzymes and the protective properties of cells. In a severe form of acute alcoholic hepatitis that threatens the patient's life, corticosteroid drugs are used. A contraindication to their appointment is the presence of infection and gastrointestinal bleeding.

Ursodeoxycholic acid is prescribed as a hepatoprotector. It also has choleretic properties and regulates lipid metabolism. The drug S-adenosylmethionine is used to correct the psychological state. With the development of Dupuytren's contractures, initially they are treated with physiotherapeutic methods (electrophoresis, reflexology, exercise therapy, massage, etc.), and in advanced cases they resort to surgical correction.

Liver cirrhosis requires symptomatic treatment and treatment of emerging complications (venous bleeding, ascites, hepatic encephalopathy). In the terminal stage of the disease, donor liver transplantation may be recommended for patients. This operation requires strict abstinence from alcohol for at least six months.

Forecast and prevention

The prognosis directly depends on the stage of alcoholic liver disease, strict adherence to medical recommendations and the complete rejection of alcohol. The stage of steatosis is reversible and, with proper therapeutic measures, the liver function normalizes within a month. The development of cirrhosis in itself has an unfavorable outcome (survival for 5 years in half of patients) and threatens with the occurrence of liver cancer. Prevention of alcoholic liver disease involves abstinence from alcohol abuse.