Chronic alcoholic hepatitis symptoms. Can alcohol cause hepatitis C? Manifestation of alcoholic hepatitis

The damaging effects of alcohol on liver cells are well known. Due to the fact that this organ has an excellent ability for self-regeneration and renewal, pronounced destructive processes do not occur in all people who abuse alcohol.

Moreover, very often after an autopsy of a deceased alcoholic, numerous pathologies of internal organs are found, but the liver is found to be in normal condition. However, a complex such as alcohol and hepatitis C guarantees progressive liver destruction and significantly reduces human life expectancy.

Let us remember that any hepatitis is caused by a virus. Unlike bacteria, viruses are not cells and therefore cannot undergo developmental stages on their own. They require living cells to replicate themselves. Moreover, not just any cells, but cells of a certain type. For example, respiratory viruses infect cells in the mucous membrane of the respiratory tract. The herpes virus establishes itself in the nervous system. Hepatitis C virus is in the liver.

Viral particles (virions) invade hepatocytes (liver cells), penetrate their nuclei, where they are integrated into the process of protein replication.

As a result, the cell begins to produce viral proteins, which then acquire an envelope and become full-fledged virions, leave the hepatocyte, infect the neighboring one, etc.

Consequences of damage to hepatocytes by viruses:

• the synthesis of liver proteins and enzymes, which play a vital role in the coordinated functioning of the whole organism, decreases;
• the detoxification function of the organ worsens;
• the efficiency of metabolic processes decreases (transformation of carbohydrates, fats);
• the organ’s ability to self-regenerate is significantly reduced;
• Over time, hepatocytes are replaced by connective tissue.

The hepatitis C virus completely reduces the functionality of the liver, and in the long term, if left untreated, leads to degeneration of its tissue and cirrhosis.

The effect of alcohol on the liver

The effects of alcohol are not as unconditional as the process described above that occurs with hepatitis C. This is due, first of all, to the colossal ability of the liver to recover. However, against the background of other factors (long-term use of medications, drugs, chronic liver diseases, hereditary causes), the damaging effects of alcohol can be very serious.

Involvement of the liver in ethanol metabolism

Alcohol from any drink undergoes decomposition in the liver. This biochemical process consists of two stages:

1. Dehydrogenation of ethanol to acetaldehyde.
2. Oxidation of acetaldehyde to acetic acid.

The intermediate substance, acetaldehyde, is poisonous to the body. When it accumulates, a person feels unwell. In particular, hangover syndrome is associated precisely with the fact that the liver does not have time to oxidize all the acetaldehyde formed.

Metabolism of ethanol is possible only thanks to special liver enzymes.

Deterioration of liver function leads to a change in the rate of ethanol decomposition.

This explains why alcohol and hepatitis C, when combined, greatly enhance the toxic effect of the former not only on the liver, but also on the entire body.

Alcoholic liver disease

Changes in the functions and structure of the liver under the influence of alcohol are called alcoholic liver disease.

The development of the pathological process is associated with the toxic effects of ethanol and acetaldehyde on hepatocytes:

• the amount of produced enzymes decreases, incl. those involved in lipid metabolism;
• fats that must be processed settle in the liver, inside hepatocytes, as well as between them, further worsening the functions of the organ;
• normal liver tissue degenerates, the liver increases in size.

This stage is called “fatty liver” (“” or “steatosis”).

In some patients, the stage of alcoholic hepatosis develops into alcoholic hepatitis with risk. In 10%-20% of patients the process ends with cirrhosis of the liver.

The development and rate of progression of alcoholic liver disease are individual and determined by several factors, including:

• hereditary characteristics of ethanol metabolism (for example, too rapid dehydrogenation to acetaldehyde and slow oxidation to acetic acid);
• quantity and frequency of alcohol consumption;
• additional damaging factors (long-term use of medications,).

Among the latter, hepatitis C and alcohol are factors that enhance and accelerate degenerative processes in the liver.

As shown above, ethanol in some cases causes hepatitis of a non-infectious nature. This can be either chronic long-term degeneration of the liver tissue, which is practically asymptomatic, or acute alcoholic hepatitis with symptoms:

• the patient turns yellow;
• the color of stool and urine changes;
• body temperature rises;
• other symptoms of intoxication are observed.

Exacerbation of alcoholic hepatitis against the background of viral liver damage occurs more often, with more severe symptoms.

How alcohol consumption in hepatitis C affects the course of the disease

In numerous studies conducted on the effect of alcohol in hepatitis C on the condition of the liver and the course of the disease, the following theses have been convincingly proven:

• the immunosuppressive effect of alcohol reduces phagocytosis of macrophages - impairs cellular immunity;
• alcohol increases the replication of the hepatitis C virus;
• those who drink more than 10 g of ethanol per day increase their viral load;
• the amount of virus in the blood increases with increasing alcohol consumption and vice versa;
• refusal to drink reduces the release of virions from hepatocytes;
• Drinking patients have higher levels of iron in liver tissue, which may further contribute to hepatocyte damage;
• In heavy drinking patients, the effectiveness of interferon treatment is reduced.

Alcohol and hepatitis C add up and intensify their destructive effects on the liver. Ethanol disrupts cellular immunity, leads to damage to hepatocytes and increased viral replication in them.

The effect of alcohol on the liver after hepatitis C AVT

Based on the above points, in particular about the effect of alcohol on the liver and its immunosuppressive effect, the obvious conclusion is that after antiviral therapy (AVT) for hepatitis C, you should stop drinking alcohol:

• with fibrosis;
• with cirrhosis;
• with hepatocellular carcinoma.

In most cases, the condition of the liver in these groups of patients does not allow alcohol to be tolerated.

Since these diseases are progressive, alcohol tolerance worsens over time.

In the absence of fibrosis and sustained virological response (SVR), doctors also recommend abstaining from alcohol. This is due to several factors:

• the virus can remain in the body, while test methods are not able to track it, because they all have a sensitivity threshold and can simply make mistakes;
• even if the virus has been successfully eliminated, the liver requires a recovery period, and the longer it lasts, the better.

Despite the fact that in the vast majority of cases, when SVR is achieved, the virus is completely eliminated, no one can give a 100% guarantee in each specific case.

In the absence of a virological response after AVT for hepatitis C, the standard risks from drinking alcohol, listed in the previous paragraphs, remain.

Consequences of alcohol consumption in hepatitis C

If a person continues to drink alcohol with hepatitis C, he or she risks the following consequences:

• progression of the disease to the stage of cirrhosis;
• transformation of cirrhosis into hepatocellular carcinoma.

These consequences also develop in people who do not drink alcohol. However, among patients with chronic hepatitis C, the transformation of the disease into the stage of cirrhosis and cancer occurs more often and faster than in patients who do not drink at all.

Is it possible to drink alcohol if you have hepatitis C?

Based on the fact that even small doses of alcohol can aggravate the course of hepatitis C, it is advisable for people with HCV infection to completely stop drinking alcoholic beverages.

Useful video

More information about the effects of alcohol on the liver in the following video:

Conclusion

1. Alcohol is not recommended for hepatitis C. Ethanol enhances the damaging viral effect and weakens the antiviral immune response at the cellular level.
2. Conducting antiviral therapy in patients who drink alcohol is not advisable, because ethanol significantly reduces the effectiveness of treatment.
3. If therapy is successful, you should abstain from drinking alcohol after AVT for hepatitis C for at least 1-3 years.
4. The consequence of alcohol consumption in hepatitis C is progressive damage to hepatocytes and liver dystrophy.
5. In the presence of fibrosis, cirrhosis or malignancy, alcohol is completely contraindicated.

Version: MedElement Disease Directory

Alcoholic hepatitis (K70.1)

Gastroenterology

general information

Short description

Alcoholic liver disease is a liver disease caused by long-term intake of toxic doses of ethanol. Alcoholic liver disease combines various disorders of the structure of the parenchyma Parenchyma is a set of main functioning elements of an internal organ, limited by 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 systematic consumption of alcoholic beverages.

"Alcoholic hepatitis"- a term adopted in ICD-10 to designate acute degenerative and inflammatory liver lesions resulting from exposure to alcohol and capable of transforming into cirrhosis of the liver Liver cirrhosis is a chronic progressive disease characterized by degeneration and necrosis of the liver parenchyma, accompanied by its nodular regeneration, diffuse proliferation of connective tissue and 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 harbinger or initial and obligatory stage of cirrhosis.

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

Note. Acute episodes of toxic liver necrosis of alcoholic etiology, along with acute alcoholic hepatitis, are designated 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;
- moderate form;
- severe form.

The degree of severity can also be determined using scales (see section "Prognosis"). In accordance with the score obtained, alcoholic hepatitis can be divided into severe and non-severe.

Etiology and pathogenesis

Etiology

Alcohol is a direct hepatotoxic agent. Its metabolism involves a number of enzymatic systems that convert ethanol into acetaldehyde, and then acetaldehyde dehydrogenase Acetaldehyde dehydrogenase is an enzyme found in the human liver and is responsible for the breakdown of acetaldehyde (converts acetaldehyde into acetic acid).
(ALDH) is metabolized into 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 persistent complexes with proteins, impaired mitochondrial function, and stimulation of fibrogenesis.

The risk of developing alcoholic liver disease occurs when drinking more than 40-80 g of pure ethanol per day. Drinking more than 80 g of pure ethanol for 10 years or more increases the risk of liver cirrhosis. There is no direct correlation between the degree of liver damage and the amount of alcohol consumed: 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 Structural changes in the liver required for alcoholic hepatitis:
- perivenular damage to hepatocytes;
- balloon dystrophy and necrosis;
- presence of Mallory bodies (alcoholic hyaline);
- leukocyte infiltration;
- pericellular fibrosis.
1.2 Symptoms that are not necessary for the diagnosis of alcoholic hepatitis:
- fatty liver;
- identification of giant mitochondria, acidophilic bodies, oxyphilic hepatocytes;
- fibrosis of the hepatic veins;
- proliferation of bile ducts;
- cholestasis.

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

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

Inflammatory infiltration of 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 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 its prevalence is the main indicator in predicting 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-collagenous proteins.

2. Chronic alcoholic hepatitis:

2.1 Chronic persistent hepatitis: 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 enlarged 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, progression of the process in some cases is observed even after stopping the use of alcoholic beverages as a result of the addition of an autoimmune destructive reaction.

Epidemiology

Sign of prevalence: Common

Age. Acute alcoholic hepatitis most often develops at the age of 25-35 years after heavy drinking and 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 average age of a patient with alcoholic hepatitis is about 50 years, with the onset of alcohol consumption at age 17 years.

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 drink and abuse alcohol, 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 significance of the sex ratio in the group of patients remains unknown.

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

Risk factors and groups

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

Clinical picture

Clinical diagnostic criteria

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

Symptoms, course

Anamnesis
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 based on three of the above signs):

The patient consumes alcoholic beverages in large quantities and has a constant desire to consume them;

Spending most of your time purchasing alcohol and consuming 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;

Continuing to drink alcohol despite worsening psychological and physical problems of the patient;

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

The need to drink alcohol to reduce withdrawal symptoms.

Alcohol abuse(detected by the presence of one or two signs):

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

Repeated use of alcohol in life-threatening situations.

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

Types of clinical course of alcoholic hepatitis:

1. Acute alcoholic hepatitis:

1.1 Asymptomatic or mild course with 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 digestive disorder 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 Jaundice variant - determined in the presence of jaundice. The most common variant of acute alcoholic hepatitis (35% of cases). Jaundice is usually not accompanied by itching and is often moderate.

1.4 Cholestatic variant (in 5-13% of cases): symptoms of intrahepatic cholestasis Cholestasis is a violation of the movement of bile in the form of stagnation in the bile ducts and (or) ducts.
(skin itching, jaundice, light-colored stool, 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
Hepatomegaly is characteristic Hepatomegaly is a significant enlargement of the liver.
. The liver is enlarged in almost all patients, often compacted, has a smooth surface, and is painful. The pain is diffuse.
Possible splenomegaly Splenomegaly - persistent enlargement of the spleen
, cutaneous telangiectasia Telangiectasia is 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 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 and 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 observed: pneumonia, sinusitis, pyelonephritis Pyelonephritis - inflammation of predominantly 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
. Isolated cases of peritonitis are possible 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 diagnosing alcoholic hepatitis is the presence of an alcohol history and specific histological signs (see section “Etiology and Pathogenesis”). Clinical and laboratory parameters play a significant role. Liver imaging plays a lesser role in diagnosis.

Instrumental studies

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

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

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 nodes.

4. Laparoscopy Laparoscopy (peritoneoscopy) is the study of the abdominal organs by examining them using medical endoscopes inserted into the peritoneal cavity through a puncture of the abdominal wall.
with a liver biopsy 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 needle biopsy of the liver is often impossible due to contraindications (primarily coagulopathy) and is associated with a large number of diagnostic errors.

5. When needle biopsy of the liver with histological examination they 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 varying degrees, pronounced fibrosis with a perisinusoidal arrangement of collagen fibers;
- intrahepatic cholestasis to varying degrees.
At the advanced stage of acute alcoholic hepatitis, as a rule, there are contraindications to needle biopsy of the liver (in these cases, transjugular biopsy can be performed).

6. Magnetic resonance imaging has high sensitivity and specificity in diagnosing hepatic steatosis Liver 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 made based on evidence of alcohol abuse and evidence of liver disease. Not a single change in laboratory marker has been definitively linked specifically to alcoholic hepatitis. The etiology of liver disease detected by laboratory testing may vary. Additionally, alcohol can be one of a number of factors that cause liver damage. The specific role of alcohol in the development of liver damage may 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 during abstinence;

Increasing the concentration of carbohydrate-free transferrin;
- macrocytosis (average erythrocyte volume > 100 μm 3), associated with increased blood alcohol content and toxic effects on the bone marrow; the specificity of this sign is 85-91%, sensitivity - 27-52%.

Signs of liver damage:
1. Increase in the level of aminotransferases with a predominance of AST by more than 2 times (in 70% of cases). Increase in 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) or other or combined etiology of liver damage (eg, viral hepatitis, acetaminophen use, etc.).

2. Increased alkaline phosphatase levels and hyperbilirubinemia are possible.

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

Multiple excesses of the level of gamma-glutamyltransferase (in 70% of patients with alcoholic liver disease, GGTP activity is within normal values);
- in the cholestatic form - increased alkaline phosphatase;

Increased Ig A.

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 biliary tract;
- neoplastic formations;
- cholecystopancreatitis;
- chronic pancreatitis.

The decisive factor is considered to be a correctly collected alcohol history, negative tests for infectious agents and visualized patency of the bile ducts. However, in the setting of suspected combined liver damage, 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 proliferation of fibrous connective tissue, occurring, for example, as a result of inflammation.
and sclerosis Sclerosis is a hardening of an organ caused by the replacement of its dead functional elements with 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 syndrome (disseminated intravascular coagulation, consumption coagulopathy, thrombohemorrhagic syndrome) is impaired blood clotting due to massive release of thromboplastic substances from tissues.
;
- renal failure;
- peritonitis (rare).

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Treatment

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

2. There are significant discrepancies in drug therapy between Western and CIS recommendations.
3. Many drugs do not have an evidence base (or have a weak one) and are used either traditionally or based on a small number of studies.

4. Treatment approaches change over time. The information set out 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");
- severity of the process;
- age of the patient;
- 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 deficiencies of proteins, vitamins and microelements (especially potassium, magnesium and phosphorus).
Deficiencies of folic acid, vitamin B6, vitamin A and thiamine are among the most common.
Micronutrient levels (eg, selenium, zinc, copper and magnesium) are often altered and, in some cases, are thought to be involved in the pathogenesis of all types of alcohol-related illness.
Difficulties arise in choosing a diet for concomitant diabetes mellitus or obesity, since the spectrum of nutritional disorders 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 2000 kcal/day for an adult ).
There is evidence of the beneficial effects (when introduced into the diet) of branched-chain amino acids (BCAAs).
Evidence of the effectiveness of introducing polyunsaturated fatty acids into the diet is still doubtful.
As an alternative route for administering nutrients (for nausea, vomiting, changes in psychological status), an endoscopically inserted enteral tube with a programmable pump can be used. Parenteral nutrition (partial or additional) is used extremely rarely.

Physical activity not recommended in the acute phase. In the future, it should be aimed at weight loss (if there is concomitant obesity). Persons with chronic alcoholic hepatitis, which occurs without significant symptoms, usually do not require restriction of physical activity.

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

Medicines

US and UK recommendations
1. Systemic corticosteroids (prednisolone, methylprednisolone) - prescribed only for severe forms of concomitant liver failure for 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) - currently has no solid evidence of effectiveness in the treatment of alcoholic hepatitis. Of course, vitamin deficiency identified during blood serum testing is subject to drug correction, if it is impossible to correct it with a balanced diet.
4. Antibacterial therapy is carried out only if infectious complications develop.
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. Ademethionine (heptral).

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

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

Surgery. Liver transplantation.

Forecast

Mild 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 rate 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 - dysfunction of the blood coagulation system
The 30-day mortality rate is less than 5%.
Overall, the one-year mortality rate after hospitalization for alcoholic hepatitis is about 40%.

Used to predict mortality Maddray coefficient(MDF): 4.6 x (difference between prothrombin time in the patient and control) + serum bilirubin in mmol/l.
If the coefficient is more than 32, the probability of death during the current hospitalization exceeds 50%.
Some studies suggest that MDF may not be an accurate predictor of mortality in patients with alcoholic hepatitis, especially those receiving glucocorticoids.

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

Alternative prognosis 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 have shown the highest predictive accuracy in some studies.

Hospitalization

Hospitalization for alcoholic liver disease can be carried out both emergency and planned. Patients without signs of severe inflammation, liver failure, or complications can be treated on an outpatient basis.

Prevention

Primary prevention. Avoiding alcohol abuse.

Prevention of complications
Patients recently discharged from hospital after an acute attack of alcoholic hepatitis should generally be monitored intensively for 2 weeks. Subsequent periodic visits to the doctor are necessary at intervals of weeks to several months.
The purpose of monitoring patients is to determine whether they are responding to therapy (including monitoring electrolyte levels and liver test results), as well as monitoring alcohol cessation and encouraging sobriety.
It should be borne in mind that complete abstinence from alcohol is observed in no more than 1/3 of patients, 1/3 of patients significantly reduce their alcohol consumption and the remaining third ignores the doctor’s recommendations. The latter patients require joint work of a hepatologist and a narcologist.

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

Immunizing patients with alcoholic liver disease against common infectious pathogens, including hepatitis A virus, hepatitis B virus, pneumococci, and influenza A virus, appears to be a very reasonable approach.

Information

Sources and literature

1. The Merk manual. Guide to Medicine. Diagnostics and treatment /ed. Beers Mark H./trans. from English edited by Chuchalina A.G., M.: Litterra, 2011
2. Damianov I. Secrets of pathology / translation from English. edited by 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 diagnosed 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., Mayevskaya M.V., Ivashkin V.T.
   1. http://www.rmj.ru/ - Russian medical journal. Independent publication for medical 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 medical practitioners - No. 1, 2004

XI Congress KARM-2019: Treatment of infertility. VRT

Alcoholic hepatitis is a terrible name that fully justifies itself. This name refers to the cause of a serious illness, in many cases fatal. Medication measures in the early stages provide a good opportunity for recovery and increase life expectancy. Let's look at the causes, symptoms, methods of treatment of this insidious disease, which speaks of itself not from the first days of damage to one of the main, multifunctional organs of the human body, namely the liver.

In the International Classification of Diseases, the term "Alcoholic hepatitis" was registered in 1995. The term “Alcoholic hepatitis” is the medical characteristics of inflammatory, degenerative changes, and liver damage. The cause of the disease is primarily alcohol abuse. The disease is alcoholic hepatitis, which progresses to cirrhosis of the liver, liver failure, failure of the liver to function normally in the body as a whole.

Cirrhosis, a liver disease caused by alcoholic hepatitis.

Liver cirrhosis is the last stage of the chronic form of one of the hepatitises, in this case alcoholic. With cirrhosis of the liver, the connective tissue of the liver is replaced, the liver becomes overgrown with fatty tissue and degrades.

Alcoholism is, first of all, the abuse of alcoholic beverages in any form. All alcohol contains ethanol. Ethanol is quite a toxic substance, and when it enters the body in systematic excessive doses, it affects the liver and destroys other organs. People who consume a lot of alcohol suffer from a lack of protein and vitamin foods, since they get 40% of their calories from alcohol-containing drinks and systematically disrupt their normal diet. It is impossible not to mention alcoholic gastritis, which a person dependent on alcohol has. Alcoholic gastritis – poor absorption of vitamins; the vitamins that enter the body do not actually play a positive role, since they “pass” by important systems.

Acetaldehyde is a substance formed in the cells and tissues of the liver and is directly related to liver damage. This is a whole mechanism that triggers a series of chemical reactions that damage liver cells.

Alcoholic hepatitis, a process of constant inflammatory processes, a chain reaction of liver damage by toxins and accompanying breakdown products of alcohol. Alcoholic hepatitis, as a rule, remains in a chronic form for many years, developing after 6-7 years after alcohol abuse began.

Violation of such norms for alcohol consumption (daily norm) leads to cirrhosis of the liver.

1. Men - 80 g per day.
2. Women – 30 – 40 g per day.
3. Teenagers – 15 – 20 g per day.

Exceeding these standards, a man, woman, or teenager is already doomed to develop cirrhosis of the liver.

Manifestation of alcoholic hepatitis

Alcoholic hepatitis has two forms.

Progressive:

1. Light form;
2. Medium shape;
3. Severe form.

The progressive form has small focal liver damage, developing into cirrhosis of the liver. 15–20% is alcoholic hepatitis. With timely drug treatment, a stabilization effect is achieved, which allows stabilizing the processes of inflammation, with residual effects of the disease that persist throughout life.

Persistent:

Stable form of the disease. In most cases, complete reversibility of inflammatory processes in the liver can be observed with complete cessation of alcohol consumption. If you continue to drink alcohol without giving it up, the reversibility stage passes into the stage of progressive alcoholic hepatitis.

Rare cases of alcoholic hepatitis can be detected only after laboratory tests, which significantly delays the start of the treatment process. Pronounced symptoms may not manifest themselves in a feeling of heaviness in the area of ​​the right hypochondrium, attacks of mild nausea, fullness of the stomach, belching with an admixture of bitterness (bile).

The histomorphological manifestation of persistent hepatitis is fibrous formations on the liver tissue, balloon cell degeneration affected by Mallory bodies. In the absence of symptoms of fibrosis, with a mild course of the disease, the clinical picture of the “sleepy state” of alcoholic hepatitis can last for 5 or 10 years, even with minimal alcohol consumption.

Progressive form, characteristic symptoms:

• Weakness;
• Nausea;
• Vomit;

Moderate, severe form manifests itself:

• Fever;
• Disease Jaundice;
• Nosebleeds;
• Pain in the right hypochondrium;

Clinical picture of the body’s chemical reactions:

• Increased bilirubin;
• Increased immunoglobulin;
• Increased gammaglutamyl transpeptidase;

In persistent hepatitis, there are high levels of transaminase activity and moderate thymol tests.

The process of the active chronic stage of hepatitis is characterized by:

• Development of liver cirrhosis;
• Under the influence of ethanol, an increase in alcoholic hyaline (Mallory bodies);

Changes in ultrastructural stellate reticuloepitheliocytes, hepatocytes.

Ultrastructural changes in the above processes show the level of damage by ethanol to the digestive, circulatory, gastrointestinal and liver organs.

For any form of hepatitis in the chronic stage, diagnosis is carried out using ultrasound of the abdominal cavity. It is necessary to study and observe organs such as the liver and spleen. When examining with ultrasound diagnostics, it is possible to track changes in the structure of the liver (organ degeneration), a significant enlargement of the spleen, the diameter of the portal vein and other changes in the liver and spleen are determined.

Doppler ultrasound (USDG) is used to establish the cause or exclude the degree of increase in pressure in the portal vein of the liver (portal hypertension). Radionuclide hepatosplenoscintigraphy can confirm or refute this diagnosis. Such research is carried out using radioactive isotopes.

The development of alcoholic hepatitis has a chronic and acute period

Acute alcoholic hepatitis (AAH) - Rapidly progressive, inflammatory destruction, active processes of liver damage.

In the clinical form of acute alcoholic hepatitis, there are 4 variants of the course of the disease:

• Icteric;
• Latent;
• Fulminant;
• Cholestatic.

Long-term alcoholism, its manifestation in the OAS according to statistics in 60-80% of cases, 5% of which leads to cirrhosis of the liver. The more severe the disorders associated with liver function, the more acute the question of the course of acute alcoholic hepatitis becomes. The excesses of the formation of liver cirrhosis have the most severe consequences in the acute form of alcoholic hepatitis.

Long-term drinking bouts, the cause and onset of manifestations of alcoholic hepatitis and already acquired cirrhosis of the liver. Symptoms worsen every day, the prognosis for recovery of such a patient is reduced to the minimum indicators for recovery.

The icteric form is one of the most common in all types of hepatitis, and especially in alcoholic hepatitis.

Symptoms of jaundice:

• Yellow coloration of the sclera, mucous membrane of the eyes, and skin (without skin rashes);
• Weakness;
• Pain in the right hypochondrium;
• Heaviness in the area of ​​the right hypochondrium;
• Sudden weight loss (anorexia state);
• Attacks of nausea;
• Attacks of vomiting;
• Diarrhea;
• Enlarged liver;
• Hand trembling.

With liver enlargement, a progressive process that is accompanied by thickening of the liver tissue, in a state of cirrhosis the parenchyma becomes lumpy, and the organ is very painful on palpation. Background manifestations include ascites, splenomegaly, telangiectasia and palmar erythema.

As the disease progresses, side infections also develop, such as bacterial peritonitis, urinary infection, septicemia, and pneumonia. If the diagnosis of liver failure (hepatoreanal syndrome) is added to the listed infections, the patient’s condition worsens significantly, in some cases, it can lead to death.

To confirm the latent type of alcoholic hepatitis, the so-called state of the “sleepy form” of the course, an analysis is carried out using a biopsy of liver tissue. In the study of parenchymal biopsy, increased transminase plays a role. Transminase, its level increases with the abuse of alcohol-containing drinks.

In 10-13% of cases, the course of alcoholic hepatitis is expressed as a cholestatic variant, in which symptoms manifest themselves according to the icteric form (dark urine, colorless feces, the skin, sclera, and mucous membranes of the eyes turn yellow). With pain in the hypochondrium and fever, clinical symptoms may be similar to the disease - cholangitis. In order not to confuse one disease with another, laboratory tests are performed for blood counts and tissue biopsy. Acute alcoholic hepatitis is severe in its course with a protracted form.

Progressive symptoms of Fulminant acute alcoholic hepatitis, manifested in aggravated icteric conditions, hemorrhagic syndrome (bleeding), renal and liver failure. Death occurs due to hepatorenal syndrome, hepatic coma.

Chronic alcoholic hepatitis, symptoms and treatment

As we wrote above, this disease has “sleepy” states, a latent form of the disease, in which symptoms may be absent or minimally manifested.

Increased transmyase activity, increase and dominance of AST and ALT cells. Increased indicators of cholestasis. There are no portal hypertensive signs. Analyzes for histological changes corresponding to processes of inflammation of a morphological nature without the development of cirrhotic changes are also manifestations of alcoholic chronic hepatitis.

It is quite difficult to make an accurate and timely diagnosis for a patient due to the reasons for the course of alcoholic syndrome (binge). The doctor makes conclusions taking into account the signs of alcoholism (alcohol dependence).

Alcohol addiction, criteria for making a diagnosis:

• Constant desire to drink alcohol;
• Violation of alcohol dosage standards, drinking large quantities every day;
• Purchasing alcoholic beverages becomes a priority for the patient;
• Avoidance of work due to constant state of alcohol intoxication;
• Drinking alcohol in dangerous doses, registering with a neuropsychiatric department;
• Increased binge drinking, violations of rules of conduct in public places under the influence of alcohol;
• Psychological states with a pronounced aggressive mood towards other people;
• Signs of withdrawal syndrome (intoxication syndrome, headaches, hand tremors);
• Repeated intake of alcohol in order to relieve withdrawal symptoms the next day (popularly the process is called “hangover”).

Based on two or three of the above manifestations of alcoholism, the doctor can make a diagnosis of alcohol dependence.

Treatment of alcoholic hepatitis

Treatment of alcoholic hepatitis includes many etiological factors on which the scheme is based. This is an energy diet With mandatory increased protein consumption, as we have already mentioned, with alcoholism, protein consumption is reduced due to the consumption of a large number of calories through alcohol consumption.

In acute, severe forms, drug treatment is prescribed with the administration of liver hepatoprotectors to maintain the organ. Removing toxins using intoxication procedures, such as blood hemolysis, drinking large amounts of water, at least 2-2.5 liters per day. Fortifying the body with vitamins B and C.

The first and most important thing in the treatment of alcoholic hepatitis, of all forms, is a complete abstinence from ethanol-containing (alcohol) drinks in any form.

Statistics on complete abstinence from alcohol among patients are very low, no more than 1/3 of all alcohol addicts. With the help of conversations with the doctor, the same number of patients quit this addiction themselves, using medication, and the prognosis for recovery in this group is quite good. A group of patients who categorically do not listen to the doctor and continue to drink alcohol are registered in psychological dispensaries with a narcologist and hepatologist for further management of such a patient.

The risk group of such patients may face the impossibility of prescribing antipsychotics for treatment, since such drugs cannot be prescribed for liver failure, which may already be developing in the body at the time of the chronic form of alcoholic hepatitis.

Jaundice manifestations go away the moment the patient gives up alcohol completely. Diseases such as ascites and encephalopathy go away. In the case of further malignant or minimal alcohol intake in the chronic stage of the disease, it leads to the fatal outcome of the patient (death).

Studies conducted in the USA have shown that a characteristic nutritional deficiency, disturbances in the consumption of protein foods, and water are inherent in every person suffering from alcoholic hepatitis; accordingly, the level of liver damage is directly related to the indicators of gross violations of food intake standards.

The norm for the proper functioning of the body, the stable operation of all systems and organs, is the consumption of at least 2000 calories with a high protein index, one kilogram of a person’s weight is 1 gram of protein food. A complete supply of B vitamins, folic acid. In case of sudden weight loss of the patient (anorexia), tube feeding or parenteral nutrition is used. In the case of anorexia, the usual way of consuming food, essential microelements and calories is hampered, the body does not accept food due to the development of the disease and causes vomiting.

Due to the correlation of calorie intake, it was noticed that the group of patients who take over 2,500-3,000 calories have a higher percentage of recovery. The other side of the coin is increased mortality when consuming 1000 calories per day.

Diet No. 5, principles, food exclusions

Diet No. 5 was developed in 1920 by the physician Pevzner. His arsenal includes 15 therapeutic diets (tables) for different groups of diseases. To date, Pevzner diets are effective in the treatment of various diseases.

Diet principles No. 5.

Products allowed for consumption:

• Rye bread (yesterday's baked goods);
• Products made from soft dough (filling – boiled meat, fish, apples, cottage cheese);
• Milk soup with pasta;
• Soups with vegetable infusions (cereals, cabbage soup, beetroot soup, fruit soup);
• Low-fat fish (fillet, baked, boiled, dumplings, meatballs);
• Poultry meat (low-fat, skinless, boiled poultry, beef, rabbit, turkey, chopped or whole);
• Milk sausages, children's sausage;
• Pilaf with a high content of carrots and boiled meat;
• Stuffed cabbage rolls;
• Dairy products (yogurt, kefir, low-fat yogurt, cottage cheese, low-fat, non-spicy cheese);
• Vegetable oil;
• Butter (in small doses);
• Cereals (oatmeal, buckwheat);
• Dried fruits;
• Krupeniki;
• Egg white omelette without yolk;
• One yolk per day;
• Boiled, stewed or raw vegetables (green peas, broccoli, boiled onions, carrots, beet);
• Boiled zucchini salads (squash caviar);
• Seafood (boiled);
• Fruits and berries (not sour, in the form of compotes, jelly, mousses, jellies);
• Vegetable juices;
• Green tea;
• Rose hip decoction;
• Coffee with cream, milk;
• Spices, parsley, dill, and sour cream sauce are allowed in moderate doses.

Product exclusions:

• Butter dough (products);
• Fresh bread;
• Puff pastry;
• Fried pies;
• Soup (mushroom, fish broth, sorrel cabbage soup, okroshka);
• Fish (canned, fatty, smoked, salted);
• Meat (smoked meats, brains, kidneys, liver, fatty streaky pork, lamb, poultry skin, goose, duck, fatty and smoked sausages);
• Fat sour cream, fermented baked milk, cream, feta cheese, fat homemade cottage cheese;
• Pig lard, lamb, chicken and mutton fat;
• Legumes;
• Fried eggs;
• Radish, spinach, sorrel, garlic, green onions;
• Pickled vegetables;
• Salted and marinated mushrooms;
• Chocolate, cakes, pastries with cream;
• Horseradish, mustard, hot pepper;
• Strong coffee, strong tea;
• Complete exclusion of alcoholic beverages of any kind.

Why is it worth adhering to diet No. 5 in treatment combined with medication?

The diet is designed in such a way that it provides adequate nutrition and helps normalize the functioning of the gastrointestinal tract and liver. Following a diet guarantees the accumulation of glycogen in the liver, which leads to the normalization of fat and cholesterol metabolism. Bile secretions are well stimulated, and all activity of the gastrointestinal tract is normalized.

As a rule, the diet is prescribed not only during the treatment of acute forms of alcoholic hepatitis, during the treatment of cholecystitis, cholelithiasis, liver cirrhosis in the absence of liver failure, and postoperative periods.

Diet No. 5 for the daily diet is:

1. 70 grams of fat;
2. 50 grams of carbohydrates;
3. 100 grams of protein.
4. The energy amount is 2600-3000 kcal.
5. Meals are divided into 4-5 meals a day, not in large portions.

The basis of nutrition is boiled food, in rare cases stewed. Products must be coarsely chopped, without chopping. Meat and fish in large boiled pieces, one per serving. The process of sautéing vegetables (sautéing) when preparing gravy and frying is excluded. Frying is completely eliminated. Cold dishes and cold water should not be in the diet due to excessive irritation of the gastrointestinal tract, which leads to a slower process of food digestion.

Examples of diet recipes No. 5 for every day

Monday

• The first breakfast is a one-protein omelette, rice porridge with milk, tea.
• Second breakfast – lazy cottage cheese dumplings with low-fat sour cream.
• Lunch – cabbage soup without sorrel, stewed carrots, a piece of boiled meat, dried fruit soup.
• Afternoon snack – biscuits, tea.
• Dinner - boiled pasta, low-fat cheese, still mineral water.

Tuesday

• First breakfast - salad of raw carrots and apples, steamed cutlets (meat, fish), coffee with milk;
• Second breakfast – one apple.
• Lunch – potato or vegetable soup (mashed potatoes), stewed cabbage, meat or boiled fish, jelly.
• Afternoon snack – rosehip decoction, one biscuit.
• Dinner – buckwheat cereal, still mineral water.
• Before bed – a glass of low-fat kefir.

Wednesday

• The first breakfast is a mixture of low-fat cottage cheese with low-fat sour cream, oatmeal.
• Lunch - boiled chicken, vegetable soup, boiled rice, fresh fruit compote.
• Afternoon snack – mashed potatoes, boiled meat, rosehip decoction.
• Before bed – a glass of low-fat kefir.

Thursday

• First breakfast - buckwheat porridge, a little butter, coffee with milk, low-fat cottage cheese with low-fat sour cream.
• Second breakfast – one baked apple.
• Lunch – beetroot soup, boiled meat with pasta (naval pasta).
• Afternoon snack – one biscuit cookie.
• Dinner – mashed potatoes, stewed meat, vegetable salad, still water.
• Before bed – a glass of low-fat kefir.

Friday

• First breakfast - oatmeal, butter, coffee with milk.
• Second breakfast – baked apple.
• Lunch – borscht without frying, noodles with boiled meat, low-fat sour cream, berry jelly.
• Afternoon snack – biscuits, not strong tea.
• Dinner – mashed potatoes, boiled raba, vegetable salad, still mineral water.
• Before bed – a glass of low-fat kefir.

Saturday

• First breakfast – steamed chicken cutlet, buckwheat porridge, tea.
• Second breakfast – carrot puree, apple jam.
• Lunch – milk soup with pasta, curd babka, low-fat sour cream, uzvar.
• Afternoon snack – fruit jelly.
• Dinner – semolina porridge with prunes with low-fat milk, still mineral water.
• Before bed – a glass of low-fat kefir.

Sunday

• First breakfast - boiled potatoes, pieces, unsalted herring, tea with a slice of lemon.
• Second breakfast – baked apple.
• Lunch – cabbage soup without frying or meat, vermicelli, steamed poultry cutlets, compote.
• Afternoon snack – biscuits, rosehip infusion.
• Dinner – curd pudding, egg white omelette, still mineral water.
• Before bed – a glass of low-fat kefir.

When treating alcoholic hepatitis, it is extremely important to completely abstain from alcohol, adhere to diet No. 5 with its exceptions and the introduction of foods and elements into the diet. Drink as much liquid as possible without gas (mineral water), include vitamins B and C in your daily diet.

Remember that your timely visit to the doctor for a consultation with possible complaints or a desire to get rid of alcohol addiction (alcoholic hepatitis) is your road to recovery and prolongation of life.

There are several types of viral hepatitis. Botkin's disease is a benign disease that provokes necrosis of functional liver cells. Hepatitis A is considered an intestinal infection and is caused by the fecal-oral route of transmission. The most dangerous viral pathologies include hepatitis B. Because of it, a large number of patients die every year. Moreover, the direct cause of death is not the disease itself, but the complications it causes (liver cirrhosis, oncology). Whether it is possible to drink alcohol if you have hepatitis A and B is a pressing question among many sick people. Doctors are unanimous in this case: drinks containing ethyl alcohol cause great harm to everyone without exception.

Clinical manifestations at different stages of Botkin's disease vary. To determine an accurate diagnosis, the patient is referred for laboratory tests, ELISA and RIA. With hepatitis A, the need for hospitalization arises only in particularly difficult cases. The treatment regimen includes drug therapy and a strict diet. You should avoid alcohol even if you have an uncomplicated viral pathology. Hepatitis B is often accompanied by hepatitis D. Under the current circumstances, there is little chance of a complete recovery.

The causative agent of hepatitis is highly resistant to the negative effects of external factors and has long viability. The hepatitis A virus enters the body through water and food. A contact-household method of transmission is also possible. Many people are highly susceptible to the pathogen.

At risk are pre-pubescent children, patients with weakened immune systems, and people leading an antisocial lifestyle. The spread of the virus occurs in an integrative or productive manner. In the latter case, full-fledged virions are formed. Integrative replication leads to integration of viral DNA.

Ethyl alcohol negatively affects the body of any person. The liver performs a filtration function. When drinking strong drinks, it is she who is responsible for neutralizing toxic compounds that arise during the breakdown of ethanol. A parenchymal organ affected by the hepatitis virus is not able to function fully, so the risk of intoxication increases significantly.

Ethyl alcohol is not only present in alcohol. Its substitutes are no less dangerous than vodka. These include moonshine, beer products, some cosmetics, tinctures, cologne and technical liquids. With systematic alcohol abuse, the patient develops electrolyte imbalance and alcoholic fibrosis. Spider veins may appear, decreased libido, and enlarged mammary glands (in men).

Is alcohol acceptable for hepatitis A and B?

Treatment of viral hepatitis involves the establishment of certain restrictions. Alcoholic drinks are definitely included in this list. They will have to be replaced with compotes, fruit drinks, kvass, juices, kefir and weak tea. Ignoring these recommendations is fraught with accelerated progression of pathological changes.

Contrary to popular belief, there is no safe dose of alcohol. Ethyl alcohol is present even in non-alcoholic beer. The person who drinks it may have a desire to continue relaxing. Abuse of alcoholic beverages is prohibited for any disease, there are no exceptions.

A patient suffering from viral hepatitis needs to focus on the prescribed therapy. To evaluate its effectiveness, the patient must regularly undergo control clinical studies. The drug regimen usually includes hepatoprotectors and immunomodulators. People who are unable to get rid of their addiction on their own should consult a narcologist. It will help relieve alcohol addiction.

The liver removes waste and toxins from the body. By drinking regularly, a person provokes the degeneration of hepatocytes. Parenchymal tissue gradually turns into connective tissue, resulting in partial dysfunction. The liver of a patient suffering from hepatitis is also subject to a powerful negative impact. The combination of these two factors leads to complete liver damage. The consequences become irreversible, signs of intoxication of the body appear.

Hepatocytes are restored within 6 months. Alcohol abuse stops the regeneration process. There is practically no chance of recovery. Liver exhaustion is accompanied by destruction of its structure.

Drinking alcohol during hepatitis treatment may result in more severe side effects. Each drug can provoke the appearance of negative symptoms, the elimination of which may require symptomatic therapy. Taking additional medications will increase the load on the damaged liver, which will negatively affect the patient’s general condition.

Is it possible to drink alcohol after treatment for hepatitis?

Drinking after completing the treatment course is not recommended. The patient will have to give up eating for at least six months. This period is for patients with no history of fibrosis. If this pathology is still present, drinks containing ethyl alcohol are strictly prohibited. Failure to comply with preventive measures and ignoring prohibitions can lead to the development of such serious pathologies as cirrhosis of the liver and alcoholic hepatitis.

To cope with a viral disease and prevent complications, the patient must:

• Follow the prescribed diet.
• Avoid physical and emotional stress.
• Forget about all harmful addictions.

By drinking alcohol, the patient negates the positive effect obtained as a result of complex treatment. For hepatitis, the patient is often prescribed interferons. This is the name for medications necessary to activate the defense mechanism. They are in the body for a limited period of time. When drinking alcohol, their period of action is significantly reduced.

Immunity against hepatitis A and B, developed after complete recovery, does not protect hepatocytes from the negative effects of ethyl alcohol. Therefore, the risk of other types of this pathology in this case will greatly increase.

What will be the consequences

People with a history of viral hepatitis should not drink alcohol to excess. This is fraught with:

Drinking has an immunosuppressive effect on the body. Because of this, the existing clinical picture is complemented by symptoms of toxic poisoning. As a result, the beneficial properties of medications are suppressed, and taking them becomes a waste of time.

It should be noted that in addition to progressive hepatitis, other diseases will appear in the anamnesis. Ethanol affects all systems of the human body. A drinking person himself brings his body to a critical state. It is strictly forbidden to drink alcohol if you have hepatitis (the etiology of the disease does not matter).

Hepatitis B is considered a terrible disease that does not go away irreversibly for the body. There are many vaccinations, as well as pharmaceuticals, that can partially or completely suppress the development of viruses.

The effectiveness of medications depends not only on the patient’s current state of health, his diet or adherence to active sports. One of the main factors in the effectiveness of therapy is the consumption of alcoholic beverages during treatment.

In the article below, we have prepared for you up-to-date information on the topic of drinking alcohol with hepatitis B, you can also ask your questions in the comments, our specialists will be happy to answer them as soon as possible.

Compatibility of alcohol with the hepatitis B virus

The presence of alcohol in the body in any quantity leads to the formation of intoxication, which causes an additional blow to the liver.

It is worth noting that alcohol means not only strong drinks, but regular beer, wine, and liqueurs. The main reason why patients with the hepatitis B virus are prohibited from drinking alcohol is the possibility of complications and other reactions that will worsen the immune system.

Combination of alcohol with antiviral drugs drugs, which are prescribed for the treatment of class B hepatitis, can cause the following ailments:

• Bloating - The problem is difficult to solve with normal bowel movements; bloating is accompanied by significant pain.
• Swelling of liver tissue, which leads to pain in the right hypochondrium.
• Loss of appetite- A person almost completely loses his appetite, which is why he begins to rapidly lose weight.
• Vein expansion against the background of general weakness of the body, it indicates a serious decrease in pressure, causing a threat to life.
• Redness of the skin is allowed, feeling of tremors and scabies.

Is it possible to drink alcohol in small quantities if you have hepatitis B?

Most of our compatriots were brought up in such a way that it is “a sin not to drink” on holiday. Doctors disagree on the amount of alcohol permissible if the hepatitis B virus is present in the body.

Some of them claim that one or two cans of beer a day will have no effect either on the condition of the liver or on the effectiveness of treatment. Another class of doctors strongly advises completely abstaining from the use of ethanol in any of its manifestations.

In general, we can draw the following conclusion: Rare consumption of no more than 14 g of ethyl alcohol is acceptable provided that the patient is under constant medical supervision and does not feel significantly unwell. 10-14 g of ethyl alcohol is equal to one average glass of wine for a feast.

It is important to consult your doctor before use.

Who should not drink alcohol if hepatitis B?

• It is strictly prohibited to consume alcoholic beverages for those persons who have there is an active development of a viral infection, as well as one of the last stages of liver damage.
• It is unacceptable for anyone who has previously suffered from alcohol addiction.
• It is also prohibited to drink beer, wine, champagne and other alcohol-containing drinks for those who directly contraindicated attending doctor.

Can I drink alcohol after being vaccinated against hepatitis B?

Our medicine has created 4 main types of vaccination against hepatitis B.

There are both synthetic and live microorganisms that are introduced for grafting. Regardless of the typology, each strain causes serious stress to the immune system. The main goal of the hepatitis B vaccine is to induce in the body the same symptoms that are characteristic of the real virus.

After the injection, the patient feels a significant deterioration in his condition, which is why he is prescribed rest and bed rest with high-quality nutrition. Doctors often advise drinking plenty of fluids, but we are not talking about alcohol.

The hepatitis B vaccine causes significant damage to the liver. If you treat the consequences of vaccination with alcoholic drinks, this will lead to an exacerbation of each symptom and a subsequent trip to the ambulance.