How to cure alcoholic hepatitis symptoms. Alcoholic hepatitis, a harbinger of cirrhosis: how to recognize and cure

Alcohol abuse is the cause of the development of alcoholic hepatitis. Currently in Russia there are more than 10 million men and women with chronic alcoholism. 21% were diagnosed with inflammation of the liver. It can be cured only with 1 and 2 degrees of the disease. The last stage is not treatable and turns into cirrhosis.

Causes of the disease

Hepatitis is a diffuse inflammation of the liver tissue. The alcoholic form of the disease is not contagious (unlike hepatitis C, which is transmitted through blood, saliva, breast milk). The cause of the pathology is the toxic damage to hepatocytes by ethyl alcohol and its decay products.

Liver damage is caused by products with any degree of strength. The amount of alcohol consumed has a greater influence on the rate of development of hepatitis. On average, pathology occurs after 4-5 years of daily drinking 70 ml of moonshine, 100 ml of vodka, 600 ml of wine, 1000-1200 ml of beer. When the dose is exceeded, tissue inflammation occurs earlier.

The rate of development of alcoholic hepatitis depends on the genetic content of acetaldehyderogenase and alcohol dehydrogenase, the enzymes responsible for the oxidation of ethyl alcohol. In people with a low concentration of AC and AL, alcohol breaks down for a long time, it “hits” the liver more. At risk are residents of Japan, Vietnam, Korea, West Africa, Siberia, Northern Europe.

The gender of the patient affects the development of the disease: women are more prone to chronic liver disease. Inflammation from alcohol develops in them three times faster than in men, hepatitis is more difficult, less treatable.

Symptoms and forms

The first months of hepatitis are asymptomatic, inflammation is detected during instrumental diagnostics of the liver (ultrasound, radiography reveal an increase in echogenicity, a decrease in the visibility of vascular structures). In a complicated form, signs appear (the same for men and women):

• Pain in the upper abdomen (under the ribs) on the right side.
• Asthenovegetative syndrome (weakness, sudden weight loss, lack of appetite).
• Cholestasia (jaundice of the skin and mucous membranes of the mouth, discoloration of feces, darkening of urine).
• Dyspeptic syndrome (nausea, belching, flatulence, bitterness in the mouth).
• Fever, often with hepatitis reaching febrile levels (above 37.5 degrees).

These symptoms may not indicate hepatitis, but other liver damage (cirrhosis, cancer). A biopsy and blood test are done to confirm the diagnosis. Inflammation is confirmed by the detection of neutrophilic leukocytosis, ESR 40–50 mm/h, increased activity of g-glutamyl transpeptidase, elevated IgA concentration.

Chronic

Persistent (remission, chronic) form of hepatitis is characterized by the stability of the patient's condition. Symptoms are mild. More often the patient complains of weakness, insomnia, lack of appetite. A moderate increase in the indicators of cholestasis syndrome is allowed. Sharp pains, no vomiting. There are no signs of renal hypertension (increased pressure in the portal vein).

Do not confuse chronic hepatitis with recovery. The absence of exacerbations does not mean that the inflammation does not progress. It happens that in an alcoholic the disease passes without acute phases. Due to easily tolerated symptoms, a person does not start treatment, continues to drink alcohol, and as a result, after a year or two, complications arise, such as cirrhosis of the liver.

Spicy

Progressive hepatitis is called when the spread of inflammation accelerates, leading to an increase in symptoms. It is clinically manifested by a rapid increase in jaundice, fever, confusion, pain in the hypochondrium (changing its character from acute to dull).

Acute hepatitis requires immediate medical attention, not only because of the suffering experienced by the patient. During this period, liver failure begins to manifest itself, which often leads to the development of coma and death. A mortal danger is an exacerbation that occurs in parallel with alcoholic cirrhosis (massive necrosis of hepatocytes, internal bleeding may begin).

Treatment Methods

Hepatitis therapy has several goals: inhibition of inflammation and fibrosis of the renal tissue, relief of symptoms, stimulation of the liver, prevention of complications (primarily cirrhosis). At stages 1–2 of the disease, the patient is prescribed a diet, drug treatment (hepatoprotectors, glucocorticoids, vitamins A, B, C, E are taken). In case of global damage to the organ (with decompensated function), transplantation is performed.

Important: it is useless to treat a patient with hepatitis if he does not stop drinking! Alcoholic drinks cause exacerbation, are not compatible with most drugs (reduce their effectiveness or cause adverse reactions). You can count on recovery if you completely refuse to drink alcohol.

Folk remedies

Herbal decoctions and tinctures alone will cope with liver hepatitis. They are allowed to be added to the medicines prescribed by the doctor - together they will rather relieve inflammation and improve well-being. Folk remedies have proven themselves well:

• To prevent exacerbation of hepatitis: a decoction of St. John's wort, fennel, rose hips. Pour a spoonful of raw materials with a liter of boiling water, hold on fire for 40 minutes. Take 3 times a day.
• For severe pain in the region of the liver: potato poultice. Mash 3 boiled potatoes, wrap in gauze, attach under the ribs (keep until cool).
• For the prevention of cirrhosis: juice from beets, radishes. Drink on a full stomach, 150 ml.

Calendula is good for the liver. A tablespoon of dried flowers is poured with 2 cups of boiling water, let it brew for 1 hour. Strained infusion is recommended to drink 2 times a day for 100 ml.

Nutrition

Fasting with hepatitis is contraindicated. The energy value of food should be at least 2000 calories per day for men and 1700 for women. Daily protein intake - at least 1 g per 1 kg of body weight, carbohydrate - more than 400 g, fat - less than 80 g. Products must necessarily contain many vitamins (especially group B, folic acid, a deficiency of which is always observed in alcoholics).

For hepatitis, diet No. 5 is prescribed. It is useful for the patient to consume such foods:

• Non-acidic varieties of fruits, berries.
• Low-fat sour cream, kefir, cottage cheese.
• Potato casserole.
• Boiled turkey, chicken breast.
• Oatmeal on the water.
• Vegetable soups.
• Boiled fish.

With a diseased liver, fried, smoked, pickled dishes, offal, mushrooms, chocolate, coffee, strong tea are prohibited. Patients with hepatitis should eat warm food - ice cream, ice-cold drinks threaten to exacerbate.

In addition to taking medications, diets, patients with alcoholic hepatitis must follow a drinking regimen. Drink water should be 100 ml 3 times a day 40-45 minutes before meals. Mineral calcium chloride waters are useful, improving the functions of a damaged liver.

Clinical recommendations necessarily relate to physical activity. With exacerbation, a lying regimen is indicated. In chronic hepatitis, regular walks in the fresh air (20–40 minutes minimum) are needed, swimming, yoga, and breathing exercises are useful. Under the ban, running, horseback riding, aerobics, weightlifting - stress, shaking provoke exacerbations.

Forecast and prevention

The Maddrey index is used to determine the severity of hepatitis and calculate the chances of survival. It is calculated according to the formula "4.6 x Prothrombin index + Serum bilirubin". When receiving an index of 32 or higher, the probability of death over 3 years is more than 70%.

The course and prognosis of hepatitis in alcoholics depend on the severity of liver dysfunction. If inflammation developed after alcoholic excesses and led to cirrhosis, then with such a “bouquet” they rarely live longer than 3 years.

Alcoholic inflammation of the liver is curable only in the absence of complications. But you will have to be patient - drug therapy lasts more than 13 months (sometimes the patient needs to take hepatoprotectors for several years). A prerequisite is a complete rejection of alcohol (even beer). If the patient continues to drink, he will not live more than a couple of years.

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They are inflammatory processes that destroy liver cells that occur as a result of alcohol abuse.

Alcoholic hepatitis can very often turn into a more serious disease - cirrhosis of the liver.

What are the causes of alcoholic hepatitis?

When alcohol is abused, acetaldehyde accumulates in the human liver, which destroys liver cells. Alcohol entering the body causes chemical processes that affect the liver. Alcoholic hepatitis is an inflammatory process that occurs as a result of exposure to alcohol toxins.
Alcoholic hepatitis is a chronic disease and manifests itself in a person after 5-7 years of prolonged drinking. The extent of liver damage in this pathology is associated with the duration of alcohol consumption, its quality and dosage.
The disease can take two forms:

• progressive;
• persistent.

The progressive form is a minor liver damage that can later lead to cirrhosis. This form accounts for approximately 20% of cases of alcoholic hepatitis.

If the patient completely stops taking alcohol and undergoes a course of treatment, then as a result, the inflammation may go away. At the same time, residual manifestations of the disease are still observed in the body.

The persistent form is a more stable form of the disease. With the refusal of alcohol, the inflammatory process can stop, while the liver is restored.

If the patient continues to take alcohol, the disease can go into a progressive stage.

What symptoms characterize the disease?

Symptoms of alcoholic hepatitis:

• heaviness in the right hypochondrium;
• nausea;
• heaviness in the stomach.

In many cases, a doctor can make a diagnosis only after conducting laboratory blood tests, which will show an increased content of enzymes.

In the persistent stage of hepatitis, liver tissue fibrosis, cell dystrophy, and the appearance of Mallory bodies are observed. If liver tissue fibrosis does not progress, this stage can last from 5 to 10 years, even if the patient drinks alcohol in small quantities.

The progressive stage of alcoholic hepatitis is characterized by the following symptoms:

• vomit;
• diarrhea;
• chills;
• yellowing of the skin and corneas of the eyes;
• heaviness in the right hypochondrium;
• acute liver failure.

At the same time, the very first laboratory tests show an increase in enzymes and bilirubin.

Chronic hepatitis often leads to cirrhosis of the liver cells. Doctors failed to establish direct signs of alcoholic etiology of liver cirrhosis. Despite this, there are violations that are characteristic of alcohol exposure. In the body, ultrastructural changes in hepatocytes occur and Mallory bodies appear. This indicates the characteristic effect of alcohol on the body.

Diagnosis of chronic hepatitis is carried out by the following methods:

• ultrasound of the spleen;
• determination of the structure of liver cells;
• determination of the size of the spleen;
• determination of the diameter of the portal vein;
• the presence of ascites.

In medical centers, Doppler ultrasound is performed, which reveals the presence of portal hypertension.
Alcoholic hepatitis can be acute or chronic.

Acute form of alcoholic hepatitis

The acute form is a degenerative lesion of liver cells, which is inflammatory in nature and is progressive. How many varieties of the disease are there? There are 4 types of acute hepatitis:

• fulminant;
• icteric;
• cholestatic;
• latent.

If the patient drinks alcohol for a long time, then in 70% of cases he develops acute alcoholic hepatitis. This disease can quickly turn into cirrhosis of the liver cells. The picture and progression of hepatitis from alcohol depends on the degree of damage to the liver.

The complication of acute hepatitis occurs under the influence of the destructive influence of alcohol on the background of the degeneration of liver cells.
Symptoms of alcoholic hepatitis usually appear in patients after prolonged drinking. Often this category of patients is already observed. In this case, the prognosis of the disease is seriously deteriorating.

The icteric form of acute hepatitis is the most common. It manifests itself with the following symptoms:

• deterioration of well-being;
• lethargy;
• headaches;
• heaviness in the right hypochondrium;
• nausea;
• vomit;
• yellowing of the skin;
• strong weight loss.

In this category of patients, there is an increase in the liver. The organ has a compacted smooth surface. If at the same time the patient has cirrhosis, then the characteristic symptoms are:

• ascites;
• tremor;
• palmar erythema.

Often bacterial infections join the disease:

• pneumonia;
• urinary tract infection;
• peritonitis;
• septicemia.

With serious complications of the disease in combination with a severe form of renal failure, a sharp deterioration in the patient's condition or death of the patient may occur.

The latent nature of the disease does not have a definite clinical picture. Its diagnosis is made on the basis of an increase in transaminases in a patient. A liver biopsy is done to make a definitive diagnosis.
The cholestatic variant is characterized by itching, dark urine, light stools, and yellowing of the skin. The patient has pain in the liver, chills. This form of the disease is protracted and has a severe course.
The fulminant variant has progressive signs of renal failure, jaundice. The patient develops hepatic encephalopathy, hemorrhagic syndrome. In severe cases, encephalopathy turns into a coma. The combination of hepatorenal syndrome and coma can lead to the death of the patient.

Chronic form of alcoholic hepatitis

In the chronic form of the disease, characteristic signs may be absent. The diagnosis is established on the basis of a blood test.

In patients, the activity of transaminases increases, the manifestations of cholestasis increase. There are no signs of portal hypertension. The patient has histological abnormalities corresponding to the inflammatory process, if there are no signs of cirrhosis.
It is difficult to establish a diagnosis of alcoholic hepatitis, because the doctor does not always have information that the patient is abusing alcohol.
Alcoholism is characterized by the following features:

1. The patient consumes alcohol for a long time and in large quantities.
2. Drinking alcohol in doses hazardous to health.
3. Drinking alcohol even when the physical and mental condition worsens.
4. withdrawal syndrome.
5. The need for alcohol to reduce withdrawal symptoms.

A doctor can diagnose alcoholism if three of these signs are present.
When alcohol is abused, the patient takes alcohol, regardless of obligations to society. With the deterioration of health, the patient still continues to take alcohol.

Treatment of alcoholic hepatitis

Treatment includes a set of the following activities:

1. A diet high in protein.
2. Medical treatment.
3. Hepatoprotectors.
4. Elimination of etiological causes.

In the treatment of alcoholic hepatitis, patients should completely stop drinking alcohol.

It often happens that the patient continues to take alcohol during treatment, sometimes in small quantities. Patients who have alcohol dependence cannot refuse alcohol during the treatment of hepatitis. Such patients should be prescribed complex treatment by narcologists and hepatologists.

These patients may experience adverse disease progression if they are unable to abstain from alcohol. Due to liver failure, these patients are not prescribed drugs for the treatment of alcoholism.

If the patient does not take alcohol, then the treatment will lead to favorable results. Jaundice, ascites and other manifestations of hepatitis will pass. If a patient with alcoholic hepatitis takes alcohol, hepatitis can cause serious complications, which can even lead to the death of the patient.

Often in patients with alcoholism endogenous depletion of the body is observed. It can be exacerbated by exogenous exhaustion of the patient in the event that a person replenishes the energy deficit with alcohol calories. At the same time, he consumes less food that contains the amount of calories, vitamins, proteins and carbohydrates necessary for his body.
Most patients with alcoholic hepatitis are malnourished. The level of liver damage in these patients depends on the nutritional deficiencies that the body receives.

Therefore, the main task of the treatment of alcoholic hepatitis is a diet with a high content of nutrients.

If the patient suffers from anorexia, then parenteral or tube nutrition is used.
Parenteral nutrition in alcoholic hepatitis provides the patient with the required amount of amino acids. Such nutrition normalizes the balance of calories and trace elements in the patient's body, restores the content of essential amino acids, reduces protein breakdown in liver cells, and improves metabolic processes.

Thanks to parenteral infusion, the metabolic processes in the patient's brain are improved, and thus hepatic encephalopathy is cured. Amino acids are a source of trace elements for such patients.

For patients suffering from severe forms of alcoholic hepatitis, doctors prescribe a course of treatment with antibacterial agents to prevent bacterial infections. The greatest effect in this case is given by fluoroquinolone preparations.

Currently, hepatologists use more than a thousand drugs for the complex treatment of alcoholic hepatitis. Hepatoprotectors have the most beneficial effect on the liver.

They restore liver homeostasis, increase the resistance of liver cells to pathological factors, and restore liver function. Hepatoprotectors contribute to the restoration of destroyed liver cells.

Varieties of hepatoprotectors

Hepatoprotectors are divided into 5 types:

1. Substances that contain components of milk thistle.
2. Medications containing ademetionine.
3. Ursosan containing bear bile and ursodeoxycholic acid.
4. organic matter of animal origin.
5. Medicines containing essential phospholipids.

Hepatoprotectors restore damaged liver cells, improve liver function, its ability to process various toxins.

With alcoholic hepatitis, when bile stagnates in the body due to an excess of alcoholic toxins, it harms the liver itself, while destroying it. Such a destructive effect leads to the disease of hepatitis, which is caused by stagnation of bile.

In the body of a healthy person, the processes of transformation of toxic acids into secondary and tertiary bile acids are constantly taking place in the liver. Tertiary acids include ursodeoxycholic acid. It is non-toxic and performs all the necessary functions in digestion, breaks down fat, mixes it with liquid.
This acid reduces the synthesis of cholesterol and its deposition in the gallbladder. What percentage of this substance is found in the gallbladder? Human bile contains only 5% of this acid.

In medicine, it began to be extracted from the bile of a bear for the treatment of liver diseases. Currently, physicians have synthesized ursodeoxycholic acid, which hepatoprotectors possess.

In the treatment of alcoholic hepatitis, essential phospholipids are actively used.
These drugs significantly accelerate the recovery of the liver from exposure to alcoholic toxins, reduce the destruction of liver tissues.
Phospholipids are compatible with other drugs and nutrients.

Now for the treatment of alcoholic hepatitis in medicine, a wide group of modern highly effective drugs are used that can cure the disease or stabilize the condition of the liver and the patient's body as a whole for a long time.

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Alcohol abuse is one of the most common causes of liver damage and leads to the development of alcoholic liver disease (ALD).

The highest rates of morbidity and mortality from liver cirrhosis (LC), which are directly dependent on the level of alcohol consumption, were registered in Europe (up to 9.8 liters - WHO, 1995). According to the State Statistics Committee of the Russian Federation (1998), alcohol consumption is 13 liters per person per year. Currently in Russia there are about 10 million patients with chronic alcoholism. Despite the mental and physical dependence on the intake of alcoholic beverages, ALD develops in 12-20% of cases. At the same time, 80% of deaths are associated with excessive consumption of alcohol and its toxic surrogates, leading to severe somatic pathology (hepatic coma, acute heart failure, gastrointestinal bleeding, infections, etc.). Regular alcohol abuse is also accompanied by an increased risk of accidents, injuries, and poisoning.

In the development of ABP, the type of alcoholic beverages does not matter - when determining the daily dose of alcohol, the conversion is carried out by the number of grams of ethanol per day (correspondence between 10 ml of ethanol, 25 ml of vodka, 100 ml of wine, 200 ml of beer). With daily consumption of risky doses of alcohol for several years, alcoholic fatty degeneration of the liver (AFD) develops, with daily use of critical (dangerous) doses of ethanol, alcoholic steatohepatitis (ASH) develops. Transformation into CP is possible with a daily intake of 160 g or more of ethanol per day in 7-18% of patients (Penquino I, II).

The issue of doses of alcoholic beverages that are harmless to health is debatable. When determining the boundaries of safe domestic alcohol consumption, genetic characteristics, individual sensitivity, national traditions, etc. are not taken into account. the development of symptoms of chronic alcohol intoxication (CHAI), which increases the risk of developing non-alcoholic diseases and aggravates their course. Often an alcoholic disease develops, combining both signs of mental pathology and damage to many systems and organs.

Risk factors for the development of ALD include: doses of alcohol, the nature and duration of abuse; genetic polymorphism of ethanol-metabolizing enzymes; gender (women are more likely to develop ALD); malnutrition (deficiency of nutrients); the use of hepatotoxic drugs metabolized in the liver; infection with hepatotropic viruses; immune factors.

ethanol metabolism. In the human body, alcohol metabolism occurs in three stages with the participation of alcohol dehydrogenase (ADH), microsomal ethanol-oxidation system (MEOS) and pyroxisomes. The formation of ABP is largely due to the presence of genes encoding enzymes involved in the metabolism of ethanol - ADH and aldehyde dehydrogenase (ALDH). These enzymes are strictly specific and localized mainly in the liver. When it enters the stomach, 12-25% of the alcohol introduced into the body is oxidized under the influence of gastric ADH, which converts ethanol into acetaldehyde, thereby reducing the amount of alcohol entering the portal circulation system and, accordingly, the liver. The lower gastric ADH activity in women than in men explains in part the fact that they are more sensitive to the toxic effects of alcohol. Consideration should be given to a decrease in the level of ADH in the stomach when taking blockers of H 2 -histamine receptors, which can lead to a significant increase in the concentration of alcohol in the blood.

Ethanol, entering the liver through the portal circulation system, is exposed to the action of the hepatic fraction of ADH, the coenzyme of which is nicotinamide dinucleotide (NAD+), resulting in the formation of acetaldehyde, which plays an important role in the development of ALD, and the reduction of the coenzyme to NАD*H. ADH, being a cytoplasmic enzyme, is involved in the oxidation of ethanol at a tissue alcohol concentration of not more than 10 mmol/L.

In humans, there are three main genes that code for ADH: ADH1, ADH2, and ADH3. Polymorphism at the ADH2 locus most likely results in significant differences in ethanol metabolism. Thus, the ADHb2 isoenzyme (ADH2*1 allele), which provides enhanced formation of acetaldehyde, is more common in people of the Mongoloid race, which explains their lower tolerance to alcohol, manifested by facial flushing, sweating, tachycardia, and also reveals the reasons for the higher risk of developing ALD. At the next stage, acetaldehyde is metabolized to acetic acid under the influence of cytosolic AlDH1 and mitochondrial AlDH2 enzymes in NAD-dependent reactions. About 10-15% of ethanol is metabolized in microsomes of the smooth endoplasmic reticulum with the help of MEOS, including cytochrome P 450 2E1, and many drugs are metabolized here. An increase in alcohol load leads to increased sensitivity to drugs, the formation of toxic metabolites and toxic liver damage when using therapeutic doses of drugs. Finally, catalases contained in pyroxisomes may also be involved in ethanol metabolism.

Pathogenesis. The toxic effect of ethanol is directly dependent on the concentration of acetaldehyde and acetate in the blood. When ethanol is oxidized, there is an increased consumption of the NAD+ coenzyme, an increase in the NAD * H / NAD + ratio, which plays an important role in the formation of fatty degeneration of the liver. An increase in the concentration of NAD*H leads to an increase in the synthesis of glycero-3-phosphate, promotes the esterification of fatty acids, the synthesis of triglycerides, is accompanied by a decrease in the rate of b-oxidation of fatty acids, and leads to their accumulation in the liver.

Acetaldehyde has a hepatotoxic effect, which manifests itself as a result of increased lipid peroxidation (LPO) processes, the formation of compounds with other proteins and enzymes, which leads to disruption of the function of phospholipid cell membranes. The complex of compounds of acetaldehyde with proteins, including tubulin, causes changes in the structure of hepatocyte microtubules, forming the so-called alcoholic hyaline, and contributes to the disruption of intracellular transport, protein and water retention, and the development of hepatocyte ballooning dystrophy.

Excessive formation of acetaldehyde and fatty acids leads to a decrease in the activity of mitochondrial enzymes, uncoupling of the processes of oxidation and phosphorylation, a decrease in the synthesis of adenosine triphosphate, and also enhances the synthesis of cytokines (in particular, transforming growth factor - TGFb). The latter promotes the transformation of Ito cells into fibroblasts that produce collagen. Another mechanism of collagen formation is the stimulation of Kupffer cells by LPO products.

Along with this, the role of the angiotensinogen (AGT) gene, a protein synthesized in the liver, and angiotensin II is assumed to play a role in the development of ALD. Their profibrogenic effect was established , an increase in the level of angiotensin II in the plasma of rats was found depending on alcohol motivation .

In the pathogenesis of ALD, the role of immune mechanisms is great. Violations of humoral immunity were revealed: an increase in the level of serum immunoglobulins (mainly class A immunoglobulin), their deposition in the wall of the hepatic sinusoids, the formation of antinuclear and antismooth muscle antibodies in low titers, as well as antibodies to alcoholic hyaline, etc.

Violation of cellular immunity is associated with sensitization of T-cells by acetaldehyde, the influence of immune complexes, and increased production of cytotoxic T-lymphocytes. As a result of the interaction of immunocompetent cells, pro-inflammatory cytokines (including tumor necrosis factor - TNFa) and interleukins induced by it (IL-1, IL-2, IL-6, IL-8) are released, which, with the participation of reactive oxygen species and nitric oxide leads to damage to various target cells, and ultimately to the development of multiple organ disorders.

At the same time, in patients suffering from ALD, an excessive growth of bacteria in the small intestine is found, which contributes to an increase in the synthesis of endotoxin - the lipopolysaccharide of the shell of gram-negative microbes. When released into the blood of the portal system, endotoxin, along with other negative factors (LPO metabolites), stimulates the activity of Kupffer cells, the synthesis of pro-inflammatory cytokines, especially TNF-α, with the active influence of which the development of inflammation and fibrosing processes in the liver is enhanced.

Diagnosis of HAI. Assessment of the severity of alcohol intoxication is of great medical and social importance. A significant argument is the data of world statistics: mortality due to alcohol intoxication ranks third.

To identify CAI during a mass examination, the world-famous GAGE ​​questionnaire is used, which is given below.

1. Have you ever felt that you should cut down on your alcohol consumption?
2. Did you get irritated if someone around you (friends, relatives) told you to cut down on your drinking?
3. Have you experienced guilt associated with drinking alcohol?
4. Have you ever felt the urge to drink alcohol as soon as you woke up after drinking alcohol?

The presence of positive answers to all four questions allows us to make a conclusion about the systematic use of alcohol and determines the high specificity of screening.

To assess the severity of CHAI, a questionnaire of "post-intoxication alcohol syndrome" (PAS) was proposed with a list of symptoms of CHAI.

1. Restlessness and excitement.
2. Paleness (cold and damp skin).
3. Pain in the region of the heart.
4. Hyperemia (excessive redness of the face).
5. Headache.
6. Dizziness.
7. Trembling of fingers.
8. Desire to take alcohol.
9. Yellowness of the skin.
10. Change in skin sensitivity (increase, decrease).
11. Violation of the stool (diarrhea, constipation).
12. Malaise and fatigue.
13. Nervous tension.
14. Nosebleeds.
15. Fainting states.
16. Dyspnea.
17. Edema on the legs.
18. Swelling of the face.
19. Lack of appetite.
20. Feeling of heartbeat.
21. Interruptions in the work of the heart.
22. Increased secretion of saliva.
23. The need to smoke.
24. The need to take medicine.
25. Gaps in memory of events that took place the day before.
26. Irritability and anger.
27. Vomiting and nausea.
28. The vomit is bloody.
29. Decreased sex drive.
30. Dry mouth.
31. Rash on the skin.
32. Excessive appetite.
33. Excessive thirst.
34. Excessive sweating (night sweats).
35. Wobbling gait.

When examining patients of the narcological department of the clinic of the Research Institute of Narcology of the Ministry of Health and Social Development of the Russian Federation, 15 or more positive answers to the PAS questionnaire suggested a high probability of systematic use of unsafe doses of alcoholic beverages.

In order to identify the physical symptoms of CAI, the LeGo Grid is used. Since there are no specific signs of CAI, when examining a patient, one should take into account the features of age-related changes (neurological, mental, etc.) and similar symptoms of CAI and concomitant diseases. The presence of seven or more signs of an objective assessment of physical symptoms does not exclude the possibility of CAI in the examined patient. Here is a list of physical signs of KhAI (“LeGo Grid”, 1976) modified by O. B. Zharkov, P. P. Ogurtsov, V. S. Moiseev.

• Obesity.
• Deficiency in body weight.
• Transient arterial hypertension.
• Tremor.
• Polyneuropathy.
• Muscular atrophy.
• Hyperhidrosis.
• Gynecomastia.
• Enlargement of the parotid glands.
• Coated tongue.
• The presence of a tattoo.
• Dupuytren's contracture.
• Venous plethora of the conjunctiva.
• Hyperemia of the face with the expansion of the network of skin capillaries.
• Hepatomegaly.
• Telangiectasias.
• Palmar erythema.
• Traces of injuries, burns, bone fractures, frostbite.

Laboratory diagnostics of KhAI. In patients who abuse alcohol more often than in the general population, the following are detected: an increase in the average volume of erythrocytes, serum iron levels, leukocytosis, a predominance of aspartate aminotransferase (AST) activity over alanine aminotransferase (ALT) activity (66%), an increase in alkaline phosphatase (AP) activity (24 %) and γ-glutamyl transpeptidase (γ-GT) (70-80%), triglycerides (70-80%), cholesterol (70-80%), class A immunoglobulin (60-70%). However, among the routine methods of laboratory diagnostics, there are no specific tests indicating CAI. In recent years, in specialized clinics, in order to detect alcohol abuse, the determination of carbohydrate-deficient (desialized) blood serum transferrin is used - a compound of transferrin with acetaldehyde, leading to the accumulation of iron in the liver (70-90%) and acetaldehyde-modified hemoglobin (70-80%).

clinical picture. ALD clinically manifests itself in the form of several nosological forms (according to ICD - 10): fatty liver (K ​​70.0), acute or chronic hepatitis (K 70.1), alcoholic fibrosis (K 70.2) and liver cirrhosis (K 70.3).

Railway usually asymptomatic and detected incidentally during the examination when detecting hepatomegaly or according to ultrasound, which registers a pronounced increase in echogenicity, a decrease in the visibility of vascular structures. Complaints of patients about discomfort, heaviness in the right hypochondrium are not associated with the pathological process in the liver and are explained by other reasons. On palpation, the liver is enlarged, smooth with a rounded edge. Biochemical tests are usually normal; there may be a slightly pronounced syndrome of cytolysis. In unclear cases, a needle biopsy of the liver is performed.

Alcoholic hepatitis. There are acute and chronic forms of alcoholic hepatitis.

Acute alcoholic hepatitis (AAH) is an acute progressive degenerative inflammatory liver disease. Clinical manifestations of OAH are very diverse: from mild anicteric forms to fulminant hepatitis, accompanied by severe liver failure; often leads to the development of hepatic coma and death. The course and prognosis of OAH depend on the severity of liver dysfunction. OAH is especially difficult after alcoholic excesses against the background of an already formed cirrhosis. The most common is the icteric form of OAS. Patients complain of weakness, nausea, anorexia, weight loss, dull pain in the right hypochondrium, fever, jaundice. Skin itching for this form of alcoholic hepatitis is not typical. A rarer variant (up to 13%) is the cholestatic form, accompanied by severe pruritus, intense jaundice, discoloration of feces and darkening of the urine, which requires differential diagnosis with obstructive jaundice, and when fever is added, with cholangitis. The fulminant form of OAH is fatal, fulminant in nature and is a reflection of acute massive necrosis of hepatocytes. It is clinically manifested by a rapid increase in jaundice, high fever, confusion, the appearance of a characteristic hepatic odor from the mouth. Characterized by the addition of disseminated intravascular coagulation, renal failure, hypoglycemia, infectious complications, cerebral edema develop. This form of hepatitis, especially in patients with alcoholic cirrhosis of the liver, determines a high risk of death, contributes to the progression of fibrosis in cases of regression of the clinical symptoms of OAH.

A special place in the structure of liver diseases is occupied by lesions caused by alcohol substitutes, mass poisoning of which was observed in the summer-autumn of last year (the total number of victims as of November 23, 2006 in the Russian Federation was 10,400 people). The main toxic substance is polyhexamethylene guanidine hydrochloride, which is part of disinfectants. Other potential etiological factors include diethyl phthalate, isopropyl alcohol, acetaldehyde, etc. Each of these toxic substances can cause damage to various organs and systems. However, among them, the development of toxic hepatitis, which occurs with a pronounced, slowly resolving cholestasis, is very significant. For poisoning with alcohol surrogates, the cytolysis syndrome is less characteristic (5-10 norms of aminotransferases), the synthetic function of the liver rarely suffers. The most dramatic situation - progressive liver failure - is observed in patients with background alcoholic cirrhosis.

Chronic hepatitis of alcoholic etiology, or alcoholic steatohepatitis slightly different in clinical manifestations from IDP. Patients complain of weakness, anorexia. According to palpation, an enlarged liver with a rounded edge is determined. On ultrasound, the picture resembles that of IDP. In some cases, there is a slight increase in the size of the spleen, expansion of the splenic vein, signs of portal hypertension begin to appear. Laboratory examination reveals an increase in transaminase activity with a characteristic excess of AST over ALT, in some cases a moderate increase in cholestasis syndrome is possible. Verification of the diagnosis is possible with a morphological study of the liver. A long course of ACH leads to the formation of alcoholic cirrhosis. It is not excluded that alcoholic cirrhosis can also form without pronounced signs of inflammation through perivenular alcoholic fibrosis.

Alcohol CPU. With alcoholic cirrhosis, an extraordinary variety of clinical manifestations is possible. In a significant number of patients, cirrhosis occurs latently or with few symptoms. However, many of them have an enlarged liver on examination. Complaints of weakness, dyspeptic disorders, weight loss, joint pain are non-specific. In 75% of cases, a picture characteristic of cirrhosis develops in the form of small hepatic signs - telangiectasias, palmar erythema, gynecomastia. The liver, as a rule, is enlarged, compacted, with a smooth surface, the edge is pointed; in some cases, the liver is normal or reduced in size. Perhaps a moderate increase in the size of the spleen, expansion of the portal and splenic veins, a decrease in the rate of portal blood flow (manifestation of portal hypertension), followed by the formation of varicose veins of the esophagus. With decompensation of cirrhosis, the development of edematous-ascitic syndrome, electrolyte disturbances are detected - hypokalemic alkalosis, in 33% of patients - metabolic alkalosis, hyponatremia, an increase in the content of ammonia in the blood is detected. Encephalopathy is mixed, coma may develop. A biochemical blood test shows hyperbilirubinemia, an increase in the activity of alkaline phosphatase and γ-GT, AST and ALT by no more than 6 times. Thrombocytopenia, prolongation of prothrombin time, hypoalbuminemia develops. Alcoholic etiology can be confirmed by studying the alcohol history, by excluding the viral nature of cirrhosis.

ABP is often accompanied by chronic pancreatitis, peripheral polyneuropathy, myocardiopathy, nephropathy. When evaluating the clinical picture and the course of the disease, it should be taken into account that the progression of organ pathology is determined not only by the influence of acute and chronic alcohol intoxication, but also by the pathological manifestations of the withdrawal syndrome.

The morphological criteria of ALD include fatty infiltration (small and large droplets in the 2nd and 3rd zones of the acinus), balloon degeneration of hepatocytes, acidophilic bodies - Mallory bodies or alcoholic hyaline in the form of condensed microfilaments, giant mitochondria, collagenization of the 3rd zone ( perivenular fibrosis), neutrophilic infiltration, tubular cholestasis, increased deposition of hemosiderin in the liver (Fig.).

ABP forecast. To determine the severity of alcoholic hepatitis and survival, the Maddrey index is used, calculated as 4.6 x (the difference between the patient's prothrombin time and the same indicator in the control) + serum bilirubin in mg%. The probability of a lethal outcome with a Maddrey index value of more than 32 exceeds 50%.

In recent years, the MELD (Model for End-Stage Liver Disease) system, previously developed for patients requiring liver transplantation, has been used to assess the risk of mortality in the outcome of OAH in order to determine the timing of the operation. MELD (in points) is calculated by the formula: 10 x (0.957 x loge [creatinine mg / dl] + 0.378 x loge [prothrombin time] + 0.643 x etiology of cirrhosis). It is shown that with a score of up to 40, life expectancy is limited to 3 months.

Treatment of ASG. The goal of ACH therapy is to prevent the formation of fibrosis and cirrhosis (inhibition of inflammation and fibrosis in the liver tissue, decrease in the activity of lipid peroxidation processes and biochemical parameters, excretion of toxic metabolites, decrease in endotoxemia), improve the quality of life and treat conditions associated with ACH (chronic cholecystitis, pancreatitis, peptic ulcer). disease of the stomach and duodenum, etc.).

Ethanol is the main etiological factor in the development of the disease. The basis of treatment for ALD should be a complete abstinence from alcohol. If this condition is met with IDP, ACH, the symptoms of chronic liver disease may regress, and laboratory parameters may improve. Prolonged abstinence in alcoholic cirrhosis helps to improve the protein-synthetic function of the liver, reduce the manifestations of portal hypertension, and also improve the morphological picture. It is necessary to conduct systematic conversations with patients with signs of CAI and their close circle, arguing the influence of alcohol on the occurrence of somato-neurological pathology, the development of alcohol dependence and mental illness, the risk of dangerous poisoning, as well as the possibility of serious consequences as a result of the interaction of drugs and alcoholic beverages (especially in elderly people).

It would be expedient to introduce restrictions generally accepted in the world on the sale of alcohol and to carry out educational work.

Diet. In ALD, it is advisable to prescribe a diet rich in proteins (at least 1 g per 1 kg of body weight), with a high energy value (at least 2000 kcal / day), with a sufficient content of vitamins (especially group B, folic and lipoic acids) and trace elements - zinc, selenium.

It has been established that zinc deficiency (40% of patients with Class B and C cirrhosis according to Child-Pugh) not only increases the manifestations of hepatic encephalopathy, but is in itself a sign of liver failure. It is also known that ADH is a zinc-dependent enzyme involved in the metabolism of ethanol.

It should be borne in mind that people who abuse alcohol, as a rule, have a lack of body weight, therefore, a gradual increase in protein intake from food improves liver function, which is explained by stimulation of enzymes, a decrease in catabolic processes, and normalization of the immune status.

Medical therapy for ABP. In the pathogenesis of ALD, a key role is played by damage to biological membranes, dysfunction of enzyme systems. In this regard, the use of polyunsaturated (essential) phospholipids, which have membrane stabilizing and cytoprotective properties, which replace phospholipid defects in the membrane structures of damaged liver cells by incorporating phospholipid complexes into cytoplasmic membranes, increases the activity and fluidity of membranes, and normalizes LPO processes. In the course of a twenty-year study devoted to the study of the effect of essential phospholipids on alcoholic liver damage using an experimental model - baboon monkeys, a slowdown in the progression of the disease was shown, preventing its transition to the stage of cirrhosis. Essentiale is prescribed at a dose of 500-1000 mg / day intravenously for 10-14 days, then the course of treatment is continued from 3 to 6 months at a dose of 1800 mg / day. Extensive experience in the use of essential phospholipids has confirmed the high efficacy of the drug in the treatment of patients with inactive forms of ALD - IDP, ACH.

Silymarin preparations (silibinin is the main active ingredient) are widely used in the treatment of liver steatosis and chronic alcoholic hepatitis. Silymarin has a hepatoprotective and antitoxic effect (70-105 mg/day for at least 3 months). The mechanism of its action is associated with the suppression of lipid peroxidation, as a result of which damage to cell membranes is prevented. In damaged hepatocytes, the drug stimulates the synthesis of proteins and phospholipids, resulting in the stabilization of hepatocyte membranes. The antifibrotic effect of silymarin was noted. Experimental models demonstrated a slowdown under its influence of the rate of fibrous transformation of the liver tissue, which is associated both with an increase in the clearance of free radicals and with a direct suppression of collagen synthesis.

In the treatment of alcoholic liver damage, ademetionine is used. The use of ademetionine in ALD is associated with the need for the body to replenish endogenous ademetionine, which performs one of the main functions in intermediate metabolism. As a precursor of such important compounds as cysteine, taurine, glutathione and coenzyme A, ademetionine plays an active role in the reactions of transamination, transsulfuration and aminopropylation. The use of exogenous ademetionine can reduce the accumulation and negative effects of toxic metabolites on hepatocytes, stabilize the viscosity of cell membranes, and activate the enzymes associated with them. On the other hand, ademetionine enhances the methylation of membranes and pathways, contributes to a change in membrane viscosity, improves the function of neuronal receptors, stabilizes the myelin sheath, and, penetrating the blood-brain barrier, stabilizes the activity of phosphlinergic and serotonergic systems. The combination of hepatoprotective and antidepressant properties determines the use of the drug in depressive disorders in cases of toxic liver damage. The recommended doses of ademetionine are 800 mg / day - with parenteral administration (for 2 weeks) and 1600 mg / day - per os (from 2 to 4-8 weeks).

Since 2005, the domestic drug ademetionine, Heptor, has been used in patients with alcoholic IDP, ACH, ACP. At a daily dose of 1600 mg per os, Heptor leads to a decrease in somatic and vegetative manifestations, a decrease in biochemical activity after 2 weeks of administration, has a similar safety profile and a low incidence of adverse events that do not require dose reduction or discontinuation compared to the original drug. The unique properties of Heptor allow it to be used in clinical practice for the treatment of alcoholic, toxic, drug-induced liver damage and depression. Heptor is well tolerated, so repeated courses can be recommended.

Against the background of the use of ursodeoxycholic acid (UDCA) preparations in patients with ALD, an improvement in the clinical, biochemical and histological picture was noted. This is probably due not only to its cytoprotective, anti-cholestatic, anti-apoptotic effects, but also to the suppression of the secretion of pro-inflammatory cytokines. In ABP, UDCA is prescribed at a dose of 13-15 mg/kg/day.

The feasibility of using corticosteroid hormones in ALD is controversial. However, in most randomized trials, data were obtained on a significant decrease in mortality with the use of 40 mg of Prednisolone or 32 mg of Metipred for 4 weeks in patients with severe OAH.

Given the role of pro-inflammatory cytokines in the pathogenesis of OAH, it is reasonable to use chimeric antibodies to TNFa (Infliximab, 5 mg/kg), which is significantly accompanied by a regression of clinical and laboratory parameters compared to Prednisolone.

For the same purpose, Pentoxifylline (1200 mg/day per os for 4 weeks) is used as an inhibitor of TNFa, which leads to an improvement in the quality of life and a decrease in mortality in patients with OAH.

Cases of severe course of OAH are accompanied by the development of severe hepatic encephalopathy, the correction of which is carried out by the use of lactulose (30-120 ml / day per os and / or per rectum) and ornithine-aspartate (20-40 g / day intravenously drip until the main manifestations stop this complication).

The use of antibacterial drugs (3rd generation cephalosporins, etc.) in patients with ALD is indicated to prevent and treat infectious complications, as well as to reduce endotoxemia.

Liver transplantation may be the treatment of choice for fulminant OAH.

Pathogenetically substantiated in the treatment of various nosological forms of ALD is the use of antioxidants (selenium, betaine, tocopherol, etc.). However, their effectiveness has not been proven.

In order to influence endogenous toxemia associated with bacterial contamination of the small intestine, it is advisable to include the use of prebiotics that improve the metabolism of intestinal bacteria in the treatment program for patients with alcoholic liver steatosis, ASH. Under the influence of prebiotic preparations in patients with compensated cirrhosis of alcoholic etiology, a decrease in excessive bacterial proliferation in the small intestine was noted, accompanied by a decrease in the severity of hepatic encephalopathy.

Literature

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L. Yu. Ilchenko, doctor of medical sciences, professor
RSMU, Moscow

Version: Directory of Diseases MedElement

Alcoholic hepatitis (K70.1)

Gastroenterology

general information

Short description

alcoholic liver disease is a liver disease caused by long-term use of toxic doses of ethanol. Alcoholic liver disease combines various disorders of the parenchyma structure Parenchyma - a set of basic functioning elements of the internal organ, limited by the connective tissue stroma and capsule.
liver and functional state of hepatocytes hepatocyte - the main cell of the liver: a large cell that performs various metabolic functions, including the synthesis and accumulation of various substances necessary for the body, the neutralization of toxic substances and the formation of bile (Hepatocyte)
caused by the systematic use of alcoholic beverages.

"Alcoholic Hepatitis"- a term adopted in ICD-10 for acute degenerative and inflammatory liver lesions resulting from alcohol exposure and capable of transforming into cirrhosis of the liver Cirrhosis of the liver is a chronic progressive disease characterized by dystrophy and necrosis of the hepatic parenchyma, accompanied by its nodular regeneration, diffuse proliferation of connective tissue and a deep restructuring of the liver architectonics.
.
Alcoholic hepatitis is one of the main variants of alcoholic liver disease. Just like alcoholic fibrosis, alcoholic hepatitis is considered a precursor or initial and obligatory stage of cirrhosis.

Alcoholic hepatitis can also be associated with fatty liver, alcoholic fibrosis, and cirrhosis.

Note. Acute episodes of toxic necrosis of the liver of alcoholic etiology, along with acute alcoholic hepatitis, are referred to as "alcoholic steatonecrosis", "sclerosing hyaline necrosis of the liver", "toxic hepatitis", "acute liver failure of chronic alcoholics".

Classification

Most clinicians distinguish between acute and chronic alcoholic hepatitis.

General classification of alcoholic hepatitis(Loginova A.S. et al.):

1. Chronic alcoholic hepatitis:
- with moderate activity;
- with pronounced activity;
- in combination with alcoholic hepatitis.

2. Acute alcoholic hepatitis (acute alcoholic liver necrosis):
- in combination with chronic alcoholic hepatopathy;
- developed in an intact liver;
- with intrahepatic cholestasis;
- mild (anicteric) form;
- form of moderate severity;
- severe form.

The severity can also be determined by scales (see section "Prognosis"). According to the score obtained (points), alcoholic hepatitis can be divided into severe and non-severe.

Etiology and pathogenesis

Etiology

Alcohol acts as a direct hepatotoxic agent. Its metabolism involves a number of enzymatic systems that convert ethanol to acetaldehyde, and further, acetaldehyde dehydrogenase Acetaldehyde dehydrogenase is an enzyme found in the human liver and is responsible for the breakdown of acetaldehyde (converts acetaldehyde to acetic acid).
(ALDH) metabolizes to its acetate.
The main factor in the development of alcoholic liver disease is the high content of acetaldehyde in it. This causes most of the toxic effects of ethanol, including through increased lipid peroxidation, the formation of stable complexes with proteins, impaired mitochondrial function, and stimulation of fibrogenesis.

The risk of developing alcoholic liver disease occurs with the use of more than 40-80 g of pure ethanol per day. When using more than 80 g of pure ethanol for 10 years or more, the risk of liver cirrhosis increases. There is no direct correlation between the degree of liver damage and the amount of alcohol taken: according to some data, less than 50% of people who drink alcohol in dangerous doses have severe forms of liver damage (hepatitis and cirrhosis).

Pathomorphology

1. Acute alcoholic hepatitis. Histological manifestations:
1.1 Mandatory for alcoholic hepatitis structural changes in the liver:
- perivenular lesion of hepatocytes;
- balloon dystrophy and necrosis;
- the presence of Mallory bodies (alcoholic hyaline);
- leukocyte infiltration;
- pericellular fibrosis.
1.2 Symptoms that are optional for the diagnosis of alcoholic hepatitis:
- fatty liver;
- detection of giant mitochondria, acidophilic bodies, oxyphilic hepatocytes;
- fibrosis of the hepatic veins;
- proliferation of bile ducts;
- cholestasis.

Perivenular hepatocyte damage
Acute alcoholic hepatitis is characterized by perivenular damage to hepatocytes or the third zone (microcirculatory periphery) of Rappoport's hepatic acinus. During the metabolism of alcohol, a more noticeable decrease in oxygen tension in the direction from the hepatic artery and portal vein to the hepatic vein is observed compared to the norm. Perivenular hypoxia contributes to the development of hepatocellular necrosis, which is found mainly in the center of the hepatic hexagonal lobules.

Balloon dystrophy and Mallory bodies
With balloon dystrophy of hepatocytes, swelling of individual hepatocytes is observed with an increase in their size, clarification of the cytoplasm and karyopyknosis. Karyopyknosis - the process of wrinkling of the cell nucleus during dystrophic changes in it
.
Mallory's bodies (alcoholic hyaline) are detected centrilobularly using Mallory's tricolor stain; are formed both in the cytoplasm of hepatic cells and extracellularly. Detection of alcoholic hyaline characterizes the severity of liver damage.
Alcoholic hyaline can have a fibrillar, fine and coarse granular structure. Fibrillar alcoholic hyaline is detected in the midst of acute alcoholic hepatitis. Later, when the disease subsides, it transforms into granular material.

Inflammatory infiltration by polynuclear leukocytes with a small admixture of lymphocytes is determined inside the lobule and in the portal tracts. Inside the lobule, leukocytes are detected in the foci of hepatocyte necrosis and around cells that contain alcoholic hyaline, which is associated with the leukotoxic effect of alcoholic hyaline. When the disease subsides, alcoholic hyaline is less common.

Pericellular fibrosis is an important feature of alcoholic hepatitis, and prevalence is the main predictor of the disease. Alcohol and its metabolites (especially acetaldehyde) can have a direct fibrogenic effect. Fibrous tissue is deposited along the sinusoids and around hepatocytes in the early stages of alcoholic hepatitis. Ito cells, fibroblasts, myofibroblasts, and hepatocytes synthesize various types of collagen and non-collagen proteins.

2. Chronic alcoholic hepatitis:

2.1 Chronic persistent hepatitis: the characteristic manifestations of alcoholic hepatitis are combined with moderate pericellular and subsinusoidal fibrosis in the third zone of the acinar hepatic lobule. In some cases, the portal tracts are dilated and portal fibrosis is observed. This picture can persist for 5-10 years without progressive fibrosis and transition to cirrhosis, even with continued alcohol consumption.

2.2 Chronic active hepatitis: histological picture of alcoholic hepatitis in combination with active fibrogenesis. Along with significant fibrosis, sclerosing hyaline necrosis is noted in the third zone of the lobule. After 3-5 months of abstinence, morphological changes resemble the picture of chronic aggressive non-alcoholic hepatitis.

In chronic alcoholic hepatitis, the progression of the process in some cases is observed even when drinking alcohol is stopped as a result of the addition of an autoimmune destructive reaction.

Epidemiology

Prevalence sign: Common

Age. Acute alcoholic hepatitis often develops at the age of 25-35 years after heavy drinking against the background of 10 or more years of alcohol abuse. The age range for all forms of alcoholic hepatitis can vary from 25 to 70 years. In the United States, the median age of a patient with alcoholic hepatitis is about 50 years old, with alcohol consumption starting at age 17.

Prevalence. According to the most minimal estimates, the number of patients in the population of Western countries is about 1-2%. Due to the asymptomatic course of mild forms of alcoholic hepatitis, in the population of patients who moderately consume alcohol and abuse it, the prevalence of the disease (according to biopsy data) is 25-30%.

sex ratio varies in different countries. It is believed that the rate of development of alcoholic hepatitis in women is 1.7 times higher than in men. However, given the predominance of men in the group of drinkers, the value of the sex ratio in the group of patients remains unknown.

Race. The Caucasoid race has a lower rate of development of alcoholic hepatitis than the Negroid and Mongoloid.

Factors and risk groups

Risk factors for the development and progression of the disease:
- taking from 40-80 grams of ethanol per day for 10-12 years;
- genetically determined phenotypes of enzymes that provide a high rate of ethanol metabolism and the accumulation of acetaldehyde;
- infection with hepatotropic viruses;
- overweight;
- malnutrition;
- female.

Clinical picture

Clinical Criteria for Diagnosis

Anorexia, nausea, vomiting, weight loss, right upper quadrant pain, fever, jaundice, hepatomegaly, splenomegaly, dyspepsia, weakness, nausea, vomiting

Symptoms, course

Anamnesis
The diagnosis of alcoholic hepatitis is associated with certain difficulties, since it is not always possible to obtain sufficiently complete information about the patient.

Criteria for alcohol dependence(diagnosed on the basis of three of the above signs):

The patient's use of alcoholic beverages in large quantities and the constant desire to use them;

Spending most of the time on acquiring alcohol and drinking it;

Drinking alcohol in life-threatening situations or when it violates the patient's obligations to society;

Alcohol consumption, accompanied by a decrease or cessation of the patient's social and professional activity;

Continued alcohol intake, despite the aggravation of the patient's psychological and physical problems;

Increasing the amount of alcohol consumed to achieve the desired effect;
- the appearance of withdrawal symptoms;

The need for alcohol intake to reduce withdrawal symptoms.

Alcohol abuse(revealed in the presence of one or two signs):

Alcohol use, despite the increased social, psychological and professional problems of the patient;

Reuse of alcohol in life-threatening situations.

In doubtful cases, in the diagnosis of any liver disease or if alcohol abuse is suspected, the use of a special questionnaire is recommended.

Varieties of the clinical course of alcoholic hepatitis:

1. Acute alcoholic hepatitis:

1.1 Asymptomatic or insidious course with a gradual onset (about 50% of patients). The only complaint is often dyspepsia.

1.2 The clinical picture of acute toxic liver necrosis is classically characteristic:
- fever (40%);
- dyspepsia Dyspepsia is a disorder of the digestive process, usually manifested by pain or discomfort in the lower chest or abdomen, which may occur after eating and is sometimes accompanied by nausea or vomiting.
;
- pain in the right hypochondrium (50%);
- diarrhea, nausea, vomiting;
- anorexia;
- weakness;
- weight loss.

1.3 Icteric variant - is determined in the presence of jaundice. The most common variant of acute alcoholic hepatitis (35% of cases). Jaundice is usually not accompanied by pruritus, often moderately severe.

1.4 Cholestatic variant (in 5-13% of cases): symptoms of intrahepatic cholestasis Cholestasis is a violation of the progress of bile in the form of stagnation in the bile ducts and (or) ducts.
(pruritus, jaundice, light stools, dark urine, fever).

1.5 Fulminant acute alcoholic hepatitis: may resemble all clinical variants of acute alcoholic hepatitis (except latent), but is characterized by rapid progression with the development of liver and kidney failure and rapid death.

2. Chronic alcoholic hepatitis: manifestations similar to other etiological forms of hepatitis. Dyspeptic disorders are often observed.

Objective examination
Characterized by hepatomegaly Hepatomegaly is a significant enlargement of the liver.
. The liver is enlarged in almost all patients, often compacted, has a smooth surface, painful. The pain is diffuse.
Possible splenomegaly Splenomegaly - persistent enlargement of the spleen
, cutaneous telangiectasias Telangiectasia - local excessive expansion of capillaries and small vessels.
, palmar erythema Erythema - limited hyperemia (increased blood supply) of the skin
.
Alcoholic and hepatic encephalopathy may occur Encephalopathy is the general name for brain diseases characterized by its degenerative changes.
, as well as asterixis Asterixis (symptom of "pop", falling of the hand) - inability to maintain a fixed posture, fluttering tremor - slow and irregular flexion-extension of the limbs
, as an expression of the latter.
Ascites often develops Ascites - accumulation of transudate in the abdominal cavity
, which, with severe fibrosis and obstruction of the central veins, may be resistant to diuretic therapy.

With alcoholic hepatitis, concomitant bacterial infections are often noted: pneumonia, sinusitis, pyelonephritis Pyelonephritis - inflammation predominantly of the interstitial tissue of the kidney and renal pelvis
, active pulmonary tuberculosis, gram-negative septicemia Septicemia is a form of sepsis in which the presence of pathogenic microorganisms in the blood is not accompanied by the formation of metastatic foci of purulent inflammation.
. Possible isolated cases of peritonitis Peritonitis is inflammation of the peritoneum.
and abscess Abscess - a cavity filled with pus and delimited from surrounding tissues and organs by a pyogenic membrane
lungs.

Diagnostics

The criterion for the diagnosis of alcoholic hepatitis is the presence of an alcohol history and specific histological signs (see the section "Etiology and pathogenesis"). Clinical and laboratory parameters play an important role. Imaging of the liver plays a lesser role in diagnosis.

Instrumental Research

1. Ultrasound:
- the liver parenchyma has a diffuse, hyperechoic structure;
- at the stage of cirrhosis - the corresponding sonographic picture.

2.Color duplex sonography Color duplex sonography - a non-invasive and non-radioactive diagnostic method for analyzing arteries and veins (is a combination of Doppler technology with ultrasound imaging)
: identification of the direction of hepatic blood flow, the degree of development of collateral circulation, the presence of blood clots in the vessels of the liver.

3.FEGDS FEGDS - fibroesophagogastroduodenoscopy (one of the methods for examining the upper digestive tract, which allows you to examine the inner surface of the esophagus, stomach and duodenum)
carried out to identify the presence and degree of varicose veins of the esophagus and stomach, to detect portal gastropathy (erosive-hemorrhagic gastritis) and assess the risk of bleeding.
Rectoscopy is used to identify anorectal varicose veins.

4. Laparoscopy Laparoscopy (peritoneoscopy) is a study of the abdominal organs by examining them with the help of medical endoscopes inserted into the peritoneal cavity through a puncture of the abdominal wall.
with a liver biopsy, they make it possible to describe the surface of the liver, the size of the regeneration nodes and morphologically confirm the diagnosis. These studies are carried out only in the absence of contraindications to them. For example, percutaneous puncture liver biopsy is often not feasible due to contraindications (primarily coagulopathy) and is associated with a large number of diagnostic errors.

5. When puncture liver biopsy with histological examination find:
- hepatocytes in a state of balloon and fatty degeneration;
- massive lobular infiltration with a predominance of polymorphonuclear leukocytes and areas of focal necrosis;
- Mallory bodies (sometimes), which, when stained with hematoxylin-eosin, are purple-red cytoplasmic inclusions, consisting of condensed intermediate microfilaments of the cytoskeleton;

To some extent, pronounced fibrosis with a perisinusoidal arrangement of collagen fibers;
- In varying degrees, pronounced intrahepatic cholestasis.
At the advanced stage of acute alcoholic hepatitis, as a rule, there are contraindications to puncture liver biopsy (in these cases, transjugular biopsy may be performed).

6. Magnetic resonance imaging has high rates of sensitivity and specificity in the diagnosis of hepatic steatosis Hepatic steatosis is the most common hepatosis in which fat accumulates in the liver cells.
and cirrhosis, but not hepatitis. There are no criteria for proving the alcoholic nature of the detected changes.

Laboratory diagnostics

The diagnosis of alcoholic hepatitis, like any other form of alcoholic liver disease, is based on evidence of alcohol abuse and evidence of liver disease. None of the changes in the laboratory marker has been definitively associated with alcoholic hepatitis. The etiology of liver disease detected by laboratory testing may be different. In addition, alcohol can be one of a number of factors that cause liver damage. The specific role of alcohol in the development of liver damage can be difficult to assess in a patient with potentially multifactorial liver disease.

Signs of alcohol abuse:
- a sharp increase in the level of gamma-glutamyltransferase in the blood serum and its sharp decrease against the background of withdrawal;

Increasing the concentration of non-carbohydrate transferrin;
- macrocytosis (mean erythrocyte volume> 100 microns 3) associated with high blood alcohol content and toxic effects on the bone marrow; the specificity of this feature is 85-91%, the sensitivity is 27-52%.

Signs of liver damage:
1. An increase in the level of aminotransferases with a predominance of AST by more than 2 times (in 70% of cases). Increasing AST by 2-6 times. AST levels greater than 500 IU/L or ALT greater than 200 IU/L are uncommon and suggest massive necrosis (fulminant form of alcoholic hepatitis), other or combined etiologies of liver damage (eg, viral hepatitis, acetaminophen, etc.).

2. An increase in the level of alkaline phosphatase and hyperbilirubinemia are possible.

In acute alcoholic hepatitis observed:
- neutrophilic leukocytosis up to 15-20 x 10 9 /l, sometimes up to 40x10 9 /l;
- increase in ESR up to 40-50 mm/h;
- hyperbilirubinemia due to direct fraction;
- an increase in the level of aminotransferases (the ratio of AST / ALT - more than 2);

Multiple excess of the level of gamma-glutamyltransferase (in 70% of patients with alcoholic liver disease, GGTP activity is within the normal range);
- with a cholestatic form - an increase in alkaline phosphatase;

Increase in IgA.

Differential Diagnosis

Differential diagnosis of alcoholic hepatitis with the following diseases is carried out:
- non-alcoholic fatty liver disease;
- viral and infectious hepatitis;
- obstruction of the bile ducts;
- neoplastic formations;
- cholecystopancreatitis;
- chronic pancreatitis.

The decisive factor is considered to be a correctly collected alcohol history, negative tests for infectious agents and visualized biliary tract patency. However, in the setting of suspected combined liver disease, it is very difficult to determine the dominant etiological cause. The most reliable diagnostic test in this case is the laboratory determination of CDT (carbohydrate-deficient transferrin).

Complications

Outcomes of alcoholic hepatitis can be:
- fibrosis Fibrosis is the growth of fibrous connective tissue, which occurs, for example, as a result of inflammation.
and sclerosis Sclerosis is a thickening of an organ due to the replacement of its dead functional elements with a connective (usually fibrous) tissue or a homogeneous hyaline-like mass.
liver;
- cirrhosis of the liver;
- hepatic encephalopathy;
- liver cancer.

Infectious complications:
- pneumonia;
- sinusitis Sinusitis - inflammation of the mucous membrane of one or more paranasal sinuses
;
- sepsis;
- liver abscess (rare);
- ICE DIC (disseminated intravascular coagulation, consumption coagulopathy, thrombohemorrhagic syndrome) - impaired blood clotting due to massive release of thromboplastic substances from tissues.
;
- renal failure;
- peritonitis (rare).

Treatment

General provisions
1. The most important principle in the treatment of alcoholic hepatitis is the avoidance of alcohol. The disease can quite quickly and completely regress (compared to hepatitis of other etiologies) with the complete abolition of alcohol intake.

2. There are significant discrepancies in drug therapy between Western and accepted in the CIS recommendations.
3. Many drugs have no (or weak) evidence base and are used either traditionally or based on a small number of studies.

4. Approaches to therapy change over time. The information below reflects the most generally accepted views at the time of writing.
5. Treatment of alcoholic hepatitis depends on many factors:

Form (see section "Classification");
- the severity of the process;
- age of the patient;
- the presence of concomitant diseases and complications.

Diet
It is important to eat a diet that contains sufficient amounts of protein and calories, as people who abuse alcohol often develop a deficiency of proteins, vitamins and trace elements (especially potassium, magnesium and phosphorus).
Deficiencies in folic acid, vitamin B6, vitamin A and thiamine are among the most common.
Trace elements (eg, selenium, zinc, copper, and magnesium) are often altered and, in some cases, are thought to be involved in the pathogenesis of all forms of alcohol disease.
Difficulties arise in the selection of a diet for concomitant diabetes mellitus or obesity, since the spectrum of malnutrition in these patients varies widely from malnutrition to obesity. The American College of Gastroenterology (ACG) and the American Association for the Study of Liver Diseases (AASLD) recommend an average of 1.2-1.5 g/kg protein and 35-40 kcal/kg body weight per day (at least 2,000 kcal/day for an adult). ).
There is evidence of a beneficial effect (when introduced into the diet) of branched-chain amino acids (BCAA).
Evidence for the effectiveness of introducing polyunsaturated fatty acids into the diet is still questionable.
As an alternative route of nutrient administration (for nausea, vomiting, changes in psychological status), an endoscopically inserted enteral tube with a programmable pump can be used. Parenteral nutrition (partial or supplementary) is extremely rare.

Physical activity not recommended in the acute phase. In the future, it should be aimed at weight loss (if there is concomitant obesity). Individuals with chronic alcoholic hepatitis that occurs without significant symptoms, as a rule, limit physical activity is not required.

Infusion therapy
It is used in inpatient treatment of severe forms of acute alcoholic hepatitis (including those with severe cholestasis and, especially, liver failure). Infusion therapy aims at detoxification, correction of acid-base balance, correction of hypoalbuminemia, correction of the coagulation system. Complex saline solutions, albumin, native plasma, or blood clotting factors are commonly used in moderate doses. The introduction of colloids try to avoid.

Medicines

US and UK recommendations
1. Systemic corticosteroids (prednisolone, methylprednisolone) - are prescribed only for severe forms of concomitant liver failure with a course of up to 4 weeks, 40 mg / day. (32 mg / day for metipred), sometimes with a progressive dose reduction by 2 times over the next 2-3 weeks until complete withdrawal. Cause side effects.
2. Pentoxifylline - 400 mg orally 3 times a day, if there are contraindications to systemic corticosteroids.
3. Antioxidant therapy (vitamins C and E and other antioxidants) - does not currently have solid evidence of effectiveness in the treatment of alcoholic hepatitis. Of course, the deficiency of vitamins revealed in the study of blood serum is subject to medical correction, if it is impossible to correct it with a balanced diet.
4. Antibacterial therapy is carried out only with the development of infectious complications.
5. Drugs such as thalidamide, misoprostol, adiponectin, and a group of probiotics have shown good effects in preliminary studies, but are not yet standard therapy.

1. Systemic corticosteroids (prednisolone) - 40 mg / day, for 4 weeks.
2. Ademetionine (Heptral).

3. Silymarin.
4. Essential phospholipids (in the absence of cholestasis), for example, Essentiale.
5 Ursodeoxycholic acid.
6. Antibacterial therapy for prophylactic purposes, short course (fluoroquinols).
7. Colchicine.

Summary. Generally recognized are measures aimed at giving up alcohol, normalizing nutrition, detoxification corrective infusion therapy, as well as prescribing systemic corticosteroids (in severe cases). In the absence of a clear evidence base, other medicines should be prescribed by the doctor, based on the patient's capabilities and his personal experience and judgment.

Surgery. Liver transplant.

Forecast

Non-severe alcoholic hepatitis is a benign disease with negligible short-term mortality. However, when alcoholic hepatitis is severe enough (development of hepatic encephalopathy, jaundice, coagulopathy), mortality can be significant.

The overall 30-day mortality in patients hospitalized with alcoholic hepatitis is about 15%, but in patients with severe forms it approaches or exceeds 50%.
In patients without encephalopathy, jaundice, or coagulopathy Coagulopathy - a violation of the function of the blood coagulation system
The 30-day mortality rate is less than 5%.
In general, one-year mortality after hospitalization for alcoholic hepatitis is about 40%.

Used to predict death Maddrey coefficient(MDF): 4.6 x (difference between prothrombin time in patient and control) + serum bilirubin in mmol/l.
With a coefficient value of more than 32, the probability of death during the current hospitalization exceeds 50%.
According to some studies, MDF may be an inaccurate predictor of mortality in patients with alcoholic hepatitis, especially those receiving glucocorticoids.

Other factors that correlate with a poor prognosis include advanced age, impaired renal function, encephalopathy, and an increase in white blood cell count during the first 2 weeks of hospitalization.

Alternative forecast scales(not widely used):
- The Combined Clinical and Laboratory Index of the University of Toronto;
- Model for end-stage liver disease (MELD);
- Glasgow alcoholic hepatitis score (GAHS);
- Asymmetric dimethylarginine (ADMA).
The last two scales in some studies showed the highest accuracy of the forecast.

Hospitalization

Hospitalization for alcoholic liver disease can be carried out both on an emergency basis and on a planned basis. Patients without signs of a pronounced inflammatory process, liver failure, complications can be treated on an outpatient basis.

Prevention

primary prevention. Refusal to abuse alcohol.

Prevention of complications
Patients recently discharged from the hospital after an acute attack of alcoholic hepatitis should generally be followed up intensively for 2 weeks. Subsequent periodic visits to the doctor are necessary at intervals of a week to several months.
The goal of monitoring patients is to determine whether they are responding to ongoing therapy (including monitoring of electrolyte levels and liver function tests), as well as to control alcohol withdrawal and encourage sobriety.
It should be borne in mind that complete abstinence from alcohol is noted in no more than 1/3 of patients, 1/3 of patients significantly reduce alcohol consumption, and the remaining third ignore the doctor's recommendations. The last patients need the joint work of a hepatologist and a narcologist.

In patients with alcoholic hepatitis who have evidence of liver cirrhosis (especially those with concomitant chronic viral hepatitis B or C), periodic monitoring is necessary to screen for hepatocellular carcinoma. The general screening algorithm includes serum alpha-fetoprotein (AFP) every 6 months and ultrasound every 12 months.

Immunization of patients with alcoholic liver disease against common infectious pathogens, including hepatitis A virus, hepatitis B virus, pneumococcus, and influenza A virus, seems to be a very reasonable approach.

Information

Sources and literature

1. The Merc manual. Medical guide. Diagnosis and treatment / ed. Beers Mark H./trans. from English. ed. Chuchalina A.G., M.: Literra, 2011
2. Damianov I. Secrets of pathology / translation from English. ed. Kogan E. A., M.: 2006
3. "Pentoxifylline for alcoholic hepatitis" Kate Whitfield, Andrea Rambaldi, Jørn Wetterslev, Christian Gluud, Cochrane Hepato-Biliary Group, The Cochrane Library, published online: oct, 2009
4. "The epidemiology and clinical characteristics of patients with newly alcohol-related liver disease: results from population-based surveillance" Sofair AN, Barry V, Manos MM, Thomas A. etc., "Journal of Clinical Gastroenterology", No. 44(4 ), 2010
5. "Treatment of alcoholic liver disease" Thomas H. Frazier, Abigail M. Stocker, Nicole A. Kershner, Luis S. Marsano, "Therapeutic Advances in Gastroenterology", No. 4(1), 2011
6. "Use of serum carbohydrate-deficient transferrin values ​​to exclude alcoholic hepatitis from non-alcoholic steatohepatitis: a pilot study" Ohtsuka T., Tsutsumi M., Fukumura A., "Alcoholism: Clinical and Experimental Research", No. 29, 2005
7. "Alcoholic liver disease" Bueverov A.O., Maevskaya M.V., Ivashkin V.T.
   1. http://www.rmj.ru/ - Russian medical journal. Independent publication for practitioners - No. 9, 2002
8. "Alcoholic hepatitis: Basic principles of treatment" Adzhigaitkanova S.K.
   1. http://www.eurolab.ua/encyclopedia/565/46022/
9. "General principles of treatment of acute alcoholic hepatitis" Bueverov A.O.
   1. http://www.rmj.ru/ - Russian medical journal. Independent publication for practicing physicians - №1, 2004

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When the shape and volume of the patient's liver changes on the background of alcoholism, alcoholic hepatitis is diagnosed. This is a degenerative disease with a risk of developing cirrhosis. It requires surgical treatment of the disease, the rejection of alcoholic beverages and the transition to a healthy lifestyle. Learn how to recognize hepatitis at home, what symptoms it is characterized by.

What is alcoholic hepatitis

In 1995, the term "alcohol hepatitis" was coined, which indicates a characteristic of liver damage due to ethanol consumption. This disease is inflammatory, causes cirrhosis. Alcohol toxins enter the liver, where acetaldehydes are formed, which damage cells. The disease becomes chronic after six years with the constant use of ethanol. Hepatitis C and alcohol are not directly related, but the development of a toxic disease contributes to the daily intake of 50-80 g of alcohol for men, 30-40 g for women and 15-20 g for adolescents.

Alcoholic hepatitis - symptoms

Depending on the form of manifestation of the disease, the following symptoms of alcoholic hepatitis are distinguished:

1. Persistent form - proceeds hidden, the patient is unaware of the disease. Signs of it can serve as heaviness in the right side under the ribs, nausea, belching, pain in the stomach. The type is detected with the help of laboratory tests, it is treated by giving up alcohol and following a diet.
2. Progressive form - it is formed in the absence of treatment of persistent hepatitis, is considered a harbinger of cirrhosis. The patient's condition worsens, foci of necrosis are observed in the liver (the cells die completely). Signs are: vomiting, diarrhea, fever, jaundice, pain in the right side. Without treatment, the disease threatens death from liver failure.

Signs of alcoholic hepatitis

Depending on the development and course of the disease, special signs of hepatitis are distinguished. The disease can be acute (icteric, latent, fulminant and cholestatic) and chronic. If the first symptoms are pronounced, pronounced (the patient may turn yellow, experience pain and deterioration), then the second may be asymptomatic and mild.

Acute alcoholic hepatitis

OAH, or acute alcoholic hepatitis, is considered a rapidly progressive disease that destroys the liver. It appears after prolonged drinking. There are four forms:

1. Icteric - weakness, pain in the hypochondrium, anorexia, vomiting, diarrhea. In men, there is jaundice without skin itching, weight loss, nausea. The liver is enlarged, thickened, smooth, painful. The patient's hands tremble, ascites, erythema, bacterial infections, fever may appear.
2. Latent - diagnosed only by a laboratory method, biopsy, latent leakage.
3. Cholestatic - rare, symptoms are severe itching, colorless feces, jaundice, dark urine, impaired urination.
4. Fulminant - symptoms progress, hemorrhages, jaundice, renal failure and liver encephalopathy are observed. Due to coma and hepatorenal syndrome, death occurs.

Chronic alcoholic hepatitis

The absence of obvious symptoms is characterized by chronic alcoholic hepatitis. It is detected only by laboratory tests - transaminase activity, cholestasis syndrome are checked. The indirect development of the disease is indicated by the criteria for alcohol dependence:

• drinking large amounts of alcohol, desire to drink;
• withdrawal symptoms;
• increase in alcohol dosage.

How to recognize hepatitis at home

To correctly recognize hepatitis at home, you need to pay attention to the patient. If he has at least one sign of an acute course of the disease, the intervention of a doctor is necessary. When observing indirect signs of involvement in alcoholism, you should also contact specialists to examine the liver and identify abnormalities in its function.

If the disease is not treated in time, complications are possible, up to the death of the patient against the background of liver necrosis:

• high blood pressure;
• intoxication of the body;
• hypertension, varicose veins;
• jaundice, cirrhosis.

Is toxic hepatitis contagious?

According to doctors, alcoholic toxic hepatitis is considered a non-contagious disease, because it occurs as a result of poisoning the body with a chemical substance. It develops against the background of long-term use of alcoholic beverages in large quantities, affects only the patient's body. For treatment, it is important to eliminate the destructive factor and increase the functionality of the organs.

How to treat alcoholic hepatitis

To effectively treat alcoholic hepatitis of the liver, you must definitely stop drinking alcohol and consult a doctor. He will prescribe complex therapy, including:

• detoxification - droppers, intravenous or oral cleansing drugs;
• visiting a psychologist, narcologist to eliminate a bad habit;
• energy diet, it is recommended to consume more proteins;
• surgical or drug treatment - you can remove foci of necrosis, take methionine and choline to replenish the lipid function of the organ;
• intramuscular injection of vitamins, potassium, zinc, nitrogen-containing substances;
• the use of corticosteroids in severe disease;
• taking hepatoprotectors (Essentiale, Ursosan, Heptral);
• elimination of etiology factors;
• taking antibiotics with the development of bacterial, viral infections or the development of a severe form of the disease.

Doctors forbid self-treatment, since liver damage can be serious and lead to uncontrolled consequences. If the case is very severe and neglected, it may require liver transplantation, the engraftment prognosis is average. As a strengthening treatment after elimination of symptoms and acute course, traditional medicine based on corn stigmas, milk thistle can be used.

These rules are used to prevent the occurrence of a recurrence of the disease:

• reduction of doses of alcohol or complete rejection of it;
• compliance with medication, refusal of alcohol during treatment;
• proper nutrition, complete in calories and BJU.

Diet for alcoholic hepatitis of the liver

In the majority of patients with alcoholic hepatitis in the clinical history, there was an exhaustion of the body due to the lack of good nutrition. To improve health and reduce the severity of the liver, a special diet is needed. The diet for alcoholic hepatitis includes the following recommendations:

• rejection of fatty meat, lard, fish, eggs, canned and smoked foods;
• a ban on mushrooms, seasonings and sauce, pastries, white bread, strong tea, coffee;
• you can not eat nuts, onions, garlic, sorrel, radish, confectionery, ice cream;
• do not abuse the intake of carbonated water, fatty cheeses, cottage cheese, sour cream, butter;
• a categorical ban on alcohol, nicotine;
• products can be steamed, baked, boiled;
• inclusion in the diet of cereals, dried toast, bran, dairy products, veal, lean fish, fat-free cottage cheese, chicken;
• it is useful to eat vegetables, fruits, green tea, dried fruits, green vegetables, figs;
• meals 5-6 times a day, separate - do not mix proteins with carbohydrates in one meal, eat fruits separately.

Alcoholic hepatitis

Studies have shown that 1 average resident of Germany accounts for about 9.5 liters of alcohol per year, and 10 liters per resident of Russia. The gap is small, but the amount is very dangerous, because with such an active consumption of strong drinks, a person runs the risk of getting cirrhosis of the liver, which is preceded by alcoholic hepatitis. This disease develops from drinking alcohol, leading to inflammatory liver damage that can develop into cirrhosis. It has many forms, is difficult to diagnose, requires long-term treatment and recovery.

About what is alcoholic hepatitis, what are its symptoms and treatment, we will now tell.

Types of alcoholic hepatitis

Alcoholic hepatitis is divided into several types, depending on the symptoms and course of the disease. Consider their signs and features.

Persistent form

With this form of the disease, there are very few symptoms of alcoholic hepatitis, and patients most often complain of such manifestations:

• Nausea and belching.
• Pain on the right (in the region of the liver).
• Heaviness in the stomach.

The presence of liver disease is detected by laboratory tests, after which the attending physician prescribes a diet and strongly advises to give up alcoholic beverages. After six months, there is an improvement in the patient's condition, but the unpleasant consequences of this liver disease accompany a person for 5-10 years. If time does not begin to treat alcoholic hepatitis at this stage, then it flows into the next form - progressive.

progressive form of the disease

This form is observed in 20% of patients who suffer from alcoholic hepatitis, and it is a harbinger of imminent cirrhosis. Symptoms of alcoholic hepatitis in a progressive form are pronounced:

• Jaundice and fever.
• Vomiting and diarrhea.
• Severe pain in the right hypochondrium.

Non-specific symptoms may also appear, corresponding to the stage of the disease (mild, moderate, severe). If this form of liver disease is left untreated, then the patient will die, the cause of which is acute liver failure.

Forms of the disease and the causes of its development

According to the intensity of the course of the disease, the following types can be distinguished:

Features of the course of the acute form

This type of disease is seen in patients who suffer from other liver problems (cirrhosis, hepatitis) but regularly consume alcoholic beverages.

Acute alcoholic hepatitis is accompanied by the following symptoms:

• A very strong weakness.
• Jaundice.
• Pain in the hypochondrium.
• Nausea and vomiting.
• Weight loss and stool changes.

Acute alcoholic hepatitis can also occur in several forms:

• The icteric appearance is most common, the symptoms are weakness, yellowness of the skin, fever, pain.
• Cholestatic is characterized by the highest mortality. The manifestation of the disease is accompanied by jaundice, itching, colorless feces and dark urine.
• The fulminant appearance develops very quickly and is difficult to cure. But in the absence of treatment, the patient dies 14-20 days after the transition of the disease to the acute phase from hepatic-renal failure.
• Latent, characterized by an asymptomatic course and difficult diagnosis.

In all of the above cases, there is a significant increase in the liver, some patients have anorexia.

Chronic form

Classical chronic alcoholic hepatitis develops with regular alcohol consumption, but without concomitant liver disease. It is difficult to identify this form of the disease; an examination of the liver and its changes, as well as an increase in the level of transaminase, will help in making a diagnosis.

Chronic alcoholic hepatitis is almost asymptomatic, and the patient may complain of the following discomfort:

• Decreased appetite and nausea.
• Poor sleep, in men, the mammary glands increase.
• Decreased sexual activity.
• Pain in right hypochondrium and liver enlargement.
• Vascular stars, white nails.

The development of this form of the disease leads to the frequent use of alcohol, which is 70 g of pure ethanol for men, 20 g for women.

Who is at risk?

Scientists have proven that most of the alcohol, or rather the ethanol that it contains, is broken down by the liver. About 20% of ethanol is broken down in the stomach, turning into acetaldehyde. This substance destroys cells and leads to pathological changes in internal organs. Note that alcohol is doubly dangerous for women, because the ability of a woman's stomach to break down ethyl is two times lower than that of a man.

A high probability of getting hepatitis in people who have been drinking 100 g or more of pure alcohol daily for several years. 50 ml of vodka contains 20 g of alcohol, it turns out that 250 ml contains 100 g of pure alcohol, and this is already a dangerous dose.

Doctors also identify the following reasons that can accelerate the development of the disease:

1. Long-term alcohol use (more than 5 years).
2. Drinking alcohol in large quantities.
3. genetic predisposition.
4. Obesity and bad habits.
5. Overeating, lack of healthy foods high in protein.

Also, the cause of the development of the disease is poor ecology, which weakens the immune system, poor-quality food and cheap alcohol made from chemical components. And if the patient drinks strong antibiotics and other medicines, while continuing to drink alcohol, then he also falls into the risk group.

Now consider how to treat the disease and recover from it.

How is the disease diagnosed?

To diagnose the disease, modern laboratory and hardware techniques are used. Ways diagnostics depend on the patient's complaints, the clinical picture and the form of the disease. For example, if a person suffers from a latent form of the disease, then a biopsy is required, and an ultrasound of the abdominal organs will reveal the chronic form.

Most often, the following laboratory tests can be prescribed to the patient:

1. General analysis of blood and urine.
2. Biochemistry of blood and liver sample.
3. Analysis to assess blood clotting and cholesterol.

Depending on the nature of the course of the disease, ultrasound, MRI or CT may be prescribed, but these methods are ineffective. The best diagnostic option is a biopsy.

Features of treatment

Treatment usually begins after diagnosis. The main factor in the treatment of alcoholic hepatitis is diet, in these cases, treatment table No. 5 is prescribed, we will talk about it later.

For the treatment of alcoholic hepatitis, the following medicines are used:

1. Detoxification therapy may be prescribed, during which drugs are administered intravenously. The therapy helps in a short time to cleanse the body, increase its endurance and prepare the patient for drug treatment.
2. Metabolic and coenzyme therapies aimed at improving the metabolism in the cells of the body.
3. Drugs that help liver cells to remain active, and also contribute to their speedy regeneration.
4. Drugs that are analogues of the hormones of the adrenal cortex. This group of drugs suppresses the production of antibodies and inflammatory processes, prevents tissue scarring.
5. Naturally, for the treatment of any alcoholic hepatitis, the patient is prescribed a course of vitamins, including vitamins A, B, C, E and others. The disease is accompanied by a deterioration in the function of absorption of nutrients.

The above drugs are prescribed by a doctor, the dosage and duration of administration are calculated individually, depending on the form of the disease, its neglect, and diet. Note that it is necessary to abandon the use of ethyl, otherwise the therapy will be ineffective.

Features of the treatment table No. 5

A set of diets for various diseases was developed by the Soviet nutritionist Pevzner, and although they are actively criticized today, their use gives good results in the treatment of various types of alcoholic hepatitis. In particular, with this disease, treatment table No. 5 is used, which helps to solve such problems:

1. Restoration of liver function.
2. Restoration of the activity of the biliary tract.

The diet menu spares the liver, relieves the load from it and improves the work of medicines. Consider the list of prohibited foods:

Very fresh bread and flour products.
All fatty fish and meats.
Strong broths: meat fish, mushroom, okroshka, cabbage soup.
Any smoked, spicy and overly salty foods.
Dairy and sour-milk products with high fat content.
Eggs, hard boiled or fried.
Legumes, spicy and fatty sauces.
Ice cream, chocolate and sweets, products with cream.

The diet is rich in protein foods (cottage cheese, meat, fish), but all dishes should be non-fat, steamed or in foil in the oven.

The calorie content of the diet is about 3000 kcal, the daily amount of protein is 90 g, carbohydrates 400 g, and fats 80 g, but 30% of them should be vegetable. The patient must consume up to 3-4 liters of fluid per day, reducing the amount of salt to 4 g. Thus, the vital organ is unloaded, the body is cleansed, and the duration of the diet can be either 14 or 21 days.

How long does the treatment take?

With a timely visit to the hospital and the early abandonment of a bad habit, a favorable prognosis can be made. The liver is able to recover, so the treatment of alcoholic hepatitis in the initial stages gives good results, and the patient can forget about the unpleasant disease for a long time.

But remember that with a successful cure, you must avoid drinking alcohol, otherwise you can again be under a dropper. And in especially neglected cases, the likelihood of death increases.

How to avoid this disease?

To avoid most liver diseases, it is enough just not to drink alcoholic beverages, exclude fatty foods from your menu, and try to smoke less. But even if you rarely drink alcohol, and the next morning after the feast you feel a pulling pain on the right side under the ribs, then do not delay going to the doctor, because these may be manifestations of the first symptoms of alcoholic hepatitis.

Alcoholic hepatitis

Alcoholic hepatitis- These are pathological changes in the liver, characterized by signs of inflammation, fatty degeneration, fibrosis, the cause of which is the toxic effect of alcohol metabolites on the organ. With the continuation of the action of the etiological factor, liver changes turn into cirrhosis - irreversible damage. The severity of the disease is determined both by the dose and the quality and duration of alcohol intake. Hepatitis can occur in acute or chronic form. Treatment is aimed at giving up alcohol, providing a sufficiently high-calorie and nutritious diet, and normalizing the functional state of the liver.

General information

Alcoholic hepatitis is a disease that is one of the main manifestations of alcoholic liver disease, which in modern gastroenterology, along with alcoholic fibrosis, refers to the precursors or initial manifestations of liver cirrhosis. As a rule, this disease develops after five to seven years of regular use of alcohol. Pathology progresses with continued use of alcoholic beverages.

The cause of alcoholic hepatitis is long-term alcohol abuse. In men, liver damage can develop when drinking 50-80 grams of alcohol per day, in women - 30-40 grams, in adolescents - 15-20. The rate of development and progression of the disease is determined by the quantity, frequency of alcoholization, the quality of drinks consumed, the individual characteristics of the organism, and the duration of abuse.

The likelihood of developing alcoholic liver damage is higher in individuals with genetic characteristics of alcohol-metabolizing enzymes, in patients who have had viral hepatitis, as well as in initial nutritional deficiencies.

Alcohol intake is accompanied by its metabolization in the liver to acetaldehyde, which has the ability to damage hepatocytes (liver cells). The cascade of chemical reactions triggered in the body by this substance causes hypoxia of hepatocytes, and as a result, their death. As a result of toxic alcoholic damage to the liver, a diffuse inflammatory process develops in its tissue.

Classification

Alcoholic hepatitis can be either persistent or progressive. The persistent course is a relatively stable form of the disease, while in the conditions of stopping the use of alcohol, damage to liver cells is reversible. Continued alcoholization leads to a transition to a progressive form.

The progressive form (divided into mild, moderate and severe degrees according to activity) is characterized by small-focal necrotic liver damage, which often turns into cirrhosis. Timely treatment of this form leads to stabilization of the process, residual effects persist.

Depending on the course, acute and chronic alcoholic hepatitis are distinguished. The acute course is characterized by acute progressive liver damage. About 70% of cases of long-term abuse are caused by acute hepatitis, which in 4% of cases very quickly turns into cirrhosis. This form can occur in the following variants: latent, icteric, cholestatic and fulminant. Severe variants of acute alcoholic hepatitis often develop against the background of existing cirrhosis after heavy drinking.

Symptoms of alcoholic hepatitis

The latent variant of the course does not have characteristic symptoms. Patients feel some heaviness in the hypochondrium on the right, slight nausea. This variant is usually detected by the results of laboratory tests (increased transaminases). Definitive diagnosis requires a biopsy.

The icteric variant of the course is the most common. Characteristic signs are complaints of severe weakness, anorexia, pain in the right hypochondrium, diarrhea, nausea, vomiting, weight loss, yellowing of the skin, sclera. Possible increase in body temperature. The liver is enlarged, smooth (with cirrhosis - bumpy), painful on palpation. The detection of symptoms such as splenomegaly, ascites, palmar erythema (reddening of the palms), telangiectasia, indicates the presence of background cirrhosis.

The cholestatic variant of alcoholic hepatitis is less common, its characteristic features are intense pruritus, discoloration of feces, jaundice, and dark urine. This option has a protracted course. The fulminant variant is characterized by rapid progression of hepatorenal, hemorrhagic syndrome, marked changes in laboratory markers. Against the background of hepatic coma, hepatorenal syndrome, the outcome can be fatal.

The chronic course of alcoholic hepatitis is characterized by a moderate severity of clinical signs and laboratory markers. The diagnosis is based on the characteristic features found on liver biopsy, which indicate the presence of inflammation in the absence of cirrhosis.

Diagnostics

Diagnosis of alcoholic hepatitis can be associated with certain difficulties. The mild course of the disease may not be accompanied by any specific symptoms, and it can be suspected only if changes in laboratory parameters are detected.

Laboratory signs of the acute form are leukocytosis, less often - leukopenia (with the toxic effect of alcohol on the bone marrow), B12-deficiency anemia, accelerated ESR, and an increase in markers of liver damage. Ultrasound examination of the liver reveals an increase in its size, heterogeneity of the structure, smooth contours. Magnetic resonance imaging (MRI of the liver) determines collateral hepatic blood flow, concomitant damage to the pancreas.

In the chronic form, an ultrasound examination of the liver reveals a slight or moderate enlargement of the liver, an increase in its echogenicity, and a uniform structure. Laboratory parameters changed moderately. A liver biopsy with alcohol damage reveals specific signs of inflammation, fibrosis, and necrosis. The severity of damage depends on the form of the disease and its duration.

Identification during the examination of signs of liver damage should be combined with anamnestic data indicating long-term use of alcohol, as well as the presence of dependence, abuse. This is difficult, because the doctor does not always have complete information about the patient. That is why relatives should be involved in collecting a complete anamnesis, since patients often significantly underestimate the amount of alcohol they drink.

Also, characteristic external signs of alcoholic disease (alcoholism) are revealed: puffiness of the face, tremor of the hands, tongue, eyelids, atrophy of the muscles of the shoulder girdle, Dupuytren's contracture (fibrous change in the palmar tendons, leading to their shortening and flexion deformity of the hand), damage to the peripheral nervous system, and others. target organs (kidneys, heart, pancreas, central nervous system).

Treatment of alcoholic hepatitis

Therapy of this disease should be complex. The main directions of treatment are the elimination of the damaging factor, the appointment of an appropriate diet, and drug therapy. Any form of alcoholic hepatitis first of all requires the termination of the etiological factor - alcohol. Without alcohol withdrawal, the progression of damage is inevitable. In mild forms, this is already enough for the reverse development of changes in the liver.

Alcoholic hepatitis is accompanied by malnutrition in most patients. The more severe the damage to the liver, the more pronounced trophic insufficiency. The recommended energy value of the daily diet is about 2000 calories. The protein content should be 1 g per kilogram of weight. Adequate intake of vitamins, unsaturated fatty acids is required. In the case of anorexia, tube enteral or parenteral nutrition is prescribed. Amino acid infusions reduce protein catabolism (expenditure of interstitial protein reserves), improve brain tissue metabolism.

Drug therapy includes the appointment of essential phospholipids, which reduce fatty changes in the liver, have an antioxidant effect, slow down liver fibrosis, and accelerate the regeneration of its cells. Also, with alcohol damage, especially the cholestatic form, ursodeoxycholic acid preparations are prescribed, which have a cytoprotective effect. In order to achieve an antioxidant effect, blocking the production of acetaldehyde, damage to cell membranes, silymarin-containing hepatoprotectors are prescribed.

Treatment of the acute form includes detoxification therapy, administration of plasma-substituting solutions, and correction of electrolyte disturbances. In severe cases with a syndrome of hepatocellular insufficiency, glucocorticosteroids are used. Treatment of the chronic form is carried out taking into account the degree of liver damage. The presence of fibrosis requires a complete rejection of alcohol. Drug therapy includes the appointment of drugs that affect the process of fibrosis, γ-interferon, glycine.

Forecast and prevention

The basis for the prevention of alcoholic hepatitis is the restriction of alcohol consumption, in order to prevent the progression of existing liver damage - a complete refusal. In patients with mild to moderate severity of alcoholic hepatitis, with the complete cessation of the action of acetaldehyde, the prognosis is good - complete restoration of liver function is possible. Currently, in order to treat this pathology, highly effective drugs are used that can cure the disease or stabilize the patient's condition for a long time, preventing the transition to liver cirrhosis.

Treatment should be carried out by a hepatologist or gastroenterologist together with a psychotherapist and a narcologist, since the decisive factor is the refusal of alcohol. With continued action of the etiological factor, the disease is complicated by cirrhosis of the liver. This is an irreversible condition, which is the final stage of alcohol damage. In this case, the prognosis is poor. These patients are at high risk of developing hepatocellular carcinoma.

Symptoms and treatment of alcoholic hepatitis

Alcoholic hepatitis - pathological changes in the liver, which are accompanied by inflammatory signs, fatty degeneration. The etiology is due to the regular toxic effects of alcohol metabolites on the gland. With alcohol dependence, cirrhosis, a primary cancer, develops over time.

If cirrhotic processes develop only in alcoholics with "experience", then for the development of the alcoholic form of hepatitis, it is enough to use 50 g of alcohol for a long time - at least five years. According to official statistics, mortality due to acute hepatitis is 20-60%, based on the course of the disease.

How many live with alcoholic hepatitis, what symptoms manifest pathology, diagnosis and features of drug treatment - in detail in the article.

Liver and alcohol

Excessive consumption of alcoholic products on a regular basis leads to poisoning of the human body. Alcohol in large doses is poison to humans. In a small amount, ethanol is produced by the body itself, takes an active part in a number of biological and chemical processes.

Poison is the amount of alcohol that exceeds the safe daily dose. So, this is more than 30 ml of alcohol 40% degrees (vodka, whiskey), from 75 ml of 17% drink (fortified wine), from 100 ml of 11-13% alcohol (champagne) and more than 250-330 ml of beer.

Moreover, even the situation when a person does not have alcoholism is called abuse, but he uses the above dosages 4-5 times a week.

After the consumption of alcoholic products, the body tries to get rid of toxic substances - the splitting process begins in the oral cavity, then ethanol is neutralized by 20% in the stomach. The speed is due to food intake, the acidity of gastric juice. Due to gastric reactions, a component is formed - acetaldehyde, which has a toxic effect.

The rest of the amount is excreted through the lungs, enters the liver. There, ethanol is first transformed into acetaldehyde, then into acetic acid. The latter does no harm, because through several biochemical reactions it breaks down into components in the form of water and carbon dioxide.

Disease pathogenesis

With the constant use of alcohol, the enzymatic function of the liver worsens.

This is based on the fact that acetaldehyde damages liver cells, fatty transformation (steatosis) is observed.

The process goes like this:

• Lipid acids are formed in the liver cells. When ethanol enters them, the process is disrupted.
• The gland perceives a violation of the natural process as an inflammatory reaction, therefore, a high concentration of TNF is formed in it.
• As TNF levels rise, triglycerides accumulate.

Ethanol also leads to cholestatic syndrome. The patient develops early stage fibrosis. It is reversible, but if the effect of ethanol is not eliminated, then the disease will soon begin to progress.

Forms and varieties of alcoholic hepatitis

Hepatitis can be divided into two large groups - alcoholic and non-alcoholic (this category includes infectious, viral diseases that can be transmitted from a sick person). Downstream, the classification is represented by two forms - acute hepatitis - diagnosed with alcoholism in 70% of clinical pictures and a chronic illness.

Acute form and symptoms

Alcoholic hepatitis is a consequence of the negative effects of alcohol; people cannot become infected with this type of disease.

Symptoms of acute alcoholic hepatitis are most often manifested in men who have been addicted to alcohol for 3-5 years. In very rare cases, the acute course of the disease manifests itself after a few days of drinking. In this case, the strongest intoxication, inflammatory reaction and destructive processes in the liver are revealed.

Often, the alcoholic form of hepatitis appears against the background of already existing cirrhosis of the liver (alcohol is not always the cause of development). Additional provoking factors include smoking, malnutrition, taking medications that adversely affect the functionality of the liver.

For the first time, hepatitis of alcoholic origin manifests itself after the consumption of a significant dosage of alcohol.

Acute symptoms:

1. Nausea, vomiting.
2. Bitterness in the mouth.
3. Loss of appetite.
4. The body temperature rises to 38 degrees.
5. Pain in the projection area of ​​the liver.
6. Disruption of the digestive tract.
7. Increased gas formation.
8. Weakness.
9. Mental disorders.

1-3 days after the detection of clinical signs, jaundice is observed - the mucous membranes, the whites of the eyes and the skin become yellow.

The duration of the acute form varies from 3 to 5 weeks. In a mild form, blood biochemistry is relatively normal, in severe cases, the main analysis indicators increase tenfold, there are signs of hepatocellular insufficiency. To determine the degree of damage, ultrasound, CT is performed.

Forms depending on the course of an acute illness

In medical practice, there is a classification of acute hepatitis of alcoholic origin, depending on the course.

Alcoholic hepatitis: acute and chronic, clinical guidelines

Alcoholic hepatitis is considered the main variant of alcoholic pathology of the organ. He, like alcoholic fibrosis, is an indispensable harbinger of cirrhosis.

Is alcoholic hepatitis contagious?

Some believe that all serious liver diseases are contagious. There is some truth in this - hepatitis B and C are transmitted parenterally. It is not uncommon for people to die from these diseases caused by viruses.

Alcoholic hepatitis: how long do they live with it

Many people who abuse alcohol think they can do it without any serious consequences for their body. They believe that when the first signs of liver pathology appear, they will stop drinking, and their health will return to normal.

Disease pathogenesis

Among all alcoholic liver diseases (ALD), alcoholic hepatitis occupies a special place. The probability of its development is directly dependent on the frequency of consumption of alcoholic beverages and their volume. It does not matter what a person drinks - beer, vodka, wine or whiskey.

The disease develops slowly: if you regularly consume critical doses of ethanol-containing drinks, fatty liver will first occur. After a sufficiently long period of time, fatty degeneration transforms into alcoholic steatohepatitis, and everything ends with cirrhosis of the liver.

Causes and methods of diagnosis

In those who have abused alcohol for 5-7 years, specialists diagnose a chronic form of alcoholic hepatitis. The rate of progression of the disease is directly dependent on the presence of hereditary factors and the patient's health status.

However, according to studies, daily intake of even 50 g of alcohol for a long period of time can become an impetus for the development of alcoholic hepatitis. These data are primarily for men. In women, the disease occurs 2 times faster, and the dose of alcohol that can provoke its development is also less.

Diagnosing alcoholic hepatitis is easy: you just need to find out how long and how much a person drinks alcohol.

• If a person weighs 70 kg, and every day during the year he drinks 150-180 ml of vodka, then there are already characteristic changes in his liver.
• If a person's alcohol experience is more than 3 years, we can safely say that he is the "owner" of liver failure in a chronic form.

The diagnosis of alcoholic hepatitis is simple. To do this, it is enough to find out the anamnesis, examine and question the patient.

Types of alcoholic hepatitis

Persistent form

The persistent form of alcoholic hepatitis most often occurs without pronounced symptoms. For a long time, a person does not even suspect that his liver is sick.

From time to time he feels:

• heaviness in the right hypochondrium;
• slight nausea and belching;
• discomfort in the stomach.

The persistent form of this disease can be detected using laboratory tests. If detected early, it responds well to treatment. If you follow the diet prescribed by the doctor and stop drinking alcohol, you will feel better in the first 6 months.

progressive form

Progressive alcoholic hepatitis is a harbinger of liver cirrhosis. A similar pathology occurs in 20% of patients suffering from alcoholic hepatitis.

In the patient's liver, cells begin to die quickly, sometimes foci of necrosis form, and the state of human health deteriorates sharply.

The characteristic signs of the disease include:

• vomiting and diarrhea, indicating toxic damage to the body;
• fever
• jaundice;
• pain in the right hypochondrium.

acute form

Alcoholic hepatitis, depending on the degree of intensity of the development of pathology, is divided into acute and chronic.

The acute form of the disease is diagnosed in patients who already have certain liver problems (cirrhosis, chronic hepatitis), but continue to drink alcoholic beverages.

The disease can occur in one of four forms:

• icteric;
• fulminant;
• latent;
• cholestatic.

The icteric form of alcoholic hepatitis is one of the most common. However, in patients:

• yellowing of the skin and mucous membranes;
• weakness and nausea appear;
• the stool is broken;
• there is pain in the right hypochondrium;
• vomiting opens;
• weight is reduced.

The phase of exacerbation of latent hepatitis does not have pronounced symptoms. The disease can be detected only after certain laboratory tests are carried out: a blood test will show a significant increase in the level of transaminase, the result of a biopsy is the presence of a developing inflammatory process in the liver.

The cholestatic form of the disease is characterized by the appearance of:

• skin itching;
• jaundice;
• discolored feces;
• dark urine.

The fulminant form of acute alcoholic hepatitis is the most dangerous. The result of its progression is the development of hemorrhagic syndrome, renal failure and hepatic encephalopathy.

Chronic form

Alcoholic hepatitis in a chronic form is accompanied by:

• Bloating and rumbling in the abdomen;
• Decreased appetite;
• nausea;
• Pain in the right hypochondrium;
• Enlargement of the liver;
• Decreased libido;
• Hypogonadism (insufficient secretion of androgens);
• Gynecomastia (enlargement of the mammary glands in male patients);
• Sleep disturbance;
• An increase in temperature;
• The appearance of Dupuytren's contracture (shortening of the palmar tendons).

The symptoms of alcoholic hepatitis, as well as the methods of its treatment, are individual. Often, those suffering from chronic alcoholic hepatitis note the presence of only one or two (in rare cases, several) characteristic signs of this liver pathology.

Treatment of alcoholic hepatitis

Treatment of alcoholic hepatitis, like all other liver diseases, is possible only with a complete refusal to drink. Unfortunately, many people suffering from this pathology simply cannot fulfill such a condition: their craving for alcohol is too great.

According to statistics, only 30% of patients are able to stop drinking alcohol during treatment. Another 30% of patients are ready to gradually reduce the dose of alcohol they drink, and the rest, unfortunately, continue to drink during therapy. Patients in this category become regular clients of not only hepatologists, but also narcologists.

By avoiding alcohol, you can get rid of not only jaundice, but also a whole range of symptoms.

To achieve maximum results, specialists use all methods, including:

• diet therapy;
• conservative treatment;
• surgical intervention.

Due to the long-term use of alcoholic beverages, the digestive system is disrupted. In the process of treating the liver, the patient's nutrition should be balanced, vitamins, nutrients and trace elements should be supplied to his body regularly and in the required quantities.

With alcoholic hepatitis, the patient is required to follow a strict diet. Doctors recommend nutrition according to Pevzner (table number 5).

The Pevzner diet has a number of features:

• Dishes must be boiled or baked. Fried foods are prohibited.
• Spicy, salty, fatty and cold foods should be excluded from the diet.
• Foods that contain coarse fiber (stringy meat and vegetables) should be rubbed on a grater before use.
• Meals should be fractional (at least 5 times a day), portions should be small and equal in volume.
• You can not drink coffee, cocoa, carbonated drinks, grape juice and, of course, drink alcoholic beverages.
• Under the ban are broths from meat, fish, mushrooms. In priority soups from vegetables and fruits.

Medications

Alcoholic hepatitis is treated with hepatoprotectors - drugs, conditionally divided into 5 categories:

• Milk thistle-based products that can support the active work of liver cells.
• Means based on ademetionine, which protect liver cells from damage and contribute to the normalization of the outflow of bile and the removal of toxins.
• Means containing in their composition bear bile, which accelerates the recovery processes.
• Organic preparations of animal origin, contributing to the activation of intracellular renewal processes.

If hepatitis is severe, you can not do without the use of antibacterial agents: they will minimize the risk of infection. A special role in the treatment of alcoholic hepatitis is given to detoxification measures, which consist of courses of injections of special drugs that stop most of the symptoms of the pathology.

Surgery

Surgical treatment involves a liver transplant. Currently, such operations are rare and quite expensive. Liver transplantation is performed only if the patient is diagnosed with the last degree of liver failure.

It's not just the high cost of the operation. The problem, most often, is finding a donor. They can only become the owner of excellent physical and mental health, it is best if the donor is a relative of the patient. The donor will have to donate 60% of his liver: after the operation, the organ will be able to recover to its original volume.

The only way to avoid the tedious and lengthy treatment of alcoholic hepatitis and the difficulties associated with it is the prevention of the disease, which implies the refusal to drink alcohol.

Everyone should know the permissible daily dose of ethanol: men experience the first symptoms of alcohol intoxication after consuming 40 g of a substance, while women need 2 times less - 20 g.

The possibility of developing alcoholic hepatitis in a regularly drinking person is influenced by factors such as the volume of drinks consumed, lifestyle, genetics, dietary habits, etc. However, it is better not to joke with such things: if you cannot cope with addiction on your own, delay contacting a medical institution is not worth it.