Differential diagnosis of liver cirrhosis table. Differential diagnosis. Distinctive features of cirrhosis of the liver

By the word "hepatitis" an ordinary educated person living in a large city means inflammation of the liver caused by viruses. Most often, the cause is drug addiction, sexual contact, blood manipulation and other possible ways of infection. Sometimes they recall alcoholic liver disease, cirrhosis and other conditions that are united by common symptoms and principles of treatment.

General information

But it turns out that sometimes you don’t need to be at risk, use drugs, visit dubious nail salons and use alcohol surrogates to develop hepatitis. Sometimes it occurs without any connection with alcohol intake or with a viral infection. This disease is called autoimmune hepatitis.

For the first time, cases of incomprehensible liver damage began to be recorded since the early 1950s, mainly in young women. They suffered from chronic hepatitis, but at the same time, the level of gamma globulins in their blood was increased. A characteristic feature of this condition was a good response to the use of hormones.

Then, with the improvement of laboratory methods, it turned out that it often occurs in patients with SLE, or systemic lupus erythematosus, which occurs almost exclusively in women. Therefore, in the middle of our century, this disease was called "lupus hepatitis". Then came the era of intensive research on this disease. In the following decades, diagnostic criteria were developed and many drugs were tested. The greatest success was achieved in the treatment of this disease with corticosteroid hormones, as well as cytostatics - immunosuppressants. It can be considered that it is in the treatment of autoimmune hepatitis that hepatology has achieved significant success - it is with this pathology that the right treatment for the first time has led to a significant increase in life expectancy in patients.

Currently, this disease, despite careful study, remains largely mysterious.

But we can recall diseases such as diabetes mellitus and NUC (ulcerative colitis). Despite complete information and understanding of the mechanisms of pathogenesis, the world situation (especially in relation to the first one) is very far from favorable. What is this pathology from modern positions?

Definition

Currently, there is no single generally accepted definition of the disease. Therefore, the most correct, “combined” definition can be formulated as follows: autoimmune hepatitis is a chronic process of inflammation and necrosis in the liver that occurs for unknown reasons, with the circulation of a significant amount of autoantibodies to tissues in the blood, an increase in the level of gamma globulins, which responds well to treatment with immunosuppressants.

Etiology and epidemiology

This disease is simply “lost” against the background of a huge number of chronic viral hepatitis B and C, against the background of alcoholic liver damage. Even in the countries of the European Union, with a perfect level of diagnosis, the prevalence does not exceed two cases per 10 thousand people. Women are three times more likely to develop autoimmune hepatitis than men.

Perhaps this is due to the fact that women are generally more prone to the development of autoimmune pathology than men. Such "big" diseases as systemic scleroderma, systemic lupus erythematosus, rheumatoid arthritis are more common in women. After all, the childbearing function involves the bearing of an organism that is genetically different from the mother. This requires both a great intensity of the immune background, and its tolerance to someone else's (paternal) genetic material.

The chances of getting sick with autoimmune hepatitis are high in two periods of life: both in young (25 years) and in old (60 years) age, although recently these peaks have “flattened out”, and there is a tendency to increase the incidence, both in men and women. and in women at all stages of life.

Etiologically, there is no clear cause of the disease. Many researchers associate the appearance of autoimmune hepatitis with the environmental situation, stress, a chronic decrease in the body's immune defenses, and intoxication (alcohol and drugs). All this adversely affects the function of the immune system and liver.

About classification

Two options for the development of hepatitis have been identified:

• in the first type (occurs in 85% of all cases), patients have antinuclear antibodies and (or) antibodies to smooth muscles. Also, with this type of hepatitis, antibodies to neutrophils are found - this is typical for such a disease as primary sclerosing cholangitis (it is also referred to as connective tissue diseases). The antigen in this situation is a liver-specific protein;
• the second type of hepatitis is characterized by the presence of antibodies to microsomes of the liver and kidneys. It is detected mainly in childhood, and in adults it manifests itself in only 20% of cases. The specific antigen for this form of the disease is one of the well-known liver cytochromes - the P 450 - 2 D enzyme. Often this type of disease, in addition to liver damage, is accompanied by the development of type 1 diabetes mellitus, or autoimmune thyroiditis.

How does the disease develop, and how does the autoimmune process lead to liver damage?

Pathogenesis

The basis for the development of a pathological immune response, which ultimately leads to the emergence of autoimmune hepatitis, is the so-called cross-antigenic reactivation, or molecular mimicry. This means that if at the time of "study" of T-lymphocytes in the thymus, some proteins of the body are not studied and recognized by them, then in the future they may encounter a foreign antigen similar to them. And in the future, having met the proteins of their body that fell on the surface of the membrane, similar to enemies, T-lymphocytes successfully organize an attack on them without recognizing their own.

In short, the scheme for the development of autoimmune hepatitis looks something like this:

1. Genetic predetermination (with hepatitis of the first type).

Associated with certain alleles of the HLA system, or major histocompatibility system. It is these genes that are responsible for a powerful immune response when antigens from the outside world enter.

As we said above, in this case we are talking about “deception” of the “friend or foe” system;

1. Launching a trigger mechanism (viral hepatitis, drug aggression, herpes infection);
2. Expression of "false" antigens on the surface of hepatocytes;
3. Lymphocytes (T and B) are activated, which respond to these decoys;
4. There is a production of gamma-globulins, or autoantibodies, a pool of inflammatory mediators (cytokines, metabolites of arachidonic acid) is formed;
5. Development of alteration (damage) of liver tissues;
6. The emergence of the clinic of autoimmune hepatitis.

Here is an extremely generalized scheme of the pathogenesis of autoimmune hepatitis. But in fact, as in other systemic diseases, the “key” to the development of the disease is the false acceptance of one’s own structures as foreign and the development of an immune response.

Clinical manifestations

How does autoimmune hepatitis manifest itself? Are there any differences in the course of this hepatitis, according to which it is possible to suspect the presence of immune inflammation of the liver?

Debut

In the initial period of the disease, there are two options for the development:

• there are no differences from acute viral hepatitis with a typical picture of the disease.

There are typical clinical manifestations: jaundice, intoxication, laboratory symptom complexes of cytolysis and necrosis of liver tissues. There is weakness, loss of appetite, dark urine, discoloration of feces. ALT and AST (liver aminotransferases) increase tenfold or more. Then intense jaundice develops, skin itching appears (with cholestasis), and patients are usually hospitalized in an infectious diseases hospital with a diagnosis of acute viral hepatitis.

But, unlike viral hepatitis, there is no improvement, and the disease is progressive, and after 1-6 months, antibodies characteristic of the autoimmune process appear in the blood;

• autoimmune hepatitis can begin in a different way: symptoms appear that are not associated with liver damage, but resemble various rheumatic diseases: lupus, myocarditis, rheumatism, rheumatoid arthritis.

Often, autoimmune hepatitis manifests with a pronounced articular syndrome: polyarthritis, vascular disorders occur, and a hemorrhagic rash may appear. These patients unsuccessfully go to the doctors: the treatment does not help them, and only after 4-6 months do symptoms such as icterus of the sclera appear, the liver and spleen increase in size.

Sometimes patients are observed for several months with a fever of unknown origin, with an increase in ESR, with diagnoses of thyrotoxicosis, suspected tuberculosis, and with a host of other diagnoses. Naturally, no treatment is carried out, or, on the contrary, they treat “everything” and “from everything”.

Expanded stage

At its height, autoimmune hepatitis is manifested by a variety of symptoms of liver damage:

• fever (from 37 ° to 39 ° C), with an increase in ESR even up to 60 mmh and above;
• arthralgia - pain in the joints (large in the arms and legs);
• hemorrhagic hemorrhages in the skin, or recurrent purpura;
• sometimes - psoriasis, symptoms of focal scleroderma;
• endocrinopathy - amenorrhea, striae on the thighs and abdomen, hirsutism occurs;
• jaundice interspersed, easing during remission and rising during exacerbation;
• the liver enlarges and hardens.

Surprisingly, many patients with hepatitis, despite the pronounced manifestations, feel good.

In conclusion, the description of the symptoms, it must be said that autoimmune hepatitis "lays" the foundation for heart damage, the occurrence of glomerulonephritis, iridocyclitis, amenorrhea, lymphadenopathy, anemia, and many other syndromes.

Most patients with this liver disease have a continuous form of autoimmune hepatitis. Less often there is an alternation of exacerbations and remissions. With a continuously relapsing course, the prognosis is much worse.

Diagnostics

Given the similarity of autoimmune hepatitis and the multifaceted clinical picture, the absence of pathognomonic symptoms, it was decided by an international group to study this disease in 1999 to compile diagnostic criteria and a scoring table that helps to make a diagnosis.

The most characteristic for autoimmune hepatitis were the following criteria:

• female;
• high levels of gamma globulins;
• titers of type-specific antibodies above 1:80;
• negative blood test for viral hepatitis (PCR, ELISA);
• a liver biopsy showed lobular hepatitis and bridging necrosis, a very characteristic finding.

In summary, it should be said that if the patient has:

• the above clinic;
• he was not given a blood transfusion;
• he did not take drugs with a hepatotoxic effect;
• did not abuse alcohol;
• did not suffer from acute and chronic hepatitis of viral etiology;

and if at the same time he has a high level of gamma globulins, specific antibodies, and his ALT and AST significantly predominate over the level of alkaline phosphatase - this is “certain autoimmune hepatitis”.

Principles of treatment

Unlike viral liver diseases, in autoimmune hepatitis, the main tactics of treatment is the appointment of corticosteroid hormones. In this case, the main drug is prednisone. It acts on T - lymphocytes, causing their suppression, and inhibits the cycle of their reactions. As a result, the process of inflammation and necrosis in the liver tissues slows down.

Despite the side effects of hormones, their effect is not to improve well-being (as mentioned above, patients feel good), but to actually prolong life. Therefore, with autoimmune hepatitis, you often have to put up with some of them.

Cytostatic drugs, such as azathioprine, are also used in the treatment. But there are cases when you can not prescribe these drugs, but observe the patient. This is possible with an asymptomatic course, with low rates of transaminases. On the other hand, in case of deep dysfunctions of the organ, in the presence of decompensated cirrhosis, anemia, ascites, portal hypertension, treatment is already too late.

Therefore, absolute indications for the appointment of hormones and immunosuppressive therapy are a vivid clinical picture, progression of symptoms, and a picture of bridging and (or) multilobular necrosis proven by a histological examination of a liver biopsy.

In the treatment, hormones are used both separately and in combination with azathioprine. Hormone intake should be long - sometimes from 6 months to six months, and some patients are shown lifelong therapy. The diagnosis we are talking about is so serious that there are no absolute contraindications to the appointment of hormones.

Even diabetes, gastric ulcers, and osteoporosis, which are considered absolute contraindications to corticosteroids in other cases, are relative here.

As for azathioprine, there are still absolute contraindications: a pronounced aplastic effect with inhibition of hematopoietic function, pregnancy, severe leukopenia or malignant neoplasms.

Usually, a noticeable improvement occurs already in the first weeks after prescribing the drugs, and the normalization of laboratory parameters by the end of the year in 75% of patients with correctly selected therapy. But this is true under the condition of a decrease in the level of transferases - ALT and AST in the peripheral blood. If they are not reduced, then there is no need to wait for remission. In general, treatment failures occur in every fifth case.

Forecast

Despite all the successes in the treatment of autoimmune hepatitis, the greatest number of deaths occurs in the early period of the disease, as the most active. If the patient is not diagnosed for a long time, and he does not receive treatment, then there is a chance to live the next five years in only 50% of patients.

Under favorable circumstances, with modern immunosuppressant treatment, there is an 85% chance that the patient will live 10 years.

But the total life expectancy of a patient with the occurrence of such a process in the liver does not exceed 15 years, in extreme cases - 20 years. Therefore, when a type 2 disease occurs in children, this diagnosis still sounds like a sentence. But times are changing. Now cirrhosis of the liver (the outcome of the process) is not a "ticket to the cemetery" without any alternative. Patients with autoimmune liver disease may be on the waiting list for a liver transplant for several years, and after transplantation, life expectancy is significantly extended.

In conclusion, we should express the hope that, due to the progress of nanotechnologies and cellular techniques, in the near future it will be possible to control the development of autoimmune reactions at the cellular level, and autoimmune damage to the liver, as well as other organs and systems, will not take us by surprise.

Ascites (otherwise dropsy of the abdomen) is the accumulation of an excessive amount of fluid in the abdominal cavity. This is not a disease, but an alarming symptom of many diseases. Ascites increases the risk of serious complications, including thrombosis, so this symptom should not be underestimated. The causes of ascites include diseases such as cirrhosis of the liver, kidney failure, tumors of the abdominal cavity, and others. The main symptoms of ascites are abdominal pain, an increase in abdominal circumference, and weight gain. Therapy consists in treating the underlying disease that is causing this symptom (in many cases, cirrhosis of the liver).

• 1Mechanism of ascites formation
• 2Etiology of the disease
• 3Degrees of disease
• 4Symptoms and diagnosis of pathology
• 5Therapeutic measures

1Mechanism of ascites formation

Ascites is an excess accumulation of fluid in the peritoneal cavity (physiologically, there is about 150 ml of fluid there). Ascites is observed if the patient has more than 500 ml of fluid in the abdominal cavity. As a rule, it is a serous fluid. It contains more than 3 g/dl of protein (mainly albumin), as well as sodium, potassium and glucose in the same concentrations as in serum. The presence of neutrophils in the fluid may indicate an existing infection. And the presence of red blood cells suggests the distribution of the tumor process in the abdominal cavity.

2Etiology of the disease

The main causes of ascites include:

• increase in venous pressure in the vena cava;
• obstructed outflow of blood from the liver (for example, cirrhosis of the liver);
• obstructed outflow of lymph;
• an increase in the permeability of the vessels of the peritoneum (for example, inflammatory processes of various origins);
• decrease in plasma oncotic pressure (eg, nephrotic syndrome).

The most common diseases that cause dropsy of the abdomen:

• cirrhosis of the liver;
• tuberculosis;
• congestive circulatory failure;
• inflammation of the pancreas;
• portal vein thrombosis;
• kidney failure;
• malignant tumors located in the abdominal cavity and in the pelvic cavity.

Ascites is characterized by the following symptoms: an increase in the circumference of the abdomen, an increase in body weight, abdominal pain, a feeling of discomfort and expulsion outward in the abdominal cavity. Later symptoms are problems with sitting and walking, disorders of the gastrointestinal tract, swelling of the legs and vulva.

3Degrees of disease

Due to the volume of fluid collected in the peritoneal cavity, ascites can be divided into:

• soft (I degree);
• moderate (II degree);
• severe (III degree).

With mild ascites, diagnosis is possible only with the help of ultrasound.

The diagnosis of "moderate ascites" is made when the volume of fluid collected in the peritoneal cavity exceeds 500 ml. The belly looks like the belly of a frog. You can feel the moving fluid in the abdominal cavity. To recognize ascites, the doctor may tap on the patient's abdomen when he lies on one side, then on the other side. Then you can observe the moving fluid in the peritoneum of the patient when changing his position.

Severe ascites gives the characteristic appearance of a standing patient: a large belly and thin limbs. The patient's abdomen is greatly enlarged and dense. The navel is flattened, but an umbilical hernia may occur (more clearly visible during coughing). Blood vessels can show through the skin on the abdomen. These vessels diverge from the navel to the sides. The skin on the abdomen is thin and shiny.

4Symptoms and diagnosis of pathology

As a rule, the first symptom that is observed in patients is the tightness of habitual clothing and the need to loosen the belt. In addition, there is often a feeling of fullness, bloating, or discomfort, nausea, and (less commonly) pain.

If the volume of the collected fluid exceeds 1.5 liters (in very advanced cases), it can reach a feeling of suffocation. Long-lasting dropsy of the abdomen can lead to the development of pleural exudate (hydrothorax), i.e. collection of water in the pleural cavity, which surrounds the lungs. More often it has a right-hand drive than a left-hand drive. Pleural exudate is caused by the flow of fluid from the abdominal cavity into the pleural cavity by lymphatic vessels that pass through the diaphragm.

Ascites is difficult to recognize in an obese patient. The disease must always be differentiated from pregnancy, bladder enlargement, ovarian cancer, which can produce similar symptoms.

To diagnose ascites, the doctor prescribes a blood test, a study of liver enzymes. As a rule, samples of fluid accumulated behind the peritoneum are used to study its composition. Before a fluid sample is taken, an ultrasound is often done to help assess the size and shape of organs in the abdomen. An alternative to ultrasound is computed tomography. Imaging is of particular importance, especially if the patient is obese or the amount of fluid collected in the peritoneal cavity is small.

Sometimes additional studies are needed, for example, cytopathology. To distinguish ascites caused by hypertension from ascites due to other causes, a diagnosis of fluid taken by means of a puncture of the abdominal cavity (paracentesis) is carried out. Removal of fluid is also carried out for medicinal purposes. It is used at the beginning of the treatment of advanced stage ascites or in the case of ascites resistant to diuretic treatment.

Indications for paracentesis:

• recently diagnosed;
• in order to differentiate ascites from inflammation of the peritoneum.

The course of the procedure:

• during the procedure, the patient is in a reclining position (the body is raised);
• the doctor performs the puncture with a needle, the length of which depends on the thickness of the patient's adipose tissue;
• the puncture is carried out in a place where the presence of fluid is noted (as a rule, this is a place in the navel area);
• for the first time, a fluid volume of 50-100 ml is taken, which is then analyzed.

A sample of the liquid is tested for protein concentration, for the presence of possible bacteria. The appearance of the fluid may suggest the cause of the ascites. Straw-colored fluid occurs with cirrhosis of the liver (although it may be bilious or clear), also with heart failure or nephrotic syndrome (although in this case it may be milky). Purulent and turbid liquid occurs with purulent inflammation of the peritoneum. And with neoplasms, diseases of the pancreas and tuberculosis, the appearance of the liquid is varied (it can be a hemorrhagic, milky liquid, and in the case of tuberculosis, even transparent).

5Therapeutic measures

Ascites is a symptom of various diseases. In 80% of cases, it accompanies cirrhosis of the liver. In about 10% of cases, it is a sign of malignancy. May also occur with heart failure, tuberculosis, nephrotic syndrome, or AIDS. Approximately 5% of patients have at least two causes of ascites.

Treatment of ascites is mainly in the treatment of the underlying disease, which caused it.

Diuretics (spironolactone, furosemide) are used to reduce the fluid content in the peritoneal cavity. Patients should reduce fluid and sodium intake in their diet.

If treatment with diuretics does not bring the desired results, other methods are used to remove excess fluid from the body, including the previously mentioned drainage with a special needle. This type of treatment is used in patients with an acute form of the disease. If the disease is associated with a serious liver condition, liver transplantation is considered.

In a small number of patients who experience relapses, the treatment option is the use of valves. There are several types of them, but none of them prolong the lives of patients and, in general, they are the first step towards a liver transplant.

Bleeding from the esophagus is a serious problem requiring urgent medical attention. help. Severe bleeding if left untreated can be fatal. Small and moderate develops chronic blood loss, leading to a breakdown and complication of the underlying disease.

Causes of the disease

The causes of esophageal bleeding can be many factors, the most common include:

• stomach ulcer;
• cirrhosis of the liver;
• gastritis;
• pathology of the esophagus;
• varicose veins of the stomach;
• tumors;
• burn;
• cardiovascular diseases;
• long-term use of drugs;
• alcohol poisoning;
• prolonged negative emotions;
• hemophilia.

In medicine, there are cases that such a condition is caused by taking medications such as Nise, Aspirin, children are especially susceptible to this. Also, due to severe vomiting, which alcohol poisoning often provokes, the longitudinal membrane of the esophagus is torn and a dangerous condition develops.

Whatever the cause of esophageal bleeding, it must be treated as a critical condition.

Symptoms of the disease

Such a condition is a rather rare disease, which sometimes not only patients, but also doctors cannot determine in a timely manner. This is due to the fact that with unexpressed bleeding, there is a gradual flow of blood into the stomach, which is digested there, while not showing clear signs. Even if this pathology is accompanied by pain, experts often attribute it to gastritis. Excessive bleeding makes it difficult to identify the source of this condition. However, there are specific symptoms of the disease, as a rule, these are:

• Hematemesis. When the pathology is caused by trauma, a rush of an ulcer, then a scarlet color of blood is released. This means that she did not have time to undergo digestion, this phenomenon occurs with heavy bleeding. Slight bleeding causes coffee grounds to vomit as the fluid has been processed by gastric juices. If cherry color is released during vomiting, then varicose veins of the stomach take place.
• The patient's feces are changing, it has a rich black color. This condition occurs when blood passes through the digestive tract.
• A sharp decrease in blood pressure, manifested by dizziness, nausea, malaise, weakness.
• Tachycardia, palpitations.
• Increased need for water.
• Skin change.

The intensity of the signs depends on the degree of hemorrhage, with a slight lesion, the symptoms are sometimes not striking. If a person has at least one of the symptoms, then it is urgent to contact a specialist for diagnosis.

Diagnosis of the disease

For an accurate diagnosis, the following examination is necessary:

• how to get rid of esophageal varicose veins

• a general blood test establishes the fact of bleeding, which will show a decrease in hemoglobin and red blood cells;
• fecal analysis will help determine hidden hemorrhage;
• FGDS is an accurate method that will not only help determine the site of bleeding, but also administer a hemostatic injection and suture a burst vessel;
• Ultrasound will not help to accurately determine the location of the pathology, but will determine the condition of the internal organs;
• MRI, CT will determine the cause of the hemorrhage;
• x-ray with the introduction of a dye will detect the localization of the pathology.

First aid

When bleeding, it is important to call for medical help as soon as possible and provide competent pre-medical intervention. Since the imposition of tourniquets is not advisable here, many do not know what to do in this situation.

First of all, you need to calm down yourself. Provide the patient with complete rest. He should be in a horizontal position, which will not only limit physical activity, but help control how much blood he has lost. Since the horizontal position limits its entry into the digestive tract.

It is necessary to create comfort for the patient, you should remove unnecessary clothes from him and cover him with a blanket. An important condition is the control of blood pressure and pulse rate, which should be carried out every 10 minutes. A lower pressure increases the heart rate and indicates that a large amount of blood has been lost. If the blood pressure drops below 80 mm Hg, and the heart rate increases to 130 beats, then this is an indicator of the possibility of a shock state.

In such patients, fainting may occur, indicating extensive blood loss and requiring immediate action. In order to bring a person into consciousness, you can sprinkle him with water or let ammonia be inhaled. Ice, taken orally in small pieces, will help alleviate the condition. The patient should be transported exclusively on a stretcher in a supine position.

Treatment of pathology

Treatment of hemorrhage from the esophagus must be done in a hospital. First of all, measures are taken to stop bleeding, which include:

• the introduction of the Blackmore probe, which is located in the esophagus. Then the probe is inflated with air, due to which the cuff is inflated, pressing the vessels. In this cuff there is also a tube that does not increase the vascular lumen, through which nutrition and drugs are supplied. This device can be in the patient's body for several days, until a blood clot forms on the damaged vessel;
• with the help of an operative intervention performed by means of laparoscopy, sutures are applied to the damaged vessel or cauterization is performed using electricity or a laser;
• together with surgery, drug therapy is used, which involves the introduction of hemostatic drugs, for example, Vikasol, Calcium Chloride. Sometimes it is required to replenish the blood loss with erythromass;
• if the erosive area suggests an infection, then a course of antibiotic therapy may be required, for example, Macrolide or Cephalosporin preparations.

Patients for a long time should be on the strictest bed rest. They are forbidden to eat on their own, they receive food by intravenous administration. After they have been allowed to feed on their own, they should eat their food warm and pureed.

Esophageal bleeding is a serious disease, at the first symptoms of which it is necessary to urgently consult a doctor in order to avoid the development of complications and death.

Version: Directory of Diseases MedElement

Alcoholic cirrhosis of the liver (K70.3)

Gastroenterology

general information

Short description

Alcoholic liver cirrhosis- chronic liver pathology that develops with chronic alcohol intoxication, with the gradual death of hepatocytes, widespread fibrosis and nodes of atypical regeneration, gradually replacing the parenchyma Parenchyma - a set of basic functioning elements of the internal organ, limited by the connective tissue stroma and capsule.
; accompanied by insufficiency of hepatocyte functions 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)
and changes in hepatic blood flow leading to jaundice, portal hypertension, and ascites Ascites - accumulation of transudate in the abdominal cavity
. It is a type of alcoholic liver disease.

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

Flow period

chronic pathology. The course is more favorable with the cessation of alcohol abuse.

Classification

Alcoholic cirrhosis of the liver:

1. Active:
- with intrahepatic cholestasis;
- in combination with acute alcoholic hepatitis;
- compensated;
- decompensated.

2. Inactive.

3. With hemosiderosis of the liver.

4. In combination with late cutaneous porphyria (develops with a hereditary predisposition to it).

To assess the severity of alcoholic cirrhosis of the liver, the Child-Pugh scale and other classifications can be applied (see also the rubric "Fibrosis and cirrhosis of the liver" - K74).

Etiology and pathogenesis

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

The risk of developing alcoholic liver disease occurs with the use of more than 40 g of pure ethanol per day. When using more than 80 g of pure ethanol for 10 years or more, the risk of liver cirrhosis increases. There is no direct correlation between the degree of liver damage and the amount of alcohol taken: less than 50% of people who drink alcohol in dangerous doses have severe forms of liver damage (hepatitis and cirrhosis).
The development of the cirrhotic process occurs without clinical and histological signs of acute alcoholic hepatitis in 8-20% of patients with alcoholic liver disease (alcoholic liver fibrosis). Alcoholic liver steatosis Hepatic steatosis is the most common hepatosis in which fat accumulates in the liver cells.
without signs of fibrosis and hepatitis, as a rule, does not lead to the formation of cirrhosis.

Epidemiology

Prevalence sign: Common

Sex ratio (m/f): 2

At autopsy, liver damage is determined in 65-70% of people who abuse alcohol, and the incidence of liver cirrhosis is 10-15%.
Alcoholic cirrhosis of the liver in prevalence in developed countries significantly prevails over cirrhosis of the liver of other etiologies.

Factors and risk groups

Risk factors for the development and progression of the disease:
- taking from 40-80 grams of ethanol per day for 10-12 years;
- genetically determined phenotypes of enzymes that provide a high rate of ethanol metabolism and accumulation of acetaldehyde;
- infection with hepatotropic viruses;
- intake of hepatotoxic agents;
- overweight;
- presence of alcoholic fibrosis Fibrosis is the growth of fibrous connective tissue, which occurs, for example, as a result of inflammation.
or alcoholic hepatitis;
- female.

Clinical picture

Clinical Criteria for Diagnosis

Weakness, pain in the right hypochondrium, decreased appetite, nausea, vomiting, dyspepsia, palmar erythema, telangiectasias, petechiae, purpura, bleeding from the veins of the esophagus, dysmenorrhea, gynecomastia, Dupietren's contracture, ascites, jaundice

Symptoms, course

Clinical signs of alcoholic disease range from mild symptoms to severe liver failure and portal hypertension.

Typical symptoms:
1. Weakness, increased fatigue, decreased performance.

12. Endocrine disorders:
- dysmenorrhea Dysmenorrhea is a common name for menstrual disorders
;
- amenorrhea Amenorrhea - absence of menses for 6 months or more
;
- uterine bleeding;
- violations of secondary hair growth;
- acne Acne (acne) - inflammation of the sebaceous glands
;
- gynecomastia Gynecomastia - an increase in the mammary glands in men
;
- testicular atrophy;
- enlargement of the parathyroid glands;
- the presence of palmar erythema, telangiectasia, Dupuytren's contracture Dupuytren's contracture (synonymous with palmar fibromatosis) - painless cicatricial degeneration and shortening of the palmar tendons; It is manifested by a violation of the ability to unbend the fingers, a nodular thickening of the skin on the palms.
.
13. Ascites.

14. Other symptoms of excessive alcohol consumption (see the Diagnosis section).

The cholestatic form is manifested by jaundice, discoloration of feces, darkening of urine, pain in the right hypochondrium, itching; possible fever.

Diagnostics

The diagnostic criteria are the presence of an alcohol history and the morphological picture of liver cirrhosis.

The fact of alcoholism
1. An alcohol history is revealed by questioning the patient and relatives according to a special questionnaire, which significantly increases the likelihood of diagnosing alcoholism.
2. The most common symptomatology(alcoholic stigmas detected during examination):
- expansion of the vessels of the nose and sclera;
- enlargement of the parotid glands;
- atrophy of the muscles of the shoulder girdle;
- bright spider veins;
- gynecomastia;
- Dupuytren's contracture;
- testicular atrophy;
- the presence of lesions of other organs and systems ((pancreatitis, dilated cardiomyopathy, peripheral neuropathy).

The starting method is considered to be ultrasound, the "gold standard of diagnosis" is a liver biopsy.

1. Ultrasound:

The liver parenchyma has a hyperechoic structure;
- at the stage of cirrhosis - the corresponding sonographic picture.

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

3.FEGDS carried out to identify the presence and degree of varicose veins of the esophagus and stomach, to detect portal gastropathy (erosive-hemorrhagic gastritis) and assess the risk of bleeding.
Rectoscopy is used to identify anorectal varicose veins.

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

At puncture liver biopsy with histological examination find:
- hepatocyte steatosis is predominantly macrovesicular;
- Mallory bodies Mallory bodies - acidophilic clumps around the nucleus, formed in the cytoplasm (often hepatocytes) during protein dystrophy
;
- diffuse fibrosis and diffuse micronodular cirrhosis.

5. CT Computed tomography (CT) is a method of non-destructive layer-by-layer study of the internal structure of an object, based on the measurement and complex computer processing of the difference in X-ray attenuation by tissues of different density.
And MRI MRI - magnetic resonance imaging
have sufficient sensitivity and specificity.

6. Radionuclide liver scan: diffuse decrease in the absorption of the isotope, uneven distribution of the radioactive drug, its increased accumulation in the spleen.

Laboratory diagnostics

Signs of alcohol abuse:

1. A sharp increase in the level of gamma-glutamyl transferase (GGT) in the blood serum and its sharp decrease against the background of withdrawal. GGT is a more sensitive laboratory test (sensitivity 69-73%) than AST or ALT ALT - alanine aminotransferase
for alcoholic liver disease. The low specificity (65% to 80%) of GGT is due to its presence in many other organs and changes in the induction of microsomal enzymes by various drugs. Elevated GGT does not always indicate alcoholic liver disease.

2. Increasing the concentration of carbohydrate-free transferrin (desialized transferrin, asialotransferrin, CDT) is a relatively inexpensive, but not widely used test for detecting alcohol abuse. Data on the specificity (82% to 92%) and sensitivity (58% to 69%) of a test to detect current alcohol abuse can vary widely. The high information content of the test has been proven for young men who drink alcohol at a dose of more than 60 g / day.

3. Macrocytosis ( MCV) - this test, as a diagnostic test for detecting the fact of alcohol abuse, lacks sensitivity (27-52%), but the changes become quite sensitive (85-91%) for patients who drink alcohol more than 50 g / day (in the absence of vitamin therapy B12 or folic acid).

4. Electrolyte disorders:
- hyponatremia - often present in patients with cirrhosis of the liver;
- hypokalemia and hypophosphatemia - common causes of muscle weakness in alcoholic liver disease in general;
- hypomagnesemia can lead to permanent hypokalemia, which predisposes patients to seizures during alcohol withdrawal Withdrawal is a condition that occurs as a result of a sudden cessation of the intake (introduction) of substances that caused substance abuse, or after the introduction of their antagonists.
; T eating has low sensitivity (27-52%) and high specificity (85-91%).

Signs of liver damage:

1. Increasing the level of aminotransferases: AST AST - aspartate aminotransferase
(sensitivity - 50%, specificity - 82%) and ALT ALT - alanine aminotransferase
(sensitivity - 35%, specificity - 86%) increased in all forms of alcoholic liver disease when taking alcohol more than 50 g / day. "Classic" AST ratio AST - aspartate aminotransferase
/ ALT ALT - alanine aminotransferase
with alcoholic liver disease equal to or more than 2.

2. An increase in the level of alkaline phosphatase (with cholestasis) and hyperbilirubinemia is possible (both fractions increase to one degree or another).
3. Hypoalbuminemia (decrease in the synthetic function of the liver).
4. Increase in IgA.
5. ESR increase.
6. Anemia in alcoholic liver disease and alcoholic cirrhosis is most likely due to several causes, such as iron deficiency, gastrointestinal bleeding, folic acid deficiency, hemolysis Hemolysis - the process of destruction of red blood cells, in which hemoglobin enters the blood plasma; occurs as a result of the natural aging of erythrocytes (normal) or in various pathological (including human hereditary diseases) conditions
and hypersplenism Hypersplenism is a combination of an enlarged spleen with an increase in the number of cellular elements in the bone marrow and a decrease in formed elements in the peripheral blood.
.
7. Thrombocytopenia may be secondary to alcoholic bone marrow suppression, folic acid deficiency, or hypersplenism.

8. Coagulopathy (prothrombin time, INR International Normalized Ratio (INR) - a laboratory indicator determined to evaluate the external pathway of blood coagulation
>1.5) - there is a persistent, long-term increase.

9. Serum urea and creatinine. An increase in urea with normal creatinine indicates bleeding of the gastrointestinal tract. A simultaneous increase indicates the development of hepatorenal syndrome.

Other tests:
1. Serum folic acid (folates) - the level may be normal or low.
2. Serum ammonia does not always correlate with hepatic encephalopathy that develops with alcoholic cirrhosis of the liver. Thus, its regular, routine determination is impractical.
3. Alpha-1-antitrypsin - differential diagnosis test. With alcoholic cirrhosis of the liver, the content is normal.
4. Serum iron, ferritin, transferrin - a test for differential diagnosis with hemochromatosis. With alcoholic cirrhosis of the liver, the content is normal or slightly increased.

5. Ceruloplasmin - a test for differential diagnosis with Konovalov-Wilson's disease. In alcoholic cirrhosis of the liver, normal or slightly elevated.

6. The level of daily excretion of copper in the urine - differential diagnostic test with Konovalov-Wilson's disease.
7. Antimitochondrial antibodies (AMA) - differential diagnostic test with primary biliary cirrhosis. With alcoholic cirrhosis of the liver, the indicators are normal.

8. Antinuclear antibodies (ANA) and antibodies to smooth muscle cells (anti-smooth muscle antibody, ASMA) - a diagnostic test for autoimmune hepatitis.

Differential Diagnosis

Alcoholic cirrhosis of the liver differentiates with the following diseases:
- other forms of alcoholic liver disease;
- cirrhosis, fibrosis, sclerosis Sclerosis is a thickening of an organ due to the replacement of its dead functional elements with a connective (usually fibrous) tissue or a homogeneous hyaline-like mass.
liver of another etiology;
storage diseases (e.g. hemochromatosis Hemochromatosis (syn. hemomelanosis, bronze diabetes, siderophilia, Troisier-Anot-Choffard syndrome, pigmented cirrhosis) is a hereditary disease characterized by impaired metabolism of iron-containing pigments, increased iron absorption in the intestine and its accumulation in tissues and organs; manifested by signs of liver cirrhosis, diabetes mellitus, skin pigmentation
, Konovalov-Wilson disease Konovalov-Wilson's disease (syn. hepato-cerebral dystrophy) is a human hereditary disease characterized by a combination of cirrhosis of the liver and degenerative processes in the brain; due to impaired protein metabolism (hypoproteinemia) and copper; inherited in an autosomal recessive manner
);
- obstruction Obstruction - obstruction, blockage
bile ducts;
- chronic inflammatory diseases of the liver.

Decisive factors in diagnosis alcoholic cirrhosis:
- alcohol history;
- the absence of other, potentially possible, hepatotropic damaging agents;
- the presence of signs of cirrhosis according to the biopsy.

Complications

It is necessary to distinguish between complications of alcoholic cirrhosis of the liver and conditions associated with alcoholism.

Complications of alcoholic cirrhosis of the liver:
- portal hypertension Portal hypertension is venous hypertension (increased hydrostatic pressure in the veins) in the portal vein system.
;
-liver failure;
- hepatocellular carcinoma Hepatocellular carcinoma is the most common liver tumor. The result of malignant degeneration of hepatocytes. The main risk factors are chronic viral hepatitis, regular consumption of hepatocarcinogens, cirrhosis of the liver caused by other causes.
;
- hepatorenal syndrome Hepatorenal syndrome is a pathological condition that sometimes manifests itself in severe liver damage and manifests itself as a secondary impairment of kidney function up to severe renal failure. The development of acute liver and kidney failure is manifested by a combination of jaundice, bleeding disorders, signs of hypoproteinemia and uremia
;

Conditions associated with alcoholism:
- alcoholic gastritis;
- alcoholic pancreatitis Pancreatitis - inflammation of the pancreas
;
- alcoholic myopathy Myopathy is the general name for a number of muscle diseases caused by a violation of the contractility of muscle fibers and manifested by muscle weakness, a decrease in the volume of active movements, a decrease in tone, atrophy, and sometimes muscle pseudohypertrophy.

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We suggest that you read the article on the topic: "Differential diagnosis of liver cirrhosis" on our website dedicated to the treatment of the liver.

Diagnosis and differential diagnosis of liver cirrhosis. Viral cirrhosis of the liver. Alcoholic cirrhosis of the liver. Primary biliary cirrhosis of the liver.

Cirrhosis of the liver is, according to modern concepts, a chronic progressive liver disease of various etiologies with signs of functional liver failure and portal hypertension expressed to varying degrees.

Reliable criteria for the diagnosis of liver cirrhosis are morphological changes in the liver, so laparoscopy and biopsy help diagnose in doubtful cases.

Viral cirrhosis of the liver

Etiological criteria are indications in the anamnesis of past viral hepatitis, especially severe, but the disease can develop after anicteric form of hepatitis. A well-known aid in the diagnosis is the detection of hepatitis B surface antigen. The antigen can be detected using immunofluorescence and radioimmunoassay methods, as well as histological examination. The presence of antigen can be assumed when there are hepatocytes with a surface resembling polished glass; staining with aldehyde fuchsin or orcein is used to detect the antigen.

The initial stage of viral cirrhosis of the liver. The most frequent complaints are pains in the right hypochondrium, dyspeptic and asthenovegetative disorders appear. The liver is large, with an uneven surface, painful on palpation. Laboratory indicators - a high level of plasma protein, a sharp increase in the activity of aminotransferases.

The advanced stage of viral cirrhosis of the liver is accompanied by a rapid, clinically pronounced progression of the disease. In the clinical picture, manifestations of liver failure come to the fore: jaundice, abdominal pain, fever, transient ascites. In all patients with this liver disease, not only the liver is enlarged, but also the spleen, the latter often reaches a significant size.

Important for confirming the diagnosis of liver cirrhosis are extrahepatic signs of liver disease - spider veins, "liver" palms, gynecomastia. Along with changes in functional parameters characteristic of the initial stage, there is a significant decrease in albumin and a sharp increase in globulin fractions, thymol test reaches high numbers, cholesterol and prothrombin are reduced. Some patients experience hypersplenism.

In most cases, the diagnosis is established on the basis of anamnestic and clinical and biochemical data. Radioisotope scanning of the liver with colloidal gold or technetium plays an essential role in the diagnosis of this liver disease. A diffuse decrease in the absorption of the isotope in the liver and a “scanning” spleen, actively accumulating the isotope, indicate cirrhosis of the liver.

Laparoscopy and targeted liver biopsy reveal not only cirrhosis itself, but also its morphological type, signs of process activity.

Alcoholic cirrhosis of the liver

The etiological criteria for alcoholic cirrhosis of the liver are indications of a history of alcoholism, symptoms of previous acute alcoholic hepatitis, or a combination of cirrhosis with clinical and morphological manifestations of acute alcoholic hepatitis. Neurological and somatic manifestations of alcoholism are essential.

Alcoholic etiology is indicated by a combination of morphological features such as hepatocyte fatty degeneration, small nodular lesions, and hepatocellular fibrosis. At a later stage, a SKD variant of cirrhosis often occurs, and fatty degeneration disappears.

The most informative histological sign is alcoholic hepatitis with the formation of Mallory's hyaline and focal neutrophil infiltration.

The initial stage is most often accompanied by symptoms of acute alcoholic hepatitis - loss of appetite, pain in the liver, vomiting, sometimes short-term jaundice, cholestasis. The liver is enlarged, with a smooth surface, in some cases, with a latent course, an increase in the liver is the first and only symptom of this liver disease. Leukocytosis with a stab shift is characteristic, hyperbilirubinemia, increased activity of aminotransferases are possible.

Advanced stage of alcoholic cirrhosis of the liver. Along with the symptoms of the initial stage, malnutrition, myopathy, Dupuytren's contracture, extrahepatic vascular signs, parotid salivary gland enlargement, hair loss and testicular atrophy are found. Severe symptoms of portal hypertension are revealed: varicose veins of the esophagus and hemorrhoidal veins, ascites. Anemia appears. Dysproteinemia, an increase in bilirubin, a moderate increase in the activity of aminotransferases are detected. Immunological disorders are slightly expressed, but in some cases there is a clear increase in immunoglobulins A.

Clinical and functional criteria, especially in alcoholism, make it possible to suspect alcoholic cirrhosis. However, the criterion for a reliable diagnosis is the data of laparoscopy, which reveals an enlarged liver in the early stages with concomitant steatosis and a picture of small nodular cirrhosis, symptoms of portal hypertension. In the advanced stage, large-nodular cirrhosis is often found, signs of alcoholic hepatitis are possible.

Primary biliary cirrhosis of the liver

The etiology of this form of cirrhosis of the liver in most cases is unknown. The most significant are changes in immune responses and impaired metabolism of bile acids.

Segmental destruction and desolation of the small bile ducts, lymphoid follicles in portal infiltrates, cholestasis, detected by morphological examination, indicate primary biliary cirrhosis.

Initial stage. The clinical picture is determined by the severity of cholestasis: at first, itching with slight or no jaundice, usually with an enlarged liver. The skin is pigmented, dry, with traces of scratching. There is an increased activity of alkaline phosphatase in the blood serum, hyperlipemia and hypercholesterolemia; activity of serumal aminotransferases is increased moderately. Antimitochondrial antibodies are considered the most reliable functional criterion for primary biliary cirrhosis. Histological examination shows non-purulent inflammation of the intralobular bile ducts with their destruction. Further, proliferation of the bile ducts with destruction and periductular fibrosis is revealed.

Advanced stage of primary biliary cirrhosis of the liver. Jaundice becomes pronounced, xanthomas are often observed on the eyelids, elbows, palms, soles, buttocks. Spider veins, "liver" palms may appear. The liver is always significantly enlarged, dense. The spleen is usually palpable. Symptoms of portal hypertension appear. Changes in the skeletal system are characteristic: pain in the back and ribs, osteoporosis, enlargement of the epiphyses of bones, pathological fractures of the spine, as well as persistent bilirubinemia, hypercholesterolemia, increased levels of β-globulins, β-lipoproteins. The level of albumins and the prothrombin-educational function of the liver are reduced. Histological examination along with cholestasis reveals a picture of liver cirrhosis. Data of retrograde cholangiopancreatography are important for diagnosis, indicating the absence of extrahepatic obstruction. More informative duodenoscopy with retrograde cholangiopancreatography.

Differential diagnosis of liver cirrhosis

Liver cancer

A similar clinical picture has liver diseases such as primary liver cancer and especially cirrhosis-cancer.

Cirrhosis-cancer occurs both in persons who have had acute viral hepatitis in the past, and in patients with alcoholic liver disease. Cancer can develop against the background of long-term cirrhosis of the liver with vivid clinical symptoms or latent cirrhosis of the liver. Recognition of cirrhosis-cancer is based on the rapid progression of liver disease, exhaustion, fever, abdominal pain, leukocytosis, anemia, and a sharp increase in ESR. The correct diagnosis of primary cancer is helped by a short history of the disease, a significant, sometimes stone density of an unevenly enlarged liver. With a “typical” variant of this liver disease, there are constant weakness, weight loss, anorexia, and ascites that is not amenable to diuretic therapy. Ascites develops as a result of thrombosis of the portal vein and its branches, metastases to periportal nodes, and peritoneal carcinomatosis. Unlike cirrhosis of the liver - splenomegaly, endocrine-metabolic disorders are rare.

For the diagnosis of cirrhosis-cancer and primary liver cancer, it is advisable to use a liver scan and ultrasound. However, these are only screening tests indicating a “focal” or “diffuse” pathology without a specific diagnosis.

The criteria for a reliable diagnosis in primary liver cancer and cirrhosis-cancer are the detection of α-fetoprotein in the Abelev-Tatarinov reaction, laparoscopy with targeted biopsy, and angiography, which is especially important for cholangioma.

Accession of acute alcoholic hepatitis in patients with alcoholic cirrhosis of the liver causes jaundice with anorexia, nausea, fever, which must be differentiated from acute viral hepatitis. The correct diagnosis of acute alcoholic hepatitis against the background of liver cirrhosis is facilitated by a carefully collected history that reveals the relationship between the severity of alcoholism and clinical symptoms, the absence of a prodromal period, often associated polyneuropathy, myopathy, muscle atrophy and other somatic manifestations of alcoholism, as well as neutrophilic leukocytosis, an increase in ESR.

Fibrosis of the liver

characterized by excessive formation of collagen tissue. As an independent liver disease, it is usually not accompanied by clinical symptoms and functional disorders. In rare cases, with congenital liver fibrosis, schistosomiasis, sarcoidosis, portal hypertension develops.

Criteria for reliable diagnosis are morphological - in contrast to cirrhosis of the liver, with fibrosis, the lobular architectonics of the liver is preserved. Most often in clinical practice, alveolar echinococcosis, constrictive pericarditis, amyloidosis, and storage diseases are mistaken for liver cirrhosis. Sometimes a differential diagnosis is made with subleukemic myelosis and Waldenström's disease.

Alveolar echinococcosis

With alveolar echinococcosis, the first sign of the disease is an increase in the liver with its unusual density. Diaphragm movement is often limited. Enlargement of the spleen and violations of liver function tests detected in some patients lead to diagnostic errors. Diagnosis is aided by careful X-ray examination, especially with the use of pneumoperitoneum, as well as a liver scan. Criteria for a reliable diagnosis of echinococcosis are specific antibodies.

Constrictive pericarditis

Constrictive pericarditis (with predominant localization in the right ventricle) - one of the adhesive pericarditis, is the result of a slow overgrowth of the pericardial cavity with fibrous tissue, which limits the diastolic filling of the heart and cardiac output. The disease develops as a result of chronic tuberculous lesions of the heart shirt, injuries and wounds of the heart area, purulent pericarditis. The first signs of heart compression occur among more or less long-term well-being and are characterized by a feeling of heaviness in the right hypochondrium, enlargement and compaction of the liver, mainly the left lobe, often painless on palpation. Shortness of breath occurs only during physical exertion, the pulse is soft, small filling. Typically, an increase in venous pressure without enlargement of the heart.

For the correct recognition of the disease, it is important to take into account the anamnesis and remember that in constrictive pericarditis, stagnation in the liver precedes circulatory decompensation. The criterion for a reliable diagnosis is the data of X-ray kymography or echocardiography.

Cardiac cirrhosis of the liver

Cardiac cirrhosis of the liver, which is formed in the advanced and terminal stages of constrictive pericarditis, proceeds with persistent ascites, hepatosplenomegaly, but unlike other forms of cirrhosis, it is accompanied by high venous pressure, severe shortness of breath, swelling of the cervical veins, and cyanosis. The combination of hypertension in the system of the superior vena cava and congestion in the liver and in the portal vein with the formation of early ascites makes one suspect constrictive pericarditis, and chest radiography or echocardiography reliably recognizes it.

Benign subleukemic myelosis

Benign subleukemic myelosis (osteomyelosclerosis, myelofibrosis) is a chronic leukemia originating from the precursor cell of myelopoiesis, in most cases accompanied by the growth of fibrous tissue in the bone marrow. Clinical examination reveals an enlargement of the spleen, in most cases significant, and often the liver is also enlarged, which usually leads to an erroneous diagnosis of cirrhosis. This is facilitated by a slightly changed picture of peripheral blood: moderate neutrophilic leukocytosis with a predominance of mature forms, which grows very slowly, often for years. The development of fibrosis in the liver can lead to portal hypertension, and it is traditionally regarded as a "reliable" sign of cirrhosis. Diagnosis is aided by dissociation between the peripheral blood picture and splenomegaly. However, the criterion for reliable diagnosis is the data of trephine biopsy, which reveals pronounced cellular hyperplasia, an abundance of megakaryocytes, and proliferation of connective tissue.

Liver amyloidosis

Liver amyloidosis is usually a manifestation of a systemic disease, in the pathogenesis of which immunological disorders and changes in protein metabolism play an important role. Despite the possibility of protein shifts, especially γ-globulinemia and disorders of cellular immunity factors, the only criterion for a reliable diagnosis is the data of a puncture liver biopsy.

Hemochromatosis

Hemochromatosis is a genetically determined disease with increased absorption of iron in the intestine, elevated serum levels and excessive deposition in the liver, pancreas, reticuloendothelium, skin and other tissues. In the cirrhotic variant, hepatolienal syndrome, dysproteinemia are noted, serum iron is significantly increased, but reliable diagnosis is based on the data of a puncture liver biopsy.

Wilson-Konovalov disease

Wilson-Konovalov's disease (hepatolenticular degeneration) is a hereditary fermentopathy associated with a violation of the biosynthesis of ceruloplasmin, which is responsible for the transport of copper in the body. In the abdominal form of the disease, the hepatolienal syndrome with the rapid progression of symptoms of liver damage becomes the leading one. Criteria for reliable diagnosis - a decrease in serum ceruloplasmin, the detection of the Kaiser-Fleischer ring.

Waldenstrom's macroglobulinemia

Waldenström's macroglobulinemia is a paraproteinemic hemoblastosis, one of the types of tumors of the lymphatic system, the differentiated elements of which are represented by an M-immunoglobulin-synthesizing lymphocyte. Enlargement of the liver, spleen, lymphadenopathy can be the leading symptoms of the disease, especially in the initial stage. The criterion for reliable diagnosis is the morphological evidence of the lymphoproliferative process (puncture of the sternum, spleen, liver, lymph nodes) and the detection of monoclonal hypermacroglobulinemia of the IgM type.

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Liver cirrhosis is a diffuse pathological process that develops with excessive fibrosis and the formation of structurally abnormal nodes of regeneration.

Cirrhosis of the liver is the end stage of a wide range of liver diseases.

The variability of liver cirrhosis as a nosological form is distinguished by the peculiarities of etiological factors, the activity of the pathological process in the liver, the failure of liver function, and the degree of progression of portal hypertension.

Epidemiology

Liver cirrhosis is the cause of death of patients in 90–95% of cases of outcomes of chronic liver diseases and occupies a leading position among the causes of mortality from diseases of the digestive system.

The prevalence of liver cirrhosis in the world ranges from 25 to 400 per 100,000 population.

It has been established that patients with liver cirrhosis drink obviously hepatotoxic volumes of alcohol 2 times more often than ordinary people; also, anti-HCV in the blood serum of patients with liver cirrhosis is detected 11 times more often than in the population.

Approximately 2 million people die every year from viral cirrhosis of the liver (mainly HCV-, HBV-infectious etiology) and virus-associated hepatocellular carcinomas. Data on mortality from alcoholic cirrhosis of the liver in developed countries are approaching those for viral cirrhosis of the liver.

Etiology

The main most common causes of cirrhosis of the liver:

– alcohol abuse (over 50%);

- viral hepatitis (more often - chronic hepatitis C, less often - hepatitis B, D).

Metabolic disorders that can trigger the onset of cirrhosis of the liver:

- iron overload in hereditary hemochromatosis;

- copper overload in Wilson's disease;

– deficiency of α1-antitrypsin;

- cystic fibrosis;

- galactosemia and glycogenoses;

- hereditary tyrosinemia and telangiectasia, porphyrias.

Diseases of the biliary tract, in which cirrhosis of the liver can develop:

- extrahepatic obstruction of the biliary tract;

- intrahepatic obstruction of the biliary tract (primary biliary cirrhosis, primary sclerosing cholangitis);

- cholangiopathy in children (progressive childhood cholestasis, arteriohepatic dysplasia, cholestasis with lymphedema, Zellweger's syndrome);

- obstruction of venous outflow from the liver (Budd-Chiari syndrome, veno-occlusive disease, severe right ventricular failure);

- The toxic effects of pharmaceuticals and toxins can also trigger the onset of cirrhosis.

However, cirrhosis can be caused by immune changes (autoimmune hepatitis, graft-versus-host disease), other disease states (sarcoidosis, non-alcoholic steatohepatitis, hypervitaminosis A, cryptogenic cirrhosis).

In a quarter of cases of liver cirrhosis, the etiology remains unclear. According to most researchers, patients with cirrhosis of the liver of unknown etiology are people with unconfirmed viral and alcoholic cirrhosis of the liver due to inadequate examination.

Pathogenesis

Hepatocellular necrosis and disorders of hepatocyte regeneration, inflammation and fibrosis are interrelated processes that underlie the progression of liver cirrhosis.

Initially, hepatocytes are damaged under the direct influence of etiological agents (alcohol, virus, hepatotoxic substances, etc.) or mediated by the damaging effect of agents of autoimmune and immune aggression.

In the future, the products of cell necrosis and inflammation have a damaging effect on hepatocytes. The resulting ischemia in the central zones of the false lobules can also cause the death of hepatocytes.

An important role in the formation of necrosis is played by immunological disorders caused by dysfunction of Kupffer cells synthesizing pro-inflammatory cytokines (tumor necrosis factor-α, interleukins). The lack of bile acids in the intestine is accompanied by increased bacterial growth and, as a result, endotoxemia and additional stimulation of cytokine production. Of no small importance in the process of cytolysis of hepatocytes belongs to the difficulty in excretion and stagnation of bile, which occur due to impaired intestinal metabolism and reabsorption of bile acids, excessive absorption of lithocholic acid and destruction of cholangiocytes by toxic bile acids.

As a result of necroinflammatory processes, active connective tissue septa are formed.

Fibrogenesis is considered the most important mechanism for the formation and progression of liver cirrhosis. Hepatocellular necrosis, cytokines produced by the cellular structures of the liver, acetaldehyde (formed during the conversion of alcohol), cause degradation of the extracellular matrix space of Disse. These processes are accompanied by the activation of Ito cells, which ultimately leads to the stimulation of fibrogenesis.

Iron overload in hemochromatosis is accompanied by increased secretion of tissue inhibitors of metalloproteinases, which is accompanied by the deposition of collagen in the space of Disse with the formation of fibrils and fibronectin.

These processes underlie the "collagenization" of the sinusoids, which impedes the exchange of substances between the liver cell and the blood, which provokes the formation of portal hypertension.

Cirrhotic changes in the hepatic parenchyma and, as a result, portal hypertension, in which portosystemic shunting and hepatocellular insufficiency occur, lead to the formation of parenchymal and arterial vasodilation with a progressive decrease in systemic vascular resistance. This predisposes to a drop in effective arterial volume and a decrease in blood pressure, which creates the conditions for fluid retention and an increase in plasma volume.

In response to these processes, cardiac output and heart rate increase, which is inevitably accompanied by an increase in parenchymal blood supply and, in addition, further exacerbates portosystemic shunting, portal hypertension, and hepatocellular insufficiency.

Clinical picture

The disease can be asymptomatic for a long time.

Clinical assessment of the stage and severity of liver cirrhosis is based on the severity of portal hypertension and hepatocellular insufficiency. The stage and severity of the disease are semiquantitatively assessed using the Child-Pugh diagnostic criteria scale.

Compensated (class A) course of liver cirrhosis is characterized by the absence of icterus, ascites and bleeding from varicose veins and encephalopathy.

Subcompensated and decompensated (class B and C, respectively) course is characterized by the occurrence of ascites of varying severity, bleeding from varicose veins, spontaneous peritonitis and pleural empyema, hepatorenal syndrome and hepatic encephalopathy.

In patients with cirrhosis of the liver, various symptoms of damage to almost all organs and systems can be detected, which determine the following syndromes:

• Asthenic (fatigue, loss of appetite of varying severity, weight loss).
• Dermal (icteric staining of the skin, "varnished" tongue and lips, telangiectasia, reddening of the palmar surfaces, skin scratching, seizures in the corners of the mouth, changes in the nail plates).
• Musculoskeletal (hypertrophic osteoarthropathy, hepatic osteodystrophy, convulsions, umbilical hernia).
• Pulmonary (hypoxemia, primary pulmonary hypertension, rapid breathing, decreased lung capacity, accumulation of fluid in the pleural sinus, dilation of intrapulmonary vessels, shortness of breath).
• Cardiac (hyperdynamic circulation).
• Gastrointestinal (enlargement of the parotid salivary glands, loosening of the stool, cholelithiasis, portal hypertensive gastro- and colonopathy, symptomatic (cirrhotic) erosive and ulcerative lesions, gastritis, hepatic odor from the mouth).
• Renal (secondary hyperaldosteronism, in which fluid and sodium retention develops, "hepatic" glomerulosclerosis, renal tubular acidosis, hepatorenal syndrome).
• Hematological (folic acid deficiency and hemolytic anemia, enlarged spleen with pancytopenia, coagulation disorder, DIC, hemosiderosis).
• Endocrine (diabetes, elevated levels of parathyroid hormones due to hypovitaminosis D and secondary hyperparathyroidism, hypogonadism: in women - infertility, dysmenorrhea, disappearance of secondary sexual characteristics; in men - decreased libido, hypo- and testicular atrophy, impotence, a decrease in testosterone, feminization ).
• Neurological (hepatic encephalopathy, peripheral neuropathy, seizures).
• Portal hypertension syndrome (varicose veins - gastroesophageal, anorectal, retroperitoneal, "jellyfish head"; ascites, enlarged spleen).

Depending on the flow options, there are:

1. Subacute cirrhosis (hepatitis-cirrhosis).

Often occurs against the background of acute hepatitis with symptoms of the initial stage of liver cirrhosis. The disease lasts from 4 months to one year and is characterized by the transformation of acute hepatitis into cirrhosis of the liver, resulting in death.

2. Rapidly progressing (active) cirrhosis.

Differs in specific clinical, biochemical and morphological signs of high activity of the pathological process in the liver. From the onset of the disease, patients live for about 5 years.

3. Slowly progressive (active) cirrhosis.

A mild clinical picture of the disease is accompanied by constant biochemical and morphological activity. Portal hypertension and liver failure progress slowly. The life expectancy of patients is more than 10 years from the onset of the disease.

4. Sluggish cirrhosis.

Clinical symptoms of disease activity are not detected, the manifestation of biochemical activity is sporadic. At the same time, morphological manifestations of activity are moderately expressed. Portal hypertension develops slowly, functional failure of the liver practically does not occur. The life expectancy of such patients exceeds 15 years. The main cause of death is intercurrent diseases.

5. Latent cirrhosis.

Clinical symptoms, biochemical and morphological manifestations of disease activity are not determined. As a rule, portal hypertension and liver failure are not formed. In the prevailing number of patients, this form of liver cirrhosis does not adversely affect life expectancy.

Complications

• Bleeding from varicose veins of the digestive tract.
• Hepatorenal syndrome (malaise, thirst, dryness and decreased skin turgor, decreased urination, arterial hypotension).
• Ascites.
• Bacterial peritonitis.
• Thrombosis of the portal vein.
• hepatopulmonary syndrome.
• Accession of a secondary infection (most often with the onset of pneumonia).
• Formation of stones in the gallbladder and ducts in primary biliary cirrhosis.
• Transformation to cirrhosis-cancer.
• Liver failure.

Diagnostics

Among the laboratory and clinical indicators for the detection of liver cirrhosis, it is mandatory to conduct the following studies: hemogram, coagulogram, proteinogram, liver function tests, immunogram, as well as the determination of ANA, AMA, SMA autoantibodies, the determination of the level of α1-antitrypsin and protease inhibitor, α- serum fetoprotein, HBsAg, anti-HVC, iron metabolism indicators.

Indicators reflecting changes in liver function are considered to be markers of syndromes of cytolysis, cholestasis, synthetic inferiority of liver function, as well as the occurrence of regeneration syndrome and tumor growth.

Detection of an increased amount of non-carbohydrate transferrin, IgA, γ-glutamine transferase in the blood plasma; an increase in the average volume of erythrocytes indicates subacute and chronic alcohol intoxication.

Liver fibrosis markers are being studied, however, these markers do not reflect excessive deposition of proteins in the extracellular matrix, but tissue metabolism in general, and individually do not have specificity with respect to liver tissue. The presence in the body of other inflammatory foci is accompanied by a change in their level in the blood serum.

All patients with liver cirrhosis, regardless of the factors that caused it, are determined for markers of viral hepatitis B, C, D, which helps in determining the severity, prognosis of the disease and allows monitoring the effectiveness of treatment and vaccination.

To identify autoimmune liver damage, markers of the autoimmune process are identified; certain combinations of autoantibodies are characteristic of various autoimmune liver diseases.

Instrumental research methods are carried out: ultrasound, computed and magnetic resonance imaging, endoscopic and radionuclide studies, elastography, puncture liver biopsy.

Histomorphological examination of liver biopsy specimens in cirrhosis reveals a violation of the lobular structure of the liver, the formation of regenerate nodes (or false lobules), fibrous layers (or septa) surrounding false lobules, thickening of the hepatic trabeculae, transformation of hepatocytes (enlarged cells of the regenerative type, dysplastic hepatocytes with polymorphic , hyperchromic nuclei).

According to histomorphological criteria, macronodular, micronodular, mixed and biliary cirrhosis of the liver are distinguished.

Differential Diagnosis

In highly active forms of liver cirrhosis, it is necessary to carry out differential diagnosis with chronic active hepatitis, cholangitis, and "stagnant" liver.

As part of the clarification of the etiology of the occurrence of cirrhosis of the liver, differential diagnosis should be carried out between all its possible causes. First of all, markers of viral hepatitis B, C, D are determined and the patient is tested for alcohol abuse.

Liver cirrhosis must be differentiated from other liver diseases in which nodes are formed or fibrosis develops (nodular regenerative hyperplasia, non-cirrhotic liver fibrosis, schistosomiasis, echinococcosis, opisthorchiasis, tuberculosis, syphilis, brucellosis); malignant neoplasms of various organs with liver metastases.

The final diagnosis is established using a histological examination, in which regeneration nodes are identified.

Treatment of liver cirrhosis involves the impact on the cause of its formation - the disease that caused cirrhosis ("basic therapy"), and symptomatic intervention, depending on the expression of clinical manifestations and complications of cirrhosis.

The general principles of treatment include strict lifelong abstinence from alcohol in the presence of alcoholic cirrhosis of the liver, the use of antiviral pharmaceuticals (IFN-α and pegylated IFN-α, nucleoside analogues) for viral cirrhosis of the liver. The exception is patients with decompensated liver cirrhosis.

The use of corticosteroids is justified in liver cirrhosis as a result of autoimmune hepatitis, primary biliary cirrhosis.

The leading drugs in the treatment of liver cirrhosis are those that are aimed at reducing the severity of complications of the disease, such as bleeding from varicose veins, hepatic encephalopathy, ascites, spontaneous bacterial peritonitis.

Traditionally, patients with liver cirrhosis are prescribed drugs with hepatoprotective properties - essential phospholipids, preparations of silymarin, ademethionine, ursodeoxycholic acid.

Antifibrotic therapy is aimed at inhibiting the activation of hepatic stellate cells, preventing damage and death of hepatocytes, or slowing down the proliferation of bile duct epithelial cells, which stimulate fibrogenesis through the release of profibrinogenic agents.

The effect of hepatocyte transplantation on liver function and regression of fibrosis is being studied.

Performing orthotopic liver transplantation for cirrhosis of the liver can save the patient's life.

The prognosis for all variants of liver cirrhosis is determined by the degree of morphological changes in the liver, the tendency to progression and the lack of effective methods of treatment.

The average life expectancy is 3-5 years, rarely 10 years or more.

Prevention

Preventive measures are aimed at preventing infection with hepatitis B, C, D viruses, timely full treatment of viral hepatitis; refusal to drink alcoholic beverages, minimizing the effect of hepatotoxic substances.

In the diagnosis of cirrhosis of the liver, its differential diagnosis is of great importance. Cirrhosis today is the cause of death of about 90% of patients with chronic liver disease and occupies a leading position among other diseases of the digestive system.

The main causes, more than 60%, causing cirrhosis are alcoholism and viral infections. According to statistics, every year 2-2.5 million people die in the world only from the viral form of this disease.

Etiology

As mentioned above, the main reasons why you can earn this disease for yourself are long-term alcohol abuse and viral infections, in particular viral hepatitis C, B and D.

But there are also other provocateurs of this disease, such as:

Another fairly likely way to get sick may be a disease of the biliary tract already developed in the body: exacerbated extra- or intrahepatic obstruction of the biliary tract; children's cholangiopathy; obstructed outflow of blood from the venous pathways from the liver; excessive or improper use of pharmacological drugs, leading to toxic poisoning and, as a result, to cirrhosis of the liver.

But, surprisingly, with the modern development of medicine, there are still unknown causes of this disease.

For quite a long time, the disease may not cause any symptoms. Assessment of the stage of the disease can be traced through severe portal hypertension and hepatocellular insufficiency. An approximate estimate of those very parameters is given by the Child-Pugh diagnostic table of criteria.

This table has 3 following classes:

1. Compensated (class A);
2. Subcompensated (class B);
3. Decompensated (class C).

In class A, the course of the disease is marked by the absence of marked jaundice, nosebleeds and dilated varicose veins, ascites, and encephalopathy. Classes B and C are complicated compared to the first class, ascites is observed in an already more severe degree, spontaneous peritonitis and pleural empyema, as well as a complication of hepatic tissue encephalopathy.

The liver, being a natural filter in the human body, is subject to a high number of irritants. Although regeneration is characteristic of liver cells, one should not think that because of this, it can independently cope with most of these ailments.

Like all serious diseases, cirrhosis has its main types:

• Subacute: occurs with acute hepatitis and symptoms are present at the initial stage; the transformation of viral hepatitis into cirrhosis occurs within 0.5-1 year, a fatal outcome is possible;
• Rapidly progressive or active: has specific biochemical and clinical symptoms of severe activity of poor liver function; life expectancy from the onset of the disease is about 5 years;
• Slowly progressing or passive: this ailment is very imperceptible, but there are noticeable disturbances in the normal functioning of the liver; life expectancy within 10 years from the moment of illness;
• Sluggish (slow): symptoms of clinical activity are not expressed, and morphological activity is moderate, functional failures in the liver are not observed; death is unlikely, but possible, while the patient can live with this for more than 15 years;
• Latent: this type of this disease does not burden the sick person with obvious symptoms, the activity of liver cells is within the normal range; Almost all those who have overcome such a disease will not affect their life expectancy.

Complications in cirrhosis:

1. Ascites;
2. The formation of blood clots in the venous tract;
3. Transformation into the so-called cirrhosis-cancer;
4. Complication of secondary infection;
5. Bleeding in the digestive tract of varicose veins;
6. Liver failure;
7. Hepatorenal and hepatopulmonary syndrome;
8. Formation of stones in the bile ducts.

In order to find out the general state of affairs in cirrhosis or directly identify it, the following studies are necessary:

1. Hemogram;
2. Immunogram;
3. Proteinogram;
4. Coagulogram;
5. Liver biopsy.

These studies are the main ones in this problem, without their help it is extremely difficult to make a correct diagnosis. There are also a number of other ways to collect more detailed information about the disease in the human body.

The functional performance of the liver can be changed, and markers of such syndromes as choleostasis, cytolysis, synentic inferiority syndrome and the development of tumor growth syndrome will help to track this.

Regardless of the type of this disease, the patient must be tested for the presence of viral hepatitis B, C, D, this allows you to determine the severity of the disease, its prognosis and makes it possible to monitor the effectiveness of treatment in the future.

With autoimmune cirrhosis of the liver, an analysis is carried out to determine certain autoantibodies, their combinations make it clear what the doctor has to work with at the moment and draw up the most correct plan to combat the disease.

As it has already become clear, with any type of this ailment, you can send the patient for an additional examination, which will definitely give a better idea of ​​the situation and that stage of the disease in the patient's body. Today, medicine has already advanced far enough and should not be neglected.

In the event that it is necessary to deal with a highly active form of cirrhosis, with active viral hepatitis, cholangitis, or the so-called stagnant liver, it is necessary to conduct a differential diagnosis. This diagnosis is a method of exclusion, in which the attending physician does not try, based on the patient's tests, to make the most appropriate diagnosis. And, based on the results, excludes those forms of cirrhosis that are not suitable. First of all, the patient is examined for alcoholism and the presence of hepatitis B, C, D in the body.

This problem is also differentiated from other liver diseases that can lead the liver to the same condition.

Also, differential diagnosis is carried out with echinococcosis. With it, a gradual increase in the liver is observed, it becomes more dense and bumpy. This can be traced through a biopsy.

A more accurate and detailed diagnosis can be made, taking into account the sections of etiology, morphology and morphogenesis, the activity of cirrhosis, its functional characteristics, and the like.

Regarding the prognosis, for any type of ailment, it can be compiled based on the degree of morphological changes in the liver tissue and tendencies towards progressive development. The average life expectancy can be from 3 to 5 years, in rare cases more than 10 years.

Preventive methods can be vaccination against viral hepatitis or its timely treatment, refusal of alcohol or reduction of its consumption to 50 grams per day and, of course, examinations. At the slightest symptoms or the passage of sufficient time after the last examination, you should not waste time, but consult a doctor as soon as possible for an examination.

Cirrhosis of the liver is a chronic disease in which fibrous nodes develop in the liver, it is accompanied by hypertension and is characterized by hepatocellular insufficiency. Thanks to the advent of high-tech equipment and the availability of instrumental studies, the diagnosis of liver cirrhosis is easily feasible.

The name of the disease "cirrhosis" comes from the word kirrhos, which in Greek means - the color of orange. The most common cause of cirrhosis is the recognized alcoholism. Depending on the number of alcoholics, in different countries the presence of such cirrhosis of the liver ranges from 20 to 95%. Viral hepatitis causes it from 10 to 40% of all diseases. Hepatitis C causes cirrhosis in 40%, sometimes 80%. Hepatitis B is less reactive - it accounts for 0.5-1%.

Cirrhosis of the liver

The etiology of its origin may be drugs (Methotrexate, Isoniazid), and toxic emissions from industrial enterprises also play an important role. In addition, the etiology of its occurrence may be due to venous congestion in the liver - it is most often associated with heart failure that lasts for a long time. This disease can occur due to some hereditary diseases, for example, from hemochromatosis.

In half of patients, the cause of the primary development of cirrhosis is the combined action of factors (for example, alcoholism in combination with hepatitis B). Cirrhosis also develops as a result of insufficient patency of the bile ducts. In women during menopause, primary biliary cirrhosis of the liver is formed and is caused by the presence of cholestasis inside. The etiology of occurrence has not yet been established.

However, the etiology of secondary biliary cirrhosis was found - this is a blockage of the large biliary tract, which constantly disrupts the excretion of bile (if there is a complete blockage of the biliary tract, the obstruction is eliminated by surgical treatment, otherwise death is possible), this occurs with a diagnosis of congenital atresia bile ducts, cholelithiasis and after surgery.

Cholelithiasis

Classification of cirrhosis:

• Etiology (origin).

1. autoimmune (immunity failure);
2. metabolic;
3. viral (hepatitis);
4. unclear origin (cryptogenic, children's Indian, primary biliary cirrhosis of the liver);
5. alcoholic;
6. congenital (tyrosinosis, hemachromatosis, glycogenosis);
7. secondary biliary;
8. drug;
9. Budd-Chiari disease - thrombosis of the hepatic veins, which is observed at the level of their confluence with the inferior vena cava and leads to a violation of the outflow of blood from the liver;
10. metabolic-alimentary (occurs as a result of obesity, with severe diabetes mellitus).

    Diabetes

• building substrate.

1. macronodular (large nodules, >1 cm in diameter);
2. incomplete septal;
3. micronodular (small nodules the size of< 1 см);
4. mixed.

• There are three stages of liver failure: compensated, subcompensated and initial decompensation.
• Phases: active exists in three types - moderate, pronounced and minimal. And remission, that is, the inactive phase.

Pathological structure

The building material of cirrhosis is tissue fibrosis, the appearance of nodes and the restructuring of blood vessels. The disease of such an organ as the liver is accompanied by a diffuse process, characterized by the appearance of nodules in the parenchyma, its transformation, accompanied by the creation of false lobes, fibrosis and the formation of shunts inside the liver - they connect the liver veins with the system, the occurrence of PBC (primary biliary cirrhosis).

The transformation of morphology and pathogenesis in cirrhosis is found in many organs, which facilitates diagnosis. They are caused either by exposure to the causes that provoked cirrhosis (almost all organs of the endocrine system are affected), or by complications from cirrhosis, such as portal hypertension (ulcers or erosion of the stomach, esophagus, varicose veins, gastritis, or esophagitis - a disease esophagus, accompanied by inflammation of its mucous membrane).

Clinical picture

The main and most characteristic symptoms of this disease are interconnected with the presence of a clinic of liver failure syndromes (biochemical), as well as hilar hypertension. The manifested clinic is in direct connection with the compensatory process, and this depends on the degree of degeneration of the liver tissue and its distribution within the organ. The compensation process is mainly manifested by an increase in the liver, sometimes it is combined with an increase in the volume of the spleen. You should contact the clinic to take tests to make a diagnosis. In the early stages, the treatment of the disease is simplified.

The stage of subcompensation is most often accompanied by initial symptoms: persistent fatigue, severe weakness, decreased appetite and disability, dyspeptic disorders (intolerance to alcoholic beverages and fats, belching, bitterness in the mouth, vomiting, nausea). There is a feeling of pain, as well as heaviness in the epigastrium and on the right under the ribs, where the liver is located. In all the examples described, it is necessary to take tests in order to conduct a diagnostic study. The liver increases in volume, does not hurt or hurts slightly on palpation, is distinguished by a compacted parenchyma and a slightly pointed edge, sometimes reveals superficial tuberosity.

Objective symptoms of organ cirrhosis and clinical symptoms are visible changes on the skin. Palmar erythema occurs, it is expressed in symmetrical redness of the palms, telangiectasia (stars of redness, mainly on the skin of the torso), which is essential for the diagnosis of cirrhosis. Often manifested in the skin of the place of hemorrhage, increased bleeding in the mucous membranes, which indicates the presence of hemorrhage syndrome.

The pathogenesis reveals itself with skin itching, endocrinological disorders, for example, menstrual cycle disorders, joint pains, at this stage, the cover of underarm and pubic hair decreases, libido decreases, impotence occurs, and sometimes testicular atrophy. Subfebrile temperature (37.1-38.0 °C) is often observed, which is observed with a sluggish inflammatory process. Decompensated cirrhosis is difficult to treat, characterized by sudden weakness, urge to vomit, diarrhea, weight loss, atrophy of the muscular system (on the torso and between the ribs), high body temperature, sometimes on the contrary - its decrease, at these stages there are serious changes in the parenchyma of the organ.

Portal hypertension and progressive liver failure are usually observed in the last stage of cirrhosis of the organ - the pathogenesis is expressed by dropsy, swelling of the extremities, hemorrhage, parenchymal jaundice, varicose veins under the skin on the peritoneum - the detection of the disease is facilitated. There is a sweetish, putrid odor from the mouth, which is due to the inability of the liver to metabolize methionine. Since the affected organ is unable to function normally and remove decay products from the body, mental disorders occur (treatment by a psychiatrist), due to intoxication of the body.

Most often, an early asthenia syndrome occurs, which is expressed in mood lability, tearfulness, increased fatigue, and this requires the treatment of a neurologist. Patients are very touchy, extremely impressionable, often their reactions are hysterical, they are picky and suspicious. Their sleep is disturbed - they cannot fall asleep at night, and drowsiness sets in during the day, treatment with sleeping pills does not help. With the progression of the disease, the symptoms of encephalopathy increase. Memory decreases, consciousness disorders occur, hepatic coma develops.

Complications that lead to the death of the patient are bleeding from the gastrointestinal tract and hepatic coma. Cirrhosis is complicated by the connection of a viral infection that causes peritonitis, blood poisoning, pneumonia, portal vein thrombosis, hepatorenal syndrome. It happens that the disease turns into cancer.

Biliary cirrhosis

Depending on the origin, cirrhosis of the parenchymal organ has individual properties of development and clinic. So, primary biliary cirrhosis of the liver begins with a gradually increasing itching. At the apogee of the disease, the yellow color of the proteins of the eyes and skin increases: biochemical analyzes indicate the presence of cholestasis (the content of cholesterol, bilirubin, and bile acids in the blood increases). The clinic of biliary cirrhosis is expressed by the presence of cholestasis, tests show an increase in cholesterol, decompensation (disruption of normal functioning), the process does not occur very quickly.

There are algorithms for making a diagnosis based on instrumental signs and clinic. It is quite difficult to establish liver cirrhosis at stage 1 on the second basis. Since the disease develops slowly at the very beginning and does not have a pronounced clinic, it is known that treatment in the initial stages is much more successful than in the later ones, therefore, instrumental studies should be carried out.

Compensated and decompensated cirrhosis

Compensated cirrhosis is usually detected during the examination of a patient who applied for a completely different reason. The reason for a serious examination is the presence of an enlarged spleen of unknown origin or hepatomegaly, especially if there is evidence of the origin of cirrhosis.

Blood test

If decompensated or subdecompensated cirrhosis is present, then the clinical picture will help in diagnosing the disease - the patient's complaints about nosebleeds or dyspepsia. In addition, if after the examination, changes in the liver were detected at an early stage, which were detected when pressed with fingers: ascites, enlargement of the spleen. The diagnosis can be clarified by blood tests and instrumental examination. The following changes in blood tests are observed: thrombocytopenia, increased ESR (erythrocyte sedimentation rate), the presence of dysproteinemia, in the form of increased gamma globulin and low albumin content. The synthesis of hepatocytes is reduced - it manifests itself in a decrease in the work of cholinesterase and in the content of blood coagulation determinants, as tests show.

Often there is an increased activity of aminotransferases, however, it does not show a high intensity - it exceeds the usual norm by two to three times. Many patients have increased alkaline phosphatase activity. Thanks to blood tests, in conjunction with instrumental studies, the doctor establishes an accurate diagnosis. In staging it with cirrhosis of the liver, an examination in the X-ray room, ultrasound and radionuclide diagnostic studies play an important role.

In the early stages of cirrhosis, Ultrasound of organs detects enlargement of the spleen, as well as the liver, uneven edges and their rounding, pathogenesis of the vessels of the spleen and portal vein (serves as indirect evidence of portal hypertension, detection of dropsy and its approximate size, gallstones, chronic pancreatitis, tumors). With further progression of the disease, the echostructure of the organ changes - it becomes heterogeneous, large and small echo-positive foci are found. If there are serious changes in the structure of the parenchyma of the organ, in differential diagnosis, they manifest themselves in a decrease in its size and the number of echo-positive foci. The contours of the liver veins change, most of them are not visualized.

Examination (diagnostic) of the gastrointestinal tract, contrast radiography, detects portal hypertension.

ultrasound diagnostics

Highly accurate information (100%) about the stages of liver cirrhosis allows you to get computed tomography and MRI. They reveal the same variations in pathogenesis in the parenchymal organ that are detected and ultrasound diagnostics- at the beginning of the disease, during the examination, an enlargement of the liver is noted, then a decrease, the tuberosity of its contours is manifested, as well as the heterogeneity of the structure.

Computed multislice tomography reveals diseases accompanying cirrhosis: esophageal vein dilatation, ascites, splenomegaly. It gives accurate data on the state of organs and their sizes, based on the algorithm, excludes the presence of a tumor or detects it, detects primary liver cancer. For data processing, a special algorithm has been developed that allows you to establish an accurate diagnosis.

Examination of the liver using radionuclides, according to the information content of diagnostic measures, is somewhat less accurate in comparison with the method of ultrasound and MSCT (multispiral computed tomography), but it allows you to identify the function of the parenchymal organ at the initial stage of the disease. With reduced functionality of the liver, the spleen is visualized enlarged. Bone marrow becomes visible in the spinal column and in the pelvic bones, which indicates an unfavorable prognosis.

Often the diagnosis of cirrhosis of the parenchymal organ involves the study of the morphology of the liver parenchyma, it is taken from the patient biopsy method(blind or targeted puncture) - carried out under ultrasound control, or parenchyma sampling is carried out by laparoscopy.

Angiographic studies(blood vessels) reveal portal hypertension and its nature, if there are indications for surgical intervention.

Esophagogastroduodenoscopy reveals the presence of ulcers in the stomach and duodenum, as well as varicose veins in the esophagus.

Esophagogastroduodenoscopy

Differential Diagnosis

To establish an accurate diagnosis of the disease, perform differential analysis with hepatitis and steatosis. Such an examination takes into account the density of the organ, the distinctive features of the edge, the type of surface (tuberosity), in addition, the absence of pronounced hilar hypertension characteristic of cirrhosis in these diseases.

But it is necessary to take into account the fact that the formation of cirrhosis occurs gradually, due to the presence of active hepatitis, so it is quite difficult to distinguish between these two diseases, since the initial stage is difficult to determine.

In the acute phase, it is necessary differential diagnosis of liver cirrhosis with viral hepatitis. Cirrhosis of the organ is distinguished by the dense consistency of the parenchyma, as well as the uneven surface. To distinguish cirrhosis from liver diseases in the form of foci (infection with echinococcus, the presence of a tumor), differential diagnosis should be carried out, it helps to detect a sharp severity of disorders that are not characteristic of tumor diseases and infection with helminthic invasion of echinococcus, it is necessary to carry out angiography, laparoscopy, ultrasound diagnostics and radionuclide examinations.

Laparoscopy

Forecast

The life expectancy of patients with cirrhosis of the liver depends mainly on the degree of compensation for this disease. Approximately 50% of patients (at the time of diagnosis) with compensated cirrhosis live over seven years. If decompensated cirrhosis is detected, death occurs within three years, only 11-41% of those suffering from this disease remain alive.

If dropsy develops in patients, then only 25% of people survive this bar at three years. Cirrhosis, which is accompanied by a disease such as encephalopathy, has an even more unfavorable future - liver patients die, mostly within one year. The most favorable prognosis on the basis of etiology is cirrhosis from alcoholism, if you completely abandon alcohol.

Thus, in order to protect yourself from a serious illness, you should lead a healthy lifestyle.

The invention relates to the field of biochemical diagnostics and can be used for differential diagnosis of chronic hepatitis and liver cirrhosis. The essence of the method lies in the fact that an enzyme immunoassay determines the content of thyroglobulin in the blood serum and with an increase in the level of thyroglobulin by 2 times or more compared to the norm, chronic hepatitis is diagnosed, and with a decrease in the level of thyroglobulin by 1.5-2.5 times compared with the norm is cirrhosis of the liver. The technical result is to increase the accuracy of differential diagnosis and reduce trauma.

The invention relates to medicine and can be used in the differential diagnosis of chronic hepatitis and liver cirrhosis.

A known method for the differential diagnosis of chronic hepatitis and cirrhosis of the liver by ultrasound echography, taken as analogue (1).

A known method for the differential diagnosis of chronic hepatitis and cirrhosis of the liver by ultrasound echography and morphological examination of the liver biopsy (2), taken as a prototype.

However, the accuracy of the differential diagnosis of chronic hepatitis and cirrhosis of the liver, according to the prototype method, is relatively limited, and it is traumatic.

The aim of the present invention is to improve the accuracy of the differential diagnosis of chronic hepatitis and liver cirrhosis while reducing trauma.

The technical result is achieved by additionally carrying out an enzyme immunoassay for determining the content of thyroglobulin in the blood serum and with an increase in the level of thyroglobulin by 2 times or more compared to the norm, chronic hepatitis is diagnosed, and with a decrease in the level of thyroglobulin by 1.5-2.5 times compared with the norm is cirrhosis of the liver.

The method is carried out as follows.

The patient complains of weakness, especially in the morning, fatigue, feeling of heaviness and pain in the epigastric region and the right hypochondrium, dyspeptic symptoms - loss of appetite, intolerance to fatty foods, bloating, nausea. With a pronounced exacerbation during chronic hepatitis, weight loss, a periodic increase in body temperature are noted. The liver is enlarged and painful on palpation, its surface is smooth. Rarely, there is an increase in the spleen and sometimes - the phenomenon of "spider veins" and "hepatic palms". The activity of the process is determined by hyperenzymemia (AST, ALT, gamma-glutamyl transpeptidase, alkaline phosphatase warming), hypergammaglobulinemia and an increase in the content of immunoglobulins. In chronic viral hepatitis, HBV DNA, HCV RNA are detected in the blood serum.

An echohepatogram in chronic hepatitis: the liver tissue is compacted, intensely reflects the echo signal. Echo signals in most cases do not reach the maximum amplitude.

At laparoscopy, a large white or large mottled liver is found with damage to both lobes or only one.

With cirrhosis of the liver, as the outcome of chronic hepatitis, the clinical picture consists of hepatocellular insufficiency, portal hypertension (varicose veins of the esophagus, stomach and, less often, hemorrhoidal veins), damage to the reticuloendothelial system, hemodynamic disorders, fever, changes in the nervous and endocrine systems. Typical in liver cirrhosis are sleep disturbances - insomnia at night and drowsiness during the day. Insomnia can be exacerbated by itching that develops in the case of cholestasis, in some cases there is paresthesia in the arms and legs (feeling of numbness, crawling "goosebumps").

With subcompensated cirrhosis, patients complain of weakness and fatigue, irritability and decreased appetite, belching, dull pain in the right hypochondrium radiating to the right shoulder blade. There is an increase in temperature. The skin is dry, yellowish-gray. On palpation, the liver is enlarged, painful, its consistency is dense, the surface of the liver is uneven.

An echohepatogram in liver cirrhosis is characterized by the presence of a large number of reflected signals from sclerosed intrahepatic structures, while the amplitude of the reflected signals reaches a significant value.

The determination of the content of thyroid hormones in the blood of patients with chronic liver diseases was carried out by the enzyme immunoassay method in the blood serum and with an increase in the level of thyroglobulin by 2 times or more compared to the norm, chronic hepatitis is diagnosed, and with a decrease in the level of thyroglobulin by 1.5-2.5 times compared with the norm - cirrhosis of the liver.

Confirmation of the correctness made on. the basis of the proposed method of conclusions are the results of the morphological study of liver biopsy specimens. In liver biopsies in chronic hepatitis, stepwise and sometimes bridging necrosis is noted; lymphoid and histiocytic infiltration of lobules and portal tracts. Specific markers include opaque vitreous hepatocytes with the presence of HBsAg and hepatocytes with sand nuclei, which contain HBc Ag.

In the morphological study of liver biopsy in cirrhosis, necrosis and regeneration of the liver parenchyma are noted, which is accompanied by the formation of false lobules, diffuse proliferation of connective tissue, structural changes and deformation of the organ. The initial necrosis of hepatocytes is accompanied by hyperplasia of the preserved liver parenchyma with the formation of regeneration nodes (false lobules). In areas of massive necrosis, stromal collapse and inflammation, fibrous septa are formed, in which arteriovenous anastomoses are formed.

The method is confirmed by the following examples.

Patient E-v, 44 years old, on admission complains of fatigue, a feeling of heaviness in the epigastric region, loss of appetite and bloating. The patient lost weight by 2 kg, notes a periodic increase in body temperature. The liver is enlarged and painful on palpation. There is an enlargement of the spleen.

In the biochemical analysis of blood: Ac AT - 45 units/l, Al AT - 48 units/l; alkaline phosphatase - 195 units/l, gamma-glutamyl transpeptidase - 59 units/l, bilirubin - 41.0 μm/l. The content of immunoglobulins in the blood serum was: IgM - 155 mg% (normal 105), IgG-1890 mg% (normal 1080), IgA-345 mg% (normal 155).

This patient has HBV DNA, HCV RNA detected in the blood serum.

Ultrasound: the liver tissue is compacted, intensively reflects the echo signal. Echoes do not reach maximum amplitude.

Determination of thyroglobulin content in blood serum showed an increase in its level by 2.1 times compared with the norm (32±3.5 ng/ml). It is concluded that the patient has chronic hepatitis B-C-viral etiology.

The morphological study of liver biopsy specimens confirmed the correctness of the diagnosis. Liver biopsy specimens revealed stepwise necrosis, lymphoid infiltration of the lobules and portal tracts.

Patient G-ko, 38 years old, on admission complains of weakness, especially in the morning, pain in the epigastric region and right hypochondrium, bloating, nausea. On palpation, the liver is enlarged and painful, its surface is smooth. Splenomegaly is noted, "spider veins" are found.

In the biochemical analysis of blood: Ac AT - 50 units/l, Al AT - 54 units/l; alkaline phosphatase - 214 units/l, gamma-glutamyl transpeptidase - 67 units/l, bilirubin - 46 microns/l. The content of immunoglobulins in the blood serum was: IgM - 170 mg%, IgG - 1940 mg%, IgA - 387 mg%. This patient has HBV DNA, HCV RNA detected in the blood serum.

An echohepatogram showed thickening of the liver tissue, the presence of high-amplitude echo signals.

The thyroglobulin level is 96 ng/ml. Based on the study, the patient was diagnosed with DS: Chronic hepatitis B- and C-viral etiology.

Morphological examination of liver biopsy showed the presence of bridging necrosis, lymphoid-histiocytic infiltration of the lobules and portal tracts. Opaque vitreous hepatocytes with the presence of HBsAg and hepatocytes with sandy nuclei containing HBc Ag were revealed.

The patient underwent a course of treatment. Subsequent outpatient follow-up for 1.5 years confirmed the correctness of the diagnosis and the improvement of biochemical samples.

Patient M-va, 65 years old, complains of weakness, irritability and dull pain in the right hypochondrium; yellowish gray skin. Hyperthermia is noted. The patient is somewhat retarded.

On palpation - the liver is enlarged and painful, its consistency is dense, its surface is uneven, there is an increase in the spleen, the phenomena of "spider veins" and "hepatic palms" are noted.

The echohepatogram is characterized by the presence of a large number of reflected signals from sclerosed intrahepatic structures, the amplitude of the reflected signals reaches a maximum value.

Determination of the content of thyroglobulin in the patient's blood showed that its level is 22 ng/ml, which makes it possible to make a diagnosis of cirrhosis of the liver.

Confirmation of the correctness of the conclusions made on the basis of the proposed method are the results of a morphological study of liver biopsy specimens: necrosis and regeneration of the liver parenchyma with the formation of false lobules, diffuse proliferation of connective tissue. In areas of massive necrosis, stromal collapse and inflammation, fibrous septa are formed, in which arteriovenous anastomoses are formed.

The patient was treated. Her condition has stabilized. Follow-up observation for 15 months did not reveal the progression of liver cirrhosis, which confirms the correctness of the diagnosis.

Patient Gr-n, 54 years old, complains of fatigue, reduced appetite, pain in the right hypochondrium. The skin is dry, yellowish-gray. There is an increase in temperature.

Palpation of the liver is painful, its consistency is dense, on palpation the liver is enlarged, its surface is uneven, splenomegaly, the phenomena of "spider veins" and "hepatic palms" are noted.

Ultrasound examination reveals the presence of a large number of reflected signals from intrahepatic structures, the amplitude of the reflected signals is maximum.

In the blood, slight hyperenzymemia and hypergammaglobulinemia.

Determination of the content of thyroglobulin in the patient's blood showed that its level is 12.5 ng/ml, which makes it possible to make a diagnosis of cirrhosis of the liver.

Confirmation of the correctness of the conclusions made on the basis of the proposed method are the results of a morphological study of liver biopsies. Morphological examination of the liver biopsy shows necrosis and regeneration of the liver parenchyma with the formation of false lobules, diffuse proliferation of connective tissue, structural changes and deformation of the organ. The initial necrosis of hepatocytes is accompanied by hyperplasia of the preserved liver parenchyma with the formation of regeneration nodes. In areas of massive necrosis, stromal collapse and inflammation, fibrous septa are formed, in which arteriovenous anastomoses are formed.

The patient received treatment. He was discharged in a satisfactory condition. Follow-up observation for 19 months confirmed the correctness of the diagnosis.

According to the claimed method was carried out the diagnosis of 53 patients, which found: 24 patients - chronic hepatitis and 29 patients - cirrhosis of the liver. For 94% of these patients, follow-up follow-up confirmed the correctness of the diagnosis.

Literature

1. Diseases of the digestive system in children./Ed. A.V. Mazurin. - M., 1984, 630 p.

A method for the differential diagnosis of chronic hepatitis and cirrhosis of the liver by ultrasound examination of the liver, characterized in that an enzyme immunoassay determination of thyroglobulin content in blood serum is additionally carried out and with an increase in the level of thyroglobulin by 2 or more times compared with the norm, chronic hepatitis is diagnosed, and with a decrease in the level of thyroglobulin in the blood serum 1.5-2.5 times compared with the norm - cirrhosis of the liver.

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When making a diagnosis, it is often possible to suspect liver cirrhosis already on the basis of anamnesis - alcohol abuse, past viral hepatitis B, C and D, the presence of characteristic complaints (nosebleeds, dyspeptic disorders, weakness, abdominal pain, etc.) The results of a physical examination are taken into account: telangiectasias in the face and shoulder girdle, erythema of the palmar and digital eminences, blanching of the nails (a sign of low serum albumin), hemorrhagic diathesis (bleeding of the nasal mucosa and gums, subcutaneous petechiae and hemorrhages, localized or generalized purpura), nutritional decline and atrophy of skeletal muscles, grayish-pale skin tone or moderate scleral icterus, compacted liver with a sharp lower edge, splenomegaly with a tendency to leukothrombocytopenia, endocrine disorders (hair disorders, acne, gynecomastia, infertility, etc.). The diagnosis is supported by the detection of characteristic biochemical changes: hyperuglobulinemia, hypoalbuminemia, increased activity of aminotransferases, hyperbilirubinemia due to the conjugated pigment fraction, etc.

Ultrasound provides information about the state of the vessels of the portal system. With the help of computed tomography, a change in the size of the liver, a small amount of ascitic fluid, and a decrease in portal blood flow are determined. Esophagoscopy and X-ray examination of the esophagus can detect varicose veins of the esophagus, which is of paramount importance for the diagnosis. Using a morphological study of a liver biopsy, diffusely distributed pseudolobules surrounded by connective tissue septa are revealed. In addition, the morphological type of cirrhosis and the degree of activity of the process are established.

Recognition of the etiological forms of cirrhosis is based on history data (alcoholism, viral hepatitis, etc.), clinical features, identification of specific markers of the etiological factor (detection of antibodies to hepatitis B, C and D viruses in viral cirrhosis, alcoholic hyaline in alcoholic cirrhosis). In the diagnosis of etiological types of cirrhosis, the greatest difficulty is the distinction between primary and secondary biliary cirrhosis of the liver. Distinctive features of the first are the gradual onset of the disease with itching without pain and temperature, late development of jaundice, early onset high activity of alkaline phosphatase, which does not correspond to the degree of hyperbilirubinemia, antibodies to the mitochondroid fraction, and an increase in the content of IgM. In secondary biliary cirrhosis, along with the symptoms of cirrhosis, signs of the disease that caused it are found. Less often than in primary biliary cirrhosis, melasma, xanthoma and xanthelasma, osteoporosis are observed.

The diagnosis of liver cirrhosis in a-antitrypsin deficiency is made by determining the Pi phenotype using immunoelectrophoresis. Congestive cirrhosis, which forms in the terminal stage, proceeds with persistent ascites, hepatosplenomegaly, but unlike other forms of cirrhosis, it is accompanied by severe shortness of breath, swelling of the jugular veins, cyanosis, and high venous pressure.

Differential diagnosis of liver cirrhosis

Liver cirrhosis must be distinguished from chronic active hepatitis, liver fibrosis, liver cancer, liver echinococcosis, constrictive pericarditis, liver amyloidosis. Due to the fact that cirrhosis develops gradually, a clear distinction from chronic active hepatitis in some cases is impossible. The presence of signs of portal hypertension (varicose veins of the lower third of the esophagus) indicates the transition of hepatitis to cirrhosis. Liver fibrosis as an independent disease is usually not accompanied by clinical symptoms and functional disorders. In some cases, with congenital and alcoholic liver fibrosis, portal hypertension develops, which leads to diagnostic difficulties. Morphologically, with fibrosis, the lobular architectonics of the liver is preserved. Liver cancer is characterized by a more acute development of the disease, a pronounced progressive course, exhaustion, fever, pain, leukocytosis, anemia, and a sharply increased ESR. A pathognomonic sign of liver cancer is a positive Abelev-Tatarinov reaction - the detection of a-fetoproteins (embryonic serum globulins).

The diagnosis is confirmed by targeted biopsy data. In alveolar echinococcosis, the diagnosis is made on the basis of a hemagglutination reaction and latex agglutination with an echinococcal antigen, in which specific antibodies are determined, in some cases laparoscopy is used. With constrictive pericarditis, the first signs of heart compression are characterized by a feeling of heaviness in the right hypochondrium, an increase and thickening of the liver, mainly the left lobe. Shortness of breath occurs during physical exertion, the pulse is soft, small filling. The results of echocardiography serve as a criterion for reliable diagnosis. Liver amyloidosis is reliably diagnosed by needle biopsy data.

Ed. prof. I.N. Bronovets

"Diagnosis of cirrhosis of the liver, diagnostic signs" article from the section