Chronic hepatitis of alcoholic etiology. Alcoholic hepatitis (K70.1)

Alcoholic hepatitis is a diffuse (extensive - in all parts of the organ) inflammatory process in the liver tissue, resulting from toxic damage to the liver by alcohol and its breakdown products.
With alcoholic hepatitis, fat droplets accumulate inside hepatocytes (liver cells), and inflammation of the liver occurs and the death of some areas of its normal tissue. Over time, normal liver tissue is replaced by rough fibrous (scar) tissue (the process of fibrosis). Due to the fact that the amount of healthy liver tissue is significantly reduced, the liver ceases to cope with its functions (there are more than 500 of them in total, including the neutralization of toxic substances, the formation and storage of useful substances, etc.).
This disease usually develops 5-7 years after the start of regular alcohol consumption - 40-60 grams of ethanol (pure alcohol) per day for men and more than 20 grams for women. 10 milliliters (ml) of ethanol corresponds to 25 ml of vodka, 100 ml of wine, 200 ml of beer.

Symptoms of alcoholic hepatitis

The disease develops gradually and unnoticed by the patient.

In mild cases, alcoholic hepatitis is detected only through laboratory tests.

It usually takes about five years from the onset of liver damage to the appearance of the first symptoms. As the liver condition worsens, the number and severity of symptoms increase.

Acute alcoholic hepatitis usually develops after heavy drinking in patients with pre-existing cirrhosis of the liver (diffuse (extensive) liver disease, in which the death of liver tissue occurs and the formation of nodules from scar tissue that change the structure of the liver).
This leads to the superimposition of symptoms of hepatitis (inflammation of the liver) on the symptoms of cirrhosis and significantly worsens the prognosis.

All manifestations of alcoholic hepatitis are combined into several syndromes (a stable set of symptoms united by a single development).

• Asthenic syndrome:
  • decreased performance;
  • increased fatigue;
  • weakness;
  • daytime sleepiness;
  • decreased appetite;
  • depressed mood.

• Dyspeptic manifestations (digestive disorders):
  • decreased appetite;
  • nausea and vomiting;
  • bloating;
  • pain in the umbilical region;
  • rumbling in the stomach.

• Systemic manifestations of alcohol intoxication (the effects of alcohol on various organs):
  • peripheral polyneuropathy (damage to the nerves connecting human organs and limbs to the brain and spinal cord). Manifested by sensory disturbances and limitation of movements;
  • muscle atrophy (thinning of muscles and decrease in their volume);
  • tachycardia (rapid heartbeat) and shortness of breath (rapid breathing) due to damage to the cardiovascular system.

• Cachexia (exhaustion), weight loss.
• Low hyper-gamma globulinemia (moderate increase in gamma globulins (specific proteins of the immune system) in the blood - the norm is 8.0-13.5 grams of gamma globulins in one liter of blood).
• The De Ritis coefficient is the ratio of aspartate aminotransferase (AST, or AST) to alanine aminotransferase (ALT, or ALT): normally equal to 1. AST and ALT are specific biologically active substances involved in metabolism and normal liver function. In liver cirrhosis, the ratio of AST to ALT becomes less than 1.
• Arterial hypotension is a decrease in systolic (the first digit when measured) blood pressure below 100 millimeters of mercury.

• Syndrome of “small” liver signs (hepatocellular failure syndrome).
  • Telangiectasias (spider veins on the face and body).
  • Palmar (on the palms) and/or plantar (on the soles of the feet) erythema (redness of the skin).
  • General feminization of appearance - a man acquires part of the outlines and appearance of a woman:
    • fat deposition on the thighs and abdomen;
    • thin limbs;
    • scant hair growth in the axillary and pubic areas;
    • gynecomastia (formation and enlargement of the mammary glands in men);
    • testicular atrophy (reduction in the volume of testicular tissue, disruption of their function);
    • impotence (disorder of sexual and erectile function in men, inability to perform normal sexual intercourse).
  • Hypertrophy (enlargement) of the parotid salivary glands (symptom of the “hamster”).
  • Dilated capillary network on the face (dollar bill symptom, red face).
  • Tendency to form bruises.
  • Dupuytren's contracture (painless subcutaneous cord - tissue compaction in the form of a tourniquet) is curvature and shortening of the tendons of the palm, leading to limited function of the palm and its flexion deformation.
  • Jaundice coloration of the skin, mucous membranes of the oral cavity and sclera (the white membranes of the eyeball).
  • Leukonychia (small white stripes on the nails).
  • Symptoms of “drumsticks” (increase in the size of the fingertips, making their appearance similar to drumsticks) and “watch glasses” (increase in size and rounded change in the nail plates).

The patient's condition improves significantly after stopping alcohol intake.

Periods of sharp deterioration of the condition are associated with continued alcohol consumption, leading to the development of episodes of acute alcoholic hepatitis.

Chronic alcoholic hepatitis has less pronounced manifestations than acute hepatitis and is characterized by the symptoms described above.

Forms

There are 2 forms of alcoholic hepatitis.

• Persistent form – relatively stable, reversible (treatable) provided you stop drinking alcohol (abstaining from alcohol for 3–6 months leads to an improvement in the picture). With continued alcohol intake, it can develop into a progressive form.
• Progressive form - increasing deterioration of the condition. Occurs in every fifth case of alcoholic hepatitis. Accompanied by the formation of small foci of necrosis (cell death) in the liver, often leading to the development of cirrhosis of the liver (diffuse (extensive) liver disease, in which the death of normal tissue occurs, its gradual replacement with coarse fibrous (scar) tissue (fibrosis process) and the formation of nodes from scar tissue that changes the structure of the liver). With timely treatment of alcoholism, it is possible to stabilize the condition with the preservation of residual effects (for example, external manifestations of the syndrome of “small” liver signs and areas of fibrous (scar) changes in the liver).
  • Light level of activity - increasing the activity of transaminases (liver enzymes - substances that promote certain chemical reactions) by no more than 3 times.
  • Average degree of activity - increase in transaminase activity by 3-5 times.
  • Severe activity - increase in transaminase activity by more than 5 times.

According to the flow they distinguish spicy And chronic alcoholic hepatitis.

• Acute alcoholic hepatitis – acute (lasting less than 6 months) progressive degenerative-inflammatory (occurring with signs of inflammation and cell death) liver damage. In every twentieth patient, it relatively quickly transforms into alcoholic cirrhosis of the liver (a diffuse (extensive) liver disease in which the death of liver tissue occurs and the formation of nodules from scar tissue that change the structure of the liver). The most severe course of acute alcoholic hepatitis develops after repeated consumption of alcohol against the background of established alcoholic cirrhosis of the liver. Clinically, acute alcoholic hepatitis can be represented by four course options: latent, icteric, cholestatic And fulminant.
  • Latent variant has no symptoms and is diagnosed by increased transaminases in a patient who abuses alcohol. To confirm the diagnosis, a liver biopsy is required (taking a piece of the organ for examination).
  • AND yellowish version (most common) - among the symptoms, jaundice predominates (yellow discoloration of the skin, mucous membranes and biological fluids (for example, saliva, tear fluid)), not accompanied by itching.
  • Cholestatic variant observed in approximately every 10th patient. Accompanied by symptoms of cholestasis - stagnation of bile (jaundice, severe itching, discoloration of feces, darkening of urine). It is characterized by a protracted course (can last for years).
  • Fulminant variant characterized by rapid progression of all symptoms. May lead to the death of the patient.

• Chronic alcoholic hepatitis – long-term (lasting more than 6 months) degenerative-inflammatory liver disease, caused by alcohol intake and capable in a large number of cases of progressing to cirrhosis of the liver.

Causes

The cause of alcoholic hepatitis is the consumption of alcohol, regardless of the type of drink: either one-time consumption of large doses of alcohol, or long-term (many years) consumption of moderate doses - in terms of ethanol (pure alcohol) it is 40-60 grams.

Causes of the damaging effects of alcohol on the liver.

• The death of hepatocytes (liver cells) under the influence of alcohol occurs faster than their restoration is possible. During this time, instead of hepatocytes, connective (scar) tissue has time to develop.
• Oxygen starvation of cells, leading to their shrinkage and then death.
• Strengthening the formation of connective tissue.
• Suppression of protein formation in hepatocytes, which leads to their swelling (increased water content in them) and enlargement of the liver.

Risk factors for alcoholic hepatitis.

• Simultaneous consumption of large doses of alcohol.
• Repeated daily consumption of alcoholic beverages.
• Long-term alcohol use (8 or more years).
• Hereditary predisposition (the disease is transmitted from parents to children).
• Irrational and unbalanced diet (especially protein deficiency in food).
• Excessive nutrition, including obesity (increase in body weight due to adipose tissue).
• Infection with hepatotropic viruses (viruses that can cause inflammation of the liver and death of its cells).

Diagnostics

• Analysis of the medical history and complaints (when (how long ago) an enlarged liver, pain and heaviness in the upper abdomen, nausea, increased abdominal size, spider veins on the face and body appeared, with which the patient associates the occurrence of these symptoms).
• Life history analysis. Does the patient have any chronic diseases, are there any hereditary diseases (passed from parents to children), does the patient have bad habits, has he taken any medications for a long time, have he had tumors, has he been in contact with toxic substances ( toxic) substances.
• Physical examination. Upon examination, yellowness of the skin, an increase in the size of the abdomen, and the presence of spider veins (dilated small vessels) on the skin of the body are determined. During palpation (palpation), pain in various parts of the abdomen is assessed. Percussion (tapping) determines the size of the liver and spleen.
• Assessing the patient’s mental state for timely diagnosis of hepatic encephalopathy (a disease that develops as a result of the toxic effect of the breakdown products of normal liver cells on brain tissue and impaired blood circulation).

Laboratory research methods.

• A general blood test reveals a decrease in the number of erythrocytes (red blood cells) with the development of anemia (a decrease in the level of hemoglobin - a special substance in red blood cells that carries oxygen), a decrease in the number of platelets (blood platelets, the gluing of which ensures the initial stage of blood clotting), and less often - all blood cells. Leukocytosis (an increase in the number of leukocytes - white blood cells) can be detected, mainly due to their special variety - neutrophils.
• Biochemical blood test (to monitor the function of the liver, pancreas, the content of important microelements (potassium, calcium, sodium) in the blood).
• Biochemical markers (indicators) of liver fibrosis - PGA index:
  • prothrombin index - blood clotting indicator (P);
  • gamma-glutamyl transpeptidase is a biologically active substance that is normally involved in molecular reactions in liver tissue (G);
  • alipoprotein A1 - a protein in the plasma (liquid part) of the blood responsible for transporting “good” cholesterol (a fat-like substance that prevents the narrowing of the lumen of blood vessels) in the body - (A);
  • PGA values ​​range from 0 to 12. If PGA is 9, the probability of cirrhosis is 86%.

• An increase in proline and hydroxyproline (amino acids - constituent elements of protein) in the blood is a distinctive feature of alcoholic liver fibrosis (the growth of scar tissue in the liver without changing its structure).
• A coagulogram (analysis of blood coagulation and anticoagulation systems) reveals a slowdown in the formation of blood clots due to a decrease in the amount of coagulation factors that are formed in the liver.
• Lipidogram is a study of fat-like substances in the blood. With alcoholic liver disease, the level of triglycerides (special fat-like substances, the main source of energy for cells) in the blood increases.
• Alpha-fetoprotein is a substance that increases in the blood during liver cancer (a malignant tumor - a tumor that grows and damages surrounding tissues). Liver cancer can develop as a complication of alcoholic hepatitis if it lasts for a long time.
• Laboratory signs of long-term alcohol use. Promotion:
  • gamma-glutamyl transpeptidase activity in the blood;
  • the content of immunoglobulins A in the blood (Ig A is a special type of antibodies - proteins produced to fight foreign agents);
  • average volume of red blood cells;
  • in the blood, the activity of aspartate aminotransferase (AST, or AST) exceeds the activity of alanine aminotransferase (ALT, or ALT). AST and ALT are specific biologically active substances involved in metabolism and normal liver activity;
  • blood levels of transferrin (iron transport protein).

• Determination of markers (specific indicators) of viral hepatitis (inflammatory liver diseases caused by specific viruses).
• General urine analysis. Allows you to assess the condition of the kidneys and urinary tract
• Coprogram - stool analysis (undigested fragments of food and fat, coarse dietary fiber can be detected).

Instrumental research methods.

• Ultrasound examination (ultrasound) of the abdominal organs allows us to evaluate the size and structure of the liver and spleen.
• Esophagogastroduodenoscopy (EGD) is a diagnostic procedure during which the doctor examines and evaluates the condition of the inner surface of the esophagus (to identify pathologically (abnormally) dilated veins), stomach and duodenum using a specially optical instrument (endoscope).
• A liver biopsy (taking a piece of the liver for examination) allows you to evaluate the structure of the liver and establish a diagnosis
• Spiral computed tomography (CT), a method based on taking a series of X-rays at different depths, allows you to obtain an accurate image of the organs being examined (liver and spleen).
• Magnetic resonance imaging (MRI) - a method based on the formation of chains of water when the human body is exposed to strong magnets - allows you to obtain an accurate image of the organs being studied (liver and spleen).
• Elastography is a study of liver tissue performed using a special device to determine the degree of liver fibrosis. In the process of elastography, compression (compression) of the tissues being studied is performed using ultrasound. The speed of propagation of elastic waves depends on the elasticity of the tissue, that is, on the content of connective (scar) tissue in it. Elastography is an alternative to liver biopsy.
• Retrograde cholangiography is an x-ray method for studying the biliary system, in which contrast (a dye that makes the areas where it is located visible on x-rays) is injected into the papilla of Vater (the opening through which bile and pancreatic juice enter the duodenum). Allows you to identify the causes of deterioration in the outflow of bile. It is performed only for patients with severe cholestasis syndrome (insufficient flow of bile into the duodenum - the initial part of the small intestine).
• Consultations with a narcologist are also possible.

Assessing the severity of liver cirrhosis (diffuse (extensive) liver disease, in which the death of liver tissue occurs and the formation of nodules from scar tissue that change the structure of the liver) .

Performed by a specialist (gastroenterologist or hepatologist) according to the Child-Pugh scale. Several criteria are assessed:

• blood bilirubin level (a breakdown product of erythrocytes (red blood cells));
• level of serum albumin (the smallest proteins);
• prothrombin index (one of the indicators of blood clotting);
• the presence of ascites (free fluid in the abdominal cavity);
• hepatic encephalopathy (a disease that develops as a result of the toxic effect of decay products of normal liver cells on brain tissue and impaired blood circulation).

Depending on the severity of deviations from the norm of these criteria, the class of liver cirrhosis is established:

• A - compensated (that is, compensated - close to normal) cirrhosis of the liver;
• B – subcompensated (that is, not fully compensated) cirrhosis of the liver;
• C - decompensated (that is, with deep irreversible (that is, incorrigible by modern methods of treatment) disorders of the liver) cirrhosis of the liver.

Treatment of alcoholic hepatitis

The basis of treatment is to stop drinking alcohol.

• Diet therapy. Diet No. 5:
  • eating 5-6 times a day;
  • exclusion from the diet of spicy, fatty, fried, smoked, rough foods;
  • limiting table salt to 3 grams per day;
  • increased protein content (0.5-1.5 grams of protein per 1 kilogram of patient weight per day). With the development of hepatic encephalopathy (a disease that develops as a result of the toxic effect of decay products of normal liver cells on brain tissue and impaired blood circulation), the total amount of protein is limited to 0-30 grams per day;
  • consumption of foods with a high content of microelements (especially magnesium, zinc, selenium) and vitamins (groups B, C, A and K): fish, bananas, buckwheat, fruits and vegetables;
  • for anorexia (aversion to food), feeding through a tube (a tube inserted into the stomach cavity) or parenteral nutrition (intravenous administration of solutions of proteins, fats, carbohydrates, vitamins and minerals) is possible.

• Conservative (non-surgical) treatment.
  • Hepatoprotectors (drugs that preserve the activity of liver cells), the most effective of which are drugs made from milk thistle, a medicinal plant.
  • Preparations of ademetionine (a substance found in all tissues and fluids of the body and having various positive effects): protecting liver cells from damage;
    • improvement of bile outflow;
    • neutralization of toxic (poisonous) substances;
    • stimulation of liver cell recovery;
    • protecting the brain from damage by harmful substances produced due to liver dysfunction;
    • antidepressant effect (increasing low mood).
  • Ursodeoxycholic acid preparations (UDCA - components of bile that prevent the death of liver cells).
  • Vitamins of groups A, B, C, E are used due to their insufficient content in the body due to absorption disorders.
  • Glucocorticoids (synthetic analogs of adrenal hormones) reduce the severity of inflammation, prevent the formation of connective (scar) tissue, and suppress the production of antibodies (proteins produced by the body to fight foreign substances) that damage liver tissue.
  • Angiotensin-converting enzyme inhibitors (ACEIs are drugs that lower blood pressure, have anti-inflammatory activity and prevent the formation of connective tissue).
  • Tissue protease inhibitors (drugs that inhibit the activity of substances that cause protein breakdown) prevent the formation of connective tissue in the liver.

• Treatment of hepatic encephalopathy:
  • ​ diet therapy. With the development of hepatic encephalopathy, the total amount of protein is limited to 0-30 grams per day;
  • lactulose (synthetic analogue of lactose - milk sugar). Removes harmful substances from the intestines that accumulate due to liver dysfunction and can cause brain damage;
  • Antibacterial therapy is treatment aimed at removing microorganisms (causative agents of various diseases) from the body. Performed after identifying the type of microorganism;
  • infusion therapy (intravenous drip administration of water-salt solutions, glucose-vitamin mixtures, etc.).

The dosage and duration of use of each drug are determined individually.

• Surgery.

Transplantation (liver transplant) is performed when it is impossible to restore the normal functioning of the patient’s own liver. Most often, a transplant of part of the liver of a close relative is performed. A prerequisite is complete abstinence from alcohol for at least 6 months before transplantation.

Complications and consequences

A complication of alcoholic hepatitis is the development of liver cirrhosis (a diffuse (extensive) liver disease that develops as a result of long-term alcohol intake, in which the death of liver tissue occurs and its gradual replacement with rough fibrous (scar) tissue (fibrosis process).

In this case, small nodes of scar tissue are usually formed, which change the structure of the liver).

Complications of liver cirrhosis.

• Ascites (accumulation of fluid in the abdominal cavity). In many cases, ascites becomes refractory - that is, it does not respond to drug therapy. Such patients require repeated abdominal paracentesis - puncture (piercing) of the abdominal cavity with removal of fluid for diagnostic (composition studies) and therapeutic (reducing compression of the abdominal organs) purposes.
• Peritonitis is an inflammation of the peritoneum (the membrane lining the abdominal cavity from the inside and covering the abdominal organs).
• Varicose (the structure of the wall is changed due to increased venous pressure) expansion of the veins of the esophagus, bleeding from these veins. Symptoms of gastrointestinal bleeding:
  • bloody vomiting;
  • melena (black stool);
  • low blood pressure (less than 100/60 millimeters of mercury);
  • heart rate is more than 100 beats per minute (normal is 60-80).

• Confusion, hepatic encephalopathy (a disease that develops as a result of the toxic effect of decay products of normal liver cells on brain tissue and impaired blood circulation).
• Hepatocellular carcinoma (malignant (hard to treat, rapidly progressing) tumor of the liver that occurs due to its chronic damage (viral and/or alcoholic nature).
• Hepatorenal syndrome is severe renal failure (persistent depression of kidney function, leading to the accumulation of toxic substances in the blood due to impaired filtration) in patients with liver cirrhosis.
• Hepatopulmonary syndrome is a low oxygen content in the blood in patients with cirrhosis of the liver due to changes in blood circulation in the lungs.
• Hepatic gastropathy is a stomach disease that occurs as a result of impaired liver function and altered blood circulation.
• Hepatic colopathy is a disease of the large intestine due to impaired liver function and altered blood circulation.
• Chronic menstrual dysfunction (irregular, too heavy, scanty or absent periods).
• Infertility.

Forecast Alcoholic hepatitis liver disease depends on the stage of the disease: the prognosis is best with alcoholic fatty liver (accumulation of fatty droplets inside and between hepatocytes (liver cells) under the influence of alcohol) and the worst with the development of cirrhosis.

The prognosis is better with a complete cessation of alcohol consumption, timely comprehensive treatment, a young age and normal body weight of the patient.

Scientists have proven that the disease progresses more favorably in men than in women.

Prevention of alcoholic hepatitis

• Refusal to drink alcohol.
• Rational and balanced diet (refusal to too hot, smoked, fried and canned foods).

Additionally

• The toxic (damaging) effect does not depend on the type of drinks taken and is determined by the amount of ethanol in them.
• Alcoholic hepatitis is one of the variants of alcoholic liver disease (various disorders of the structure and function of the liver that develop as a result of long-term alcohol intake).
• Currently, much attention is paid to identifying liver fibrosis (the growth of scar tissue in the liver while maintaining its normal structure) and the presence or absence of its progression. The degree of fibrosis is determined using various scales; in Russia, the METAVIR scale is more often used.
  • F0 – no fibrosis.
  • F1 – portal fibrosis (the growth of scar tissue inside the liver around the branches of the portal vein - a vessel that brings blood to the liver from the abdominal organs) without the formation of septa (connective tissue (based on connective tissue that plays a supporting and structural function in the body) layers).
  • F2 - portal fibrosis with rare septa.
  • F3 – many septa without the formation of cirrhosis (a diffuse (extensive) liver disease in which the death of liver tissue occurs and the formation of nodules from scar tissue that change the structure of the liver).
  • F4 – cirrhosis.

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Alcoholic hepatitis is an inflammatory process. It occurs against the background of heavy consumption of alcoholic beverages. As a result, the organ is affected by toxins. The chronic form of the disease occurs 5-7 years after the onset of the inflammatory process. The scale can be serious, it all depends on the quality of alcohol consumed and its quantity.

ICD-10 code

For convenience, a special international classification of the disease was created. Thanks to her, you can understand the diagnosis anywhere in the world. Simply put, this encoding is used everywhere. Hepatitis is one of the diseases of the digestive system.

K00-K93 Diseases of the digestive system. . K00-K14 Diseases of the oral cavity, salivary glands and jaws. K20-K31 Diseases of the esophagus, stomach and duodenum. K35-K38 Diseases of the appendix [vermiform appendix]. K40-K46 Hernias. K50-K52 Non-infectious enteritis and colitis.

K55-K63 Other intestinal diseases. K65-K67 Diseases of the peritoneum

K80-K87 Diseases of the gallbladder, biliary tract and pancreas. K90-K93 Other diseases of the digestive system

K70-K77 Liver diseases.

• K70 Alcoholic liver disease (Alcoholic liver disease, Cirrhosis of the liver).
  • K70.0 Alcoholic fatty liver.
  • K70.1 Alcoholic hepatitis.
  • K70.2 Alcoholic fibrosis and sclerosis of the liver.
  • K70.3 Alcoholic cirrhosis of the liver.
  • K70.4 Alcoholic liver failure (Liver failure).
  • K70.9 Alcoholic liver disease, unspecified
• K71 Toxic liver damage.
• K72 Liver failure, not elsewhere classified. (Liver failure).
• K73 Chronic hepatitis, not elsewhere classified. (Chronic hepatitis).
• K74 Fibrosis and cirrhosis of the liver (Cirrhosis of the liver).
• K75 Other inflammatory liver diseases.
• K76 Other liver diseases.
• K77 Liver lesions in diseases classified elsewhere

ICD-10 code

K70.1 Alcoholic hepatitis

Causes of chronic alcoholic hepatitis

The name speaks for itself. The main cause of liver problems is heavy alcohol consumption. Systematic consumption of alcoholic beverages in increased quantities will sooner or later affect the condition of the liver. Alcohol contributes to disruption of the oxidative processes of cellular structures. It has a toxic effect and disables the organ. Ultimately, liver cirrhosis may develop, requiring liver transplantation.

The minimum amount of alcohol that can lead to inflammation is 20-30 grams regularly. This indicator refers to the female population. For a man it is slightly higher and amounts to 60-70 grams per day. As you can see from these statistics, a very small amount of alcohol is enough to cause serious problems. There are simply no other reasons contributing to the development of inflammation. It's all because of alcohol. Therefore, its consumption should be kept to a minimum.

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Pathogenesis

The toxic effects of ethanol lead to addiction. Ethanol has a special effect on the concentration of acetaldehyde and acetate in the blood. The oxidative process increases NAD*H / NAD+ levels. It is these indicators that play an important role in the formation of fatty liver. As soon as the concentration of the first indicator increases, an increase in the synthesis of glycero-3-phosphate occurs. As a result, fatty acids begin to actively accumulate in the liver.

Acetaldehyde has a hepatotoxic effect. It manifests itself mainly due to increased processes of lipid peroxidation. Ultimately, the functions of cell membranes are disrupted. In combination, acetaldehyde with proteins leads to a change in the structure of hepatocyte microtubules. As a result, alcoholic hyagin is formed. Intracellular transport is disrupted, and hepatocyte degeneration occurs.

Increased formation of acetaldehyde leads to a decrease in the activity of mitochondrial enzymes. As a consequence of this, the synthesis of cytokines is significantly enhanced. Cellular immunity is significantly impaired. Ultimately, the liver is severely affected. The inflammatory process begins, functionality is undermined. As a result, alcoholic hepatitis develops, which becomes chronic.

There are different points of view regarding the terminology of this type of alcoholic liver damage. L. G. Vinogradova (1990) gives the following definition: “chronic alcoholic hepatitis” is a term that denotes relapses of acute alcoholic hepatitis that occur against the background of an incompletely completed previous attack of acute alcoholic hepatitis and lead to a kind of liver damage with features of chronic hepatitis.

Histological examination can distinguish two forms of chronic alcoholic hepatitis: chronic persistent and chronic active. Morphologically chronic persistentalcoholic hepatitis combines the characteristic features of alcoholic hepatitis with moderate pericellular and subsinusoidal fibrosis in the third zone of the acinar hepatic lobule, dilation of the portal ducts, portal fibrosis, and slight portal infiltration. The clinical picture includes decreased appetite, mild pain in the liver, belching, general weakness, slight enlargement of the liver, and a slight increase in the activity of γ-glutamyl transpeptidase in the blood serum.

Chronic alcoholic active hepatitis Histologically, it combines signs of alcoholic hepatitis with active fibrosis and hyaline necrosis in the hepatic lobules; bridging and multilobular necrosis is possible with high activity of the pathological process. Clinical manifestations are characterized by severe weakness, lack of appetite, pain in the liver, jaundice, an enlarged, dense and painful liver, significant changes in liver function tests, in particular, high activity in the blood serum of γ-glutamyl transpeptidase, aminotransferases, and increased levels of immunoglobulin A in the blood.

Chronic alcoholic hepatitis can progress to liver cirrhosis even in conditions of abstinence from alcohol due to the addition of autoimmune mechanisms - sensitization of T-lymphocytes to alcoholic hyaline.

Chronic alcoholic hepatitis is a liver disease. Naturally, caused by heavy consumption of alcoholic beverages. This disease needs to be eliminated, because in most cases it develops into cirrhosis of the liver. When drinking alcoholic beverages, acedehyde is formed in the liver. It is this that severely affects liver cells. It can trigger a number of chemical reactions in the body and thereby lead to organ damage.

Symptoms of chronic alcoholic hepatitis

The clinical manifestation of this disease is limited to scant symptoms. Thus, the organ may increase slightly in size, and pain may appear. Severe pain and lack of appetite are possible. Over time, the symptoms are complemented by nausea and vomiting. No physical data available.

Often there is a disturbance in the rhythm of sleep and wakefulness. A person experiences a decrease in libido and an increase in body temperature. A number of other signs can be identified. Thus, the nails become white, spider veins appear, and palmar erythema and ascites often develop. These changes are characteristic directly of the chronic form of the disease. The symptoms described in the first paragraph appear at the initial stage.

The chronic course is characterized by the severity of symptoms, as well as their diversity. They may well appear simultaneously. If treatment is not started in time, death cannot be ruled out. This happens due to the rapid development of liver cirrhosis. Severe liver damage requires liver transplantation. The risk factor is present in people with low weight, jaundice and increased liver density. Alcoholic hepatitis, together with these factors, is fraught with aggravating consequences.

First signs

The danger lies in the fact that the disease can be asymptomatic for a long time. Signs appear in severe stages. You can suspect something is wrong based on liver dysfunction. A person begins to feel weak, he experiences increased fatigue, his appetite worsens, and his body weight decreases sharply. These are the first signs that you should pay attention to. As a rule, the pain syndrome does not particularly manifest itself at this stage. Therefore, a person most often thinks that his condition is associated with a decrease in immunity and other diseases. He is in no hurry to visit a doctor.

Over time, pain begins to manifest itself. To a greater extent, it is similar to discomfort and a feeling of heaviness in the right hypochondrium. Again, this situation does not particularly bother a person. After all, one can easily think that low-quality products were consumed. Alcoholics, as a rule, do not understand that all troubles arise from uncontrolled drinking. Gradually, nausea, vomiting and a bitter taste in the mouth are added to all the symptoms. There may be belching with bitterness. This symptom is associated with drinking alcohol and fatty foods.

Jaundice can also manifest itself. A icteric tint appears to the sclera and lining of the oral cavity. As the disease progresses, yellowing of the skin occurs. Sometimes this is accompanied by itching, as well as an enlarged liver.

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Consequences

If treatment was started on time, then there can be no consequences. In most cases, everything ends successfully. If all recommendations are followed and alcoholic beverages are excluded, there can be no consequences. Otherwise, cirrhosis and liver fibrosis may develop.

Fibrosis is a reversible stage of the process. It can be eliminated with proper treatment. Cirrhosis cannot be cured; in this case, it is possible to get rid of the problem through organ transplantation.

If treatment is started on time, and the transplant gives a positive result, then the prognosis will be favorable. But, under no circumstances should you drink alcoholic beverages. Otherwise, there is a risk of repeated inflammation. Therefore, you should always follow all the given recommendations and not deviate from them. Otherwise, death cannot be ruled out. Whether consequences occur or not, in most cases depends directly on the patient.

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Complications

It is necessary to understand that this inflammatory process has disappointing complications. The fact is that in most cases hepatitis develops into cirrhosis of the liver. It is impossible to cope with the problem at the medication level. All that is needed here is a transplant. In terms of its severity, cirrhosis is equated to a malignant tumor.

Another complication may be ascites. It is also caused by hepatitis. The main sign of a problem is a strong bulging of the abdomen. This is due to the fact that there is a large amount of free fluid in the human abdominal cavity. The type of ascites is completely determined by the amount of that same fluid. In a small form it can be 3 liters, in a medium form it can be more than 3 liters. With a high form, the amount of liquid varies up to 20-30 liters. The person is unable to move normally and has some difficulties.

It should be understood that ascites is an alarming signal. It indicates that the organ is not able to filter blood. This moment cannot be missed. Otherwise, the patient will have no more than 5 years to live.

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Diagnosis of chronic alcoholic hepatitis

The first step is to collect an anamnesis of the disease and complaints. It is important to identify how long ago the symptoms began. Important information is the amount of alcohol consumed and its frequency. It is important to collect a life history. Does the patient have any chronic processes in the body, are there any hereditary diseases? The presence of bad habits, tumors and contact with toxic substances is also taken into account.

A physical examination is then performed. During the examination, the shade of the skin, the size of the abdomen, and the presence of spider veins on the body are taken into account. Upon palpation, a person feels pain in the abdomen. In this way, the enlarged organ can also be felt. It is important to assess the patient's mental state.

If necessary, an ultrasound is performed. The full picture consists of laboratory tests, instrumental and differential diagnostics. Detailed information will be provided below.

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Analyzes

Laboratory research plays an important role. They include a complete blood count. Thanks to it, you can determine the level of red blood cells, as well as hemoglobin. It turns out that it is easy to detect leukocytosis.

In addition to the general analysis, a biochemical blood test is taken. It allows you to assess the functionality of the liver and pancreas. Biochemical markers. They are used to check blood clotting indicators and the functioning of gamma glutamyl transpeptidase. Aliproprotein A1 is monitored. It can be used to determine the condition of the liver. If proline and hydroxyproline are significantly elevated in the blood, then liver fibrosis is most likely occurring. This condition is characterized by the growth of scar tissue.

Coagulogram is also widely used. It is an analysis of the coagulation of blood systems. A lipidogram is a study of fat-like substances in the blood. Long-term use of alcohol can be determined by laboratory tests. In humans, the activity of gamma-glutamyl transpeptidase, immunoglobulins, and aspartate aminotransferase is significantly increased.

To get a complete picture, markers are determined. These are specific indicators that allow us to determine the presence of inflammatory processes in the liver that were caused by specific viruses. A general urine test is also performed. It allows you to determine the general condition of the kidneys and urinary system. A coprogram is also carried out, in other words, an analysis of stool to check for the presence of undigested food fragments and fat in it.

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Instrumental diagnostics

This research methodology is diverse. So, most often they resort to ultrasound. This will allow you to assess the condition of the abdominal organs and notice any changes in them.

Esophagogastroduodenoscopy is widely used. It is a diagnostic procedure during which a specialist is able to assess the condition of the esophagus as a whole. This allows you to identify pathologies. The stomach and duodenum can be examined. The study is carried out using a special instrument - an endoscope.

In addition, a puncture biopsy is performed. To do this, a damaged piece of liver is taken and carefully examined. This allows you to evaluate the structure of the organ and make the correct diagnosis.

Spiral computed tomography is widely used. This method involves taking x-rays at different depths. The study allows you to obtain an accurate image of the affected area. Magnetic resonance imaging has a similar effect. This technique is built on the chain of interaction between the human body and liquid. It allows you to obtain a clear image of the organ being examined.

Elastography. This technique allows you to examine liver tissue. Everything is done using a special device that allows you to determine the presence of liver fibrosis. During the procedure, special compression of the tissue being examined is performed. As a result, changes can be seen. Most often, the procedure is used as an alternative to a biopsy.

Retrograde cholangiography. This technique is based on the administration of contrast. It is usually injected into Vater's nipple. The procedure allows you to determine the deterioration of the outflow of bile. Cholangiography is performed for people with severe cholestasis syndrome.

Differential diagnosis

This type of diagnosis includes laboratory tests. Initially, a person needs to undergo a general blood test, as well as a biochemical blood test. By the level of leukocytes, hemoglobin and red blood cells, the presence of abnormalities and the inflammatory process can be determined. Particular attention is paid to blood clotting.

In addition to this procedure, a biopsy is performed. It allows you to take the affected tissue and examine it. This technique is the most reliable, but only works in conjunction with blood tests.

To determine the condition of the urinary system, a urine test is performed. It is important to determine the presence of markers. In addition, stool is examined for the presence of coarse dietary fiber or undigested food fragments. It is impossible to obtain a complete picture using instrumental or diagnostic methods alone. All studies must be conducted together.

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Treatment of chronic alcoholic hepatitis

First of all, a person needs to stop drinking any alcoholic beverages. Naturally, this is an unbearable burden for an alcoholic. Therefore, you will have to control it. Because sooner or later all this will develop into cirrhosis of the liver. This is a very serious lesion, which most often ends in death.

It is worth visiting a psychologist and narcologist. This will allow you to get rid of addiction and understand the severity of the whole process. Indeed, in most cases, a person is not able to cope with the problem on his own. All patients must strictly follow diet No. 5. Its goal is to reduce the load on the diseased organ. That is why fatty, fried and spicy foods are considered forbidden foods. It is worth giving up salt, canned food, sweets and strong teas. Preference is given to food that contains a lot of fiber, vitamins and minerals.

Naturally, it is impossible to do without medications. True, in this case you need to exercise special caution. Because medications should have a positive effect on the organ and not injure it. Hepatoprotectors are most often prescribed. This is a group of drugs that can regenerate liver cells and protect it from negative effects. It is mainly recommended to use Ursosan, Essentiale N, Heptral and Rezalut Pro. The course of treatment does not exceed one month. Detailed information about medications will be presented below.

It is important to fill a person’s diet with vitamins and minerals. Herbal teas, including those based on echinacea and mint, will be beneficial. If a person is bothered by an overexcited and stressed state, it is worth drinking a sedative. Valerian can act as it, but only in tablets! Under no circumstances should you use the tincture! 2 tablets 3 times a day are enough. In case of severe liver damage, when cirrhosis is observed, it is worth resorting to organ transplantation. Otherwise the person will not survive.

Medicines

Ursosan. The dosage of the drug is prescribed by the attending physician. In particularly severe cases, 14 mg per kilogram of weight is used. The duration of therapy can range from one month to six months. In some cases, even 2 years. Contraindications: hypersensitivity, pregnancy, impaired liver and kidney function. Side effects: pain in the liver, nausea, vomiting, allergic reactions.

Essentiale N. The dosage is 2 capsules 3 times a day. The duration of therapy depends on the person's condition. Contraindications: hypersensitivity. Side effects: extremely rarely, intestinal upset may occur.

Heptral. The drug can be used both in the form of tablets and injections. For long-term therapy, the daily dose should not exceed 4 tablets. If the drug is administered, then 400-800 mg is enough. The duration of treatment is determined by the doctor. Contraindications: hypersensitivity. Side effects: heartburn, nausea, sleep disturbance, allergic reactions.

Rezalut Pro. The drug is used 2 capsules, 3 times a day before meals. The duration of treatment depends entirely on the course of the disease. Contraindications: hypersensitivity, antiphosphalipid syndrome. Side effects: diarrhea, allergic reactions.

Traditional treatment

Traditional medicine has a lot of useful recipes. Many herbs, fruits, plants and roots can be used for treatment. True, some of them can be toxic. Therefore, independent use can lead to a lot of unpleasant consequences. Before starting treatment, you should consult a specialist.

Recipe 1. Blueberries. The beneficial properties of this berry have long been known. Its leaves contain special enzymes that help fight hepatitis. Many healers recommend using blueberry decoctions. You can use fruit drinks, juices, or simply eat the berries. Even jam will have a positive effect. The leaves themselves have special power. They are able to block viruses and protect the organ.

Recipe 2. Pumpkin. It is useful with minerals and vitamins. Its pulp can be used both for treatment and simply for nutrition. It is worth noting that using it for more than 3 months is not recommended. Traditional healers recommend consuming it fresh, about half a kilogram per day. You can cook porridge, stew it, and also eat it in the form of candied fruits. Raw pumpkin along with sour cream is especially beneficial. You can drink pumpkin juice. Pumpkin treatment is beneficial for liver cirrhosis.]

Herbal treatment

Medicinal herbs have a positive effect on many organs and systems. But it is important to understand which of them can be used and which ones to avoid.

Recipe 1. Dandelion herb. With its help, many diseases can be eliminated. Especially those associated with liver failure. When treating hepatitis, dandelion grass should be consumed fresh. Salads are quite suitable. You can use jam from them. Dandelion has a choleretic effect. A decoction of it should be consumed before each meal, half a glass. It is prepared simply, take dandelion leaves and pour boiling water over it. Then the product should be allowed to brew and cool. The root of the plant is used to combat hepatitis. It should be crushed and evaporated for an hour. Then use a tablespoon before meals.

Recipe 2. You need to take St. John's wort, calendula flowers, and chicory. Mix all this and take only 2 tablespoons of the mixture. Then fill them with two glasses of cold water. Everything is infused all night, in the morning it is boiled for 5 minutes and filtered. You can drink the product regardless of food intake. The course of treatment is 2 months.

Recipe 3. Take the grass of horsetail, yarrow and rose hips. It is important that everything is in equal proportions. After which everything is mixed and only one tablespoon is taken. The collection is poured with a glass of boiling water and infused for 2-3 hours. You can use the resulting product 3 times a day 30 minutes before meals. The duration of treatment is 2 weeks. If necessary, the course is repeated a month later.

Homeopathy

Homeopathic remedies have always been in demand. True, they are not suitable for everyone. So, there is both a positive and negative opinion about them. Among homeopathic remedies, only a few can help. Thus, the following products have earned particular popularity: Hepel and Galstena. They have a positive effect, but only if used under the supervision of an experienced homeopath. The main effect of the products is aimed at regenerating liver cells and creating a protective barrier around it. Drug therapy is long-term. It is worth noting that single-drug drugs have always been particularly tropic towards liver cells. Among them it is worth noting May celandine and milk thistle. These two drugs can eliminate most of the symptoms that occur with liver damage. Plus, they support her.

The negative opinion is that not all people resort to homeopathy. More precisely, she is not able to help everyone. The fact is that homeopathic remedies do not undergo any clinical trials, so it is difficult to say whether a positive effect will be observed.

Surgical treatment

Surgical treatment means liver transplantation. This operation is not only complicated, but also expensive. Such an intervention is only appropriate if a person has cirrhosis of the liver or the last degree of liver failure.

High-quality transplantation can only be performed in German clinics. As mentioned above, the procedure is really expensive. The complexity of this operation lies not only in the price, but also in finding a donor, because finding a person with good physical and mental characteristics is not always so easy. Some people stand in the “queue” for a new organ for years and do not always wait for it.

The operation itself is complex. The recovery period is very long. It is necessary to monitor the condition of the person and the organ. After all, it takes a long time to take root and this is not always possible. Naturally, it is best not to resort to such an operation. No one gives a 100% positive result. To avoid such a need, you should simply eliminate alcohol consumption and promptly treat pathological and inflammatory processes in the body.

Prevention

Prevention of alcoholic hepatitis is the only way to avoid this problem. After all, treatment is not only long-term, but also complex. Moreover, during the recovery period, many difficulties may arise. First of all, you should avoid consuming ethanol-containing drinks. In this case we mean alcoholic drinks of any percentage. The daily consumption dose for a woman should not exceed 20 grams, and for a man 40 grams. If these indicators are significantly higher, the likelihood of developing alcoholic hepatitis increases.

The only way to avoid this problem is to completely abstain from alcohol. If a person consumes it periodically, it is difficult to draw conclusions regarding his health. The development of alcoholic hepatitis depends entirely on the amount of alcohol consumed, a person’s lifestyle and the nature of his diet. Naturally, a special place is given to the condition of the liver. She may not be at her best initially, and alcohol will only make the situation worse.

Forecast

The prognosis depends entirely on the condition of the liver and the stage of development of the disease. The best prognosis is observed in the presence of alcoholic fatty degeneration. This condition is characterized by the presence of fat droplets inside the liver cells. This happens under the influence of alcohol. Fixing this problem is not that difficult. Therefore, the prognosis is usually favorable.

A negative course is observed in liver cirrhosis. The problem in this case can be eliminated only through transplantation. Medicines are unlikely to have the necessary effect. With cirrhosis, the prognosis is unfavorable.

A positive course is only possible if a person completely stops drinking alcohol and begins timely treatment of inflammatory processes in the body. Young age and normal body weight also affect the favorable prognosis. Finally, the disease progresses much more favorably in men than in women.

– 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. As the etiological factor continues to act, changes in the liver progress to cirrhosis - irreversible damage. The severity of the disease is determined by both 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.

ICD-10

K70.1

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, is a precursor or initial manifestation of liver cirrhosis. As a rule, this disease develops after five to seven years of regular alcohol use. The pathology progresses with continued consumption of alcoholic beverages.

Causes

Alcoholic hepatitis is caused by 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 amount and frequency of alcoholization, the quality of drinks consumed, the individual characteristics of the body, and the duration of abuse.

The likelihood of developing alcoholic liver damage is higher in individuals who have genetic characteristics of enzymes that metabolize alcohol, in patients who have had viral hepatitis, and also in those with an initial nutritional deficiency.

Pathogenesis

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

Classification

Alcoholic hepatitis can have a persistent or progressive course. The persistent course is a relatively stable form of the disease, and when alcohol consumption is stopped, the damage to liver cells is reversible. Continuation of 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 develops 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, mild nausea. This variant is usually detected by the results of laboratory tests (increased transaminases). A 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 and sclera. Possible increase in body temperature. The liver is enlarged, smooth (with cirrhosis - lumpy), painful on palpation. The detection of symptoms such as splenomegaly, ascites, palmar erythema (redness of the palms), telangiectasia indicates underlying cirrhosis.

The cholestatic version of alcoholic hepatitis is less common; its characteristic symptoms are intense skin itching, 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, pronounced changes in laboratory markers. Against the background of hepatic coma and hepatorenal syndrome, the outcome can be fatal.

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

Diagnostics

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

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

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 homogeneity of structure. Laboratory parameters were moderately changed. Liver biopsy in case of alcohol damage can reveal specific signs of inflammation, fibrosis, and necrosis. The severity of the damage depends on the form of the disease and its duration.

Identification of signs of liver damage during the examination should be combined with anamnestic data indicating long-term alcohol consumption, as well as the presence of dependence and 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 history, since patients often significantly underestimate the amount of alcohol consumed.

Characteristic external signs of alcoholic illness (alcoholism) are also 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 deformation of the hand), damage to the peripheral nervous system, other target organs (kidneys, heart, pancreas, central nervous system).

Treatment of alcoholic hepatitis

Therapy for this disease must be comprehensive. The main directions of treatment are eliminating the damaging factor, prescribing an appropriate diet, and administering drug therapy. Any form of alcoholic hepatitis first of all requires the cessation of the action of the etiological factor - alcohol. Without alcohol abstinence, progression of the damage is inevitable. In mild forms, this is already enough to reverse the development of changes in the liver.

Alcoholic hepatitis is accompanied by nutritional deficiency in most patients. The more severe the liver damage, the more pronounced the 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. Be sure to have a sufficient supply of vitamins and unsaturated fatty acids. In case of anorexia, tube enteral or parenteral nutrition is prescribed. Infusions of amino acids reduce protein catabolism (consumption of interstitial protein reserves) and improve the metabolism of brain tissue.

Drug therapy includes the prescription of essential phospholipid preparations, which reduce fatty liver disease, have an antioxidant effect, slow down liver fibrosis, and accelerate the regeneration of its cells. Also, in case of alcohol damage, especially the cholestatic form, ursodeoxycholic acid preparations, which have a cytoprotective effect, are prescribed. In order to achieve an antioxidant effect, block the production of acetaldehyde, and 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 hepatocellular failure syndrome, glucocorticosteroids are used. Treatment of the chronic form is carried out taking into account the degree of liver damage. The presence of fibrosis requires complete abstinence from alcohol. Drug therapy includes the prescription of drugs that affect the process of fibrosis, γ-interferon, glycine.

Prognosis and prevention

The basis for the prevention of alcoholic hepatitis is to limit alcohol consumption, in order to prevent the progression of existing liver damage - complete abstinence. In patients with mild to moderate alcoholic hepatitis, when the effect of acetaldehyde is completely stopped, 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 cirrhosis of the liver.

Alcoholic hepatitis is detected in approximately 35% of patients with chronic alcoholism. Clinically, it is proposed to distinguish between acute and chronic alcoholic hepatitis.

Acute alcoholic hepatitis (AAH) is an acute degenerative and inflammatory lesion of the liver caused by alcohol intoxication, morphologically characterized mainly by centroidal necrosis, an inflammatory reaction with infiltration of the portal fields predominantly by polynuclear leukocytes and the detection of alcoholic hyaline (Mallory bodies) in hepatocytes.

The disease develops predominantly in men who have been abusing alcohol for at least 5 years. However, when drinking large quantities of alcohol, acute alcoholic hepatitis can develop very quickly (within several days of alcoholic binge, especially if it is repeated repeatedly). Acute alcoholic hepatitis is predisposed by insufficient, irrational nutrition, as well as genetic burden in terms of alcoholism and alcoholic liver damage.

As a rule, alcoholic hepatitis begins acutely after a previous binge, pain in the liver area, jaundice, nausea, and vomiting quickly appear.

Histological manifestations

Acute alcoholic hepatitis is characterized by the following histological manifestations:

• perivenular centrilobular damage to hepatocytes (balloon degeneration of hepatocytes in the form of their swelling with an increase in size, clearing of the cytoplasm and karyopyknosis; necrosis of hepatocytes mainly in the center of the hepatic lobules);
• the presence of alcoholic hyaline (Mallory bodies) in hepatocytes. It is assumed that it is synthesized by the granular endoplasmic reticulum and is detected centrilobularly using a special three-color Mallory stain. Alcoholic hyaline reflects the severity of liver damage and has antigenic properties, including immune mechanisms for the further progression of alcoholic liver disease;
• as alcoholic hepatitis subsides, alcoholic hyaline is detected less frequently;
• inflammatory infiltration of segmented leukocytes and, to a lesser extent, lymphocytes of the hepatic lobules (in foci of necrosis and around hepatocytes containing inclusions of alcoholic hyaline) and portal tracts;
• pericellular fibrosis - the development of fibrous tissue along the sinusoids and around hepatocytes.

Symptoms of acute alcoholic hepatitis

The following clinical variants of acute alcoholic hepatitis are distinguished: latent, icteric, cholestatic, fulminant and a variant with severe portal hypertension.

Latent variant

The latent variant of acute alcoholic hepatitis is asymptomatic. However, many patients have complaints of poor appetite, mild pain in the liver, an enlarged liver, a moderate increase in the activity of aminotransferases in the blood serum, and the possible development of anemia and leukocytosis. To accurately diagnose the latent variant of acute alcoholic hepatitis, a puncture biopsy of the liver and histological analysis of the biopsy specimen are necessary.

Jaundice variant

The icteric variant is the most common variant of acute alcoholic hepatitis. It is characterized by the following clinical and laboratory symptoms:

• patients complain of pronounced general weakness, complete lack of appetite, rather intense pain in the right hypochondrium of a constant nature, nausea, vomiting, significant loss of body weight;
• severe jaundice appears, not accompanied by itching;
• body temperature rises, fever lasts at least two weeks;
• in some patients splenomegaly and palmar erythema are detected, in some cases ascites develops;
• in severe cases of the disease, symptoms of hepatic encephalopathy may appear;
• laboratory data: leukocytosis with an increase in the number of neutrophilic leukocytes and a band shift, an increase in ESR; hyperbilirubinemia with a predominance of the convoyed fraction, increased activity in the blood serum of aminotransferases (mainly aspartic), alkaline phosphatase, γ-glutamyl transpeptidase, decreased albumin levels and increased γ-globulins.

The icteric variant of acute alcoholic hepatitis must be differentiated from acute viral hepatitis.

Cholestatic variant

This variant of acute alcoholic hepatitis is characterized by the appearance of clinical and laboratory signs of intrahepatic cholestasis:

• intense skin itching;
• jaundice;
• dark urine;
• light-colored feces (acholia);
• the content of bilirubin in the blood is significantly increased, mainly due to the conjugated fraction, cholesterol, triglycerides, alkaline phosphatase, γ-glutamyl transpeptidase; At the same time, the increase in aminotransferase activity is small.

Fulminant variant

The fulminant variant of acute alcoholic hepatitis is characterized by a severe, rapid, progressive course. Patients are concerned about pronounced general weakness, complete lack of appetite, intense pain in the liver and epigastrium, high body temperature, jaundice increases rapidly, ascites develops, hepatic encephalopathy, renal failure, hemorrhagic phenomena are possible. Laboratory data reflect a pronounced syndrome of hepatocyte cytolysis (increased serum activity of aminotransferases, fructose-1-phosphate alvdolase, ornithine carbamoyltransferase), hepatocellular failure (decreased albumin levels in the blood, prolongation of prothrombin time), inflammation (significant increase in ESR, leukocytosis with a shift of the leukocyte formula to the left ).

The fulminant variant of acute alcoholic hepatitis can be fatal within 2-3 weeks from the onset. Death occurs from liver or hepatorenal failure.

Diagnosis of acute alcoholic hepatitis

• Complete blood count: leukocytosis (10-30x109/l) with an increase in the number of neutrophils, a band shift, an increase in ESR; some patients develop anemia;
• Biochemical blood test: increased bilirubin content in the blood to 150-300 µmol/l with a predominance of the conjugated fraction; increased activity of aminotransferases with a predominance of aspartic, γ-glutamyltan peptidase; hypoalbuminemia; hypoprothrombinemia.

The activity of serum transaminases is increased, but rarely exceeds 300 IU/l. Very high transaminase activity indicates hepatitis complicated by taking paracetamol. The AST/AlAT ratio exceeds 2/1. As a rule, alkaline phosphatase activity is increased.

The severity of the disease is best indicated by serum bilirubin levels and prothrombin time (PT), determined after administration of vitamin K. Serum IgA levels are markedly elevated; IgG and IgM concentrations increase much less; IgG levels decrease as the condition improves. The serum albumin content is reduced, which increases as the patient's condition improves, and cholesterol levels are usually elevated.

Serum potassium levels are low, largely due to inadequate dietary protein intake, diarrhea, and secondary hyperaldosteronism if fluid retention is present. The serum content of albumin-bound zinc is reduced, which in turn is due to the low concentration of zinc in the liver. This sign is not found in patients with non-alcoholic liver disease. The level of urea and creatinine in the blood is increased, which reflects the severity of the condition. These indicators are predictors of the development of hepatorenal syndrome.

According to the severity of alcoholic hepatitis, an increase in the number of neutrophils is observed, usually reaching 15–20 10 9 /l.

Platelet function is reduced even in the absence of thrombocytopenia or alcohol in the blood.

Treatment of acute alcoholic hepatitis

• Stop drinking alcohol
• Identification of aggravating factors (infection, bleeding, etc.)
• Preventing the development of acute alcohol withdrawal syndrome
• Intramuscular administration of vitamins
• Treatment of ascites and encephalopathy
• Addition of potassium and zinc
• Maintain intake of nitrogen-containing substances orally or enterally
• Consider corticosteroids for severe disease with encephalopathy but no gastrointestinal bleeding

When treating ascites, care should be taken, as there is a possibility of developing functional renal failure.

The results of the use of corticosteroids are extremely contradictory. In 7 clinical studies involving patients with mild to moderate acute alcoholic hepatitis, corticosteroids did not affect clinical recovery, biochemical parameters or progression of morphological changes. However, a randomized multicenter study showed more favorable results. The study included patients with both spontaneous hepatic encephalopathy and those with a discriminant function higher than 32. 7 days after admission, patients were prescribed methylprednisolone (30 mg/day) or placebo; Such doses were used for 28 days, and then over the course of 2 weeks they were gradually reduced, after which the intake was stopped. The mortality rate among the 31 patients receiving placebo was 35%, and among the 35 patients receiving prednisolone, it was 6% (P = 0.006). Thus, prednisolone reduced early mortality. This drug appears to be particularly effective in patients with hepatic encephalopathy. In the group of patients receiving treatment, the decrease in serum bilirubin levels and the decrease in PT were more significant. Randomized trials and a meta-analysis of all studies have confirmed the effectiveness of corticosteroids on early survival. These results are difficult to reconcile with the negative results of the previous 12 studies, many of which, however, involved only a small number of patients. There may have been a Type I error (the control group and the group of patients receiving corticosteroids were not comparable) or a Type II error (inclusion of too many patients who were not at risk of death). It is possible that patients in the latest studies were less severely ill than patients in previous studies. Corticosteroids appear to be indicated in patients with hepatic encephalopathy but no bleeding, systemic infection, or renal failure. Only approximately 25% of hospitalized patients with alcoholic hepatitis meet all of the above criteria for corticosteroid use.

Minimum nutritional and energy value of the daily diet of patients with alcoholism

Testosterone is ineffective. Oxandrolone (anabolic steroid) is useful for patients with moderate severity of the disease, but is ineffective in patients with malnutrition and low calorie intake.

Severe protein deficiency contributes to decreased immunity and the occurrence of infectious diseases, aggravates hypoalbuminemia and ascites. In this regard, the importance of good nutrition is obvious, especially in the first few days of hospital stay. Most patients can obtain adequate amounts of natural proteins from food. Improvement in the patient's condition can accelerate after the use of additional nutrition in the form of casein, which is administered using a nasoduodenal tube (1.5 g of protein per 1 kg of body weight). However, the increase in survival rate of such patients is only a trend.

Controlled studies with intravenous administration amino acid supplements gave conflicting results. In one study, daily administration of 70-85 g of amino acids reduced mortality and improved serum bilirubin and albumin levels; in another, the effect of such treatment was short-term and insignificant. In a subsequent study, the incidence of sepsis and fluid retention increased in patients receiving this treatment, although serum bilirubin levels decreased. Supplementing food with branched-chain amino acids has not been shown to affect mortality rates. Oral or intravenous amino acid supplementation should be reserved for a very small number of patients with jaundice and severe malnutrition.

Colchicine did not improve early survival of patients with alcoholic hepatitis.

Propylthiouracil. Increased metabolism caused by alcohol potentiates hypoxic liver damage in zone 3. Propylthiouracil attenuates hypoxic liver damage in animals with a hypermetabolic state; this drug has been used to treat patients with alcoholic liver disease, mainly in the cirrhosis stage. A controlled study confirmed the effectiveness of this drug, especially in the long term, in those patients who continued to drink alcohol in smaller quantities. However, propylthiouracil has never been approved for the treatment of alcoholic liver disease.

Prognosis for acute alcoholic hepatitis

The prognosis for acute alcoholic hepatitis depends on the severity of its course, as well as on the severity of abstinence from alcohol. Severe forms of acute alcoholic hepatitis can lead to death (death occurs in 10-30% of cases). Relapses of acute alcoholic hepatitis against the background of previously formed cirrhosis of the liver lead to its steady progression, decompensation and the development of severe complications (severe portal hypertension, gastrointestinal bleeding, hepatic-renal failure).

Acute alcoholic hepatitis is characterized by a high frequency of its transition to cirrhosis of the liver (in 38% of patients within 5 years); complete recovery in acute alcoholic hepatitis is observed only in 10% of patients, subject to complete cessation of alcohol intake, but, unfortunately, in some patients Abstinence does not prevent the development of liver cirrhosis. Probably, in this situation, the mechanisms of self-progression of liver cirrhosis are activated.

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Alcoholic hepatitis disease is characterized by such symptoms of liver damage as: inflammation, fatty degeneration and fibrosis, and the treatment of this disease is aimed specifically at eliminating these pathologies.

All of them arise from drinking alcohol. Alcohol toxins affect the organ and lead to disease. If, with this diagnosis, a person continues to consume alcoholic beverages, it can progress to the next stage - cirrhosis, which can no longer be cured.

Course of the disease " alcoholic hepatitis“Can occur in acute or chronic form. Therapy for this form of hepatitis includes: stopping alcohol consumption, eating high-calorie foods, and normalizing liver function with the help of medications.

K70.1– code for this disease in ICD-10.

Hepatitis from alcohol

In the international classification of diseases, diagnosis "alcoholic hepatitis" appeared in 1995. It is from this time that the history of this disease can be documented.

The term "alcoholic hepatitis" was given to the disease, which is one of the symptoms of alcoholic liver disease.

Gastroenterology classifies alcoholic liver disease and alcoholic fibrosis as the initial stage of such a serious disease as cirrhosis. How does this happen?

When alcohol enters the liver, it is metabolized into acetaldehyde, which triggers chemical reactions in the body that first lead to hypoxia of liver cells and then to their death. Due to toxic poisoning in the liver tissues, a diffuse inflammatory process develops. The development of this chronic disease usually occurs after 5-7 years of constant alcohol consumption.

Etiology of the disease

The main cause of the disease is drinking alcohol for a long time. Changes in the liver in a man begin to occur with regular daily alcohol consumption of 50-80 grams, in women at 30-40 grams per day, and in the liver of a teenager at 15-20 grams.

Depending on the quantity and quality of alcohol consumed, the duration of consumption, as well as the individual characteristics of the body, this disease progresses at different rates.

The likelihood that a person will develop alcoholic hepatitis increases if the person: is genetically predisposed to the disease, has had viral hepatitis, or has a poor diet.

Forms of alcoholic hepatitis

This disease can be either chronic or progressive. Chronic course manifests itself in a relatively stable form of the disease. If you stop drinking alcohol during this form of the disease, the liver cells will recover. If a person continues to consume alcohol, the disease becomes progressive.

Depending on the extent of the process progressive form can be mild, medium and severe. This form is characterized by the fact that a finely focal necrotic lesion appears in the liver, often turning into cirrhosis. If treatment is started in a timely manner, the development of the disease can be stopped, but residual effects will persist.

During the course of the disease they secrete acute And chronic form. The acute stage of alcoholic hepatitis is characterized by acute progressive liver damage. Acute hepatitis diagnosed in 70% of people who abuse alcohol. In 4% of these patients, the disease rapidly progresses to liver cirrhosis. Acute form this disease happens latent, icteric, cholestatic, and fulminant. After prolonged heavy drinking, serious forms of the disease often develop against the background of liver cirrhosis.

Symptoms

Latent flow Alcoholic hepatitis is not characterized by any distinctive symptoms. A person complains of heaviness in the right hypochondrium and slight nausea. The diagnosis is made when tests reveal elevated levels of transaminases, and is confirmed by a biopsy.

Jaundice the disease manifests itself most often. It is characterized by the following symptoms: anorexia, diarrhea, general weakness, nausea and vomiting, yellowness of the skin and sclera, weight loss. A person may also experience an increase in temperature.

During the examination, the doctor notes enlargement and tenderness of the liver upon palpation. The liver is smooth, while in cirrhosis it is lumpy. The following signs may also indicate underlying cirrhosis: an enlarged spleen, accumulation of fluid in the abdominal cavity, symmetrical redness of the palms, as well as the appearance of spider veins or spider veins.

Cholestatic variant Alcoholic hepatitis is rarely diagnosed and has a long course. It is characterized by symptoms such as: colorless feces and dark urine, jaundice and severe itching of the skin.

For fulminant course The disease is characterized by intensive development of hemorrhagic and hepatorenal syndromes, as well as pronounced changes in laboratory markers. Possible death due to hepatic coma and hepatorenal syndrome.

For chronic stage The disease is characterized by moderate severity of both clinical symptoms and laboratory markers. Diagnosis is made using a biopsy and is based on distinctive features that, in the absence of cirrhosis, indicate an inflammatory process.

Diagnosing this disease is quite difficult. With a mild course of alcoholic hepatitis, no distinctive signs may be observed. Only changes in the clinical parameters of a person’s blood test can help detect it.

Indicators acute stage diseases in the blood test serves increase (or rarely - decrease) in the number of leukocytes, accelerated ESR, increase markers liver damage, as well as anemia caused by a lack of vitamin B12.

A decrease in the number of white blood cells occurs due to the effect of alcohol toxins on the bone marrow. During an examination of the liver using ultrasound, it is discovered that it is enlarged, has a heterogeneous structure and smooth contours. MRI examination of organs reveals damage to the pancreas such as collateral hepatic blood flow.

Examination of the liver using ultrasound in the chronic stage shows that it is slightly or moderately enlarged, has a homogeneous structure and increased echogenicity. A blood test shows slight changes. Fibrosis, necrosis and inflammation of the liver in alcoholic lesions can be detected using a biopsy. The manifestation of these lesions depends on the duration of the disease, as well as on its form.

If the doctor reveals symptoms of liver damage during the examination, he should question the patient about his drinking habits. The patient himself does not always give complete information about himself. In addition, a person who abuses alcohol very often incorrectly estimates the amount of alcohol consumed. In such cases, the doctor must interview not only the patient himself, but also his relatives and only then give recommendations.

Prevention and prognosis

How long can a person diagnosed with alcoholic hepatitis live? If the patient is diagnosed with mild or moderate severity of the disease, and he is ready to completely stop consuming alcohol, then the prognosis is favorable. In this case, the liver can fully recover with appropriate treatment.

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