Alcoholic cirrhosis of the liver differential diagnosis. What is the differential diagnosis of liver cirrhosis according to Child Pugh and treatment

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

Liver cirrhosis is the final stage wide range liver diseases.

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

Epidemiology

Liver cirrhosis is the cause of death in 90–95% of cases of chronic liver diseases and occupies a leading place 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 amounts of alcohol 2 times more often than ordinary people; anti-HCV is also detected in the blood serum of patients with liver cirrhosis 11 times more often than in the population.

Every year, approximately 2 million people die worldwide 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 close to those for viral cirrhosis of the liver.

Etiology

The main most common reasons occurrence of liver cirrhosis:

– alcohol abuse (over 50%);

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

Metabolic disorders that can trigger liver cirrhosis:

– iron overload in hereditary hemochromatosis;

– copper overload in Wilson’s disease;

– α 1 -antitrypsin deficiency;

– cystic fibrosis;

– galactosemia and glycogenosis;

– hereditary tyrosinemia and telangiectasia, porphyria.

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

– extrahepatic obstruction of the biliary tract;

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

– cholangiopathies in children (progressive childhood cholestasis, arteriohepatic dysplasia, cholestasis with lymphedema, Zellweger syndrome);

– difficulty in 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 occurrence of cirrhosis.

At the same time, cirrhosis can be caused by immune changes (autoimmune hepatitis, graft-versus-host disease), and other painful conditions (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 liver cirrhosis of unknown etiology are persons with unconfirmed viral and alcoholic liver cirrhosis due to incomplete examination.

Pathogenesis

Hepatocellular necrosis and impaired 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 indirectly damaging effects of agents of autoimmune and immune aggression.

Subsequently, the products of cellular 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 that synthesize pro-inflammatory cytokines (tumor necrosis factor-α, interleukins). A lack of bile acids in the intestine is accompanied by increased bacterial growth and, as a consequence, endotoxemia and additional stimulation of cytokine production. Of no small importance in the process of cytolysis of hepatocytes is the difficulty of secretion and stagnation of bile, which arise due to disruption of 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 to be the most important mechanism for the formation and progression of liver cirrhosis. Hepatocellular necrosis, cytokines produced by cellular structures of the liver, acetaldehyde (formed during the transformation of alcohol), cause degradation of the extracellular matrix space of Disse. These processes are accompanied by activation of Ito cells, which ultimately leads to 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 sinusoids, which impedes the metabolism between the liver cell and the blood, which provokes the formation of portal hypertension.

Cirrhotic changes in the liver parenchyma and, as a consequence, portal hypertension, which causes portosystemic shunting and hepatocellular failure, lead to the formation of parenchymal and arterial vasodilation with a progressive decrease in systemic vascular resistance. This predisposes to a fall in effective arterial volume and a decrease blood pressure, which creates conditions for fluid retention and an increase in blood 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 aggravates portosystemic shunting, portal hypertension and hepatocellular insufficiency.

Clinical picture

Disease long time may be asymptomatic.

Clinical assessment of the stage and severity of liver cirrhosis is based on the severity of portal hypertension and hepatocellular insufficiency. Semi-quantitatively, the stage and severity of the disease is assessed using the Child–Pugh diagnostic criteria scale.

Compensated (class A) course of liver cirrhosis is characterized by the absence of jaundice, 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.

Patients with liver cirrhosis may exhibit various symptoms of damage to almost all organs and systems, which determine the following syndromes:

  • Asthenic ( fast fatiguability, loss of appetite of varying severity, loss of body weight).
  • Dermal (icteric discoloration of the skin, “varnished” tongue and lips, telangiectasia, redness of the palmar surfaces, skin scratching, jamming in the corners of the mouth, changes in the nail plates).
  • Musculoskeletal (hypertrophic osteoarthropathy, hepatic osteodystrophy, seizures, umbilical hernia).
  • Pulmonary (hypoxemia, primary pulmonary hypertension, rapid breathing, decreased vital capacity of the lungs, accumulation of fluid in the pleural sinus, dilation of intrapulmonary vessels, shortness of breath).
  • Cardiac (hyperdynamic blood circulation).
  • Gastrointestinal (enlarged parotid salivary glands, loose stools, cholelithiasis, portal hypertensive gastro- and colonopathies, symptomatic (cirrhotic) erosive and ulcerative lesions, gastritis, hepatic breath odor).
  • Renal (secondary hyperaldosteronism, in which fluid and sodium retention develops, “hepatic” glomerulosclerosis, renal tubular acidosis, hepatorenal syndrome).
  • Hematological (folate deficiency and hemolytic anemia, enlarged spleen with pancytopenia, coagulation disorders, disseminated intravascular coagulation syndrome, hemosiderosis).
  • Endocrine (diabetes, increased 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, decreased testosterone, feminization ).
  • Neurological (hepatic encephalopathy, peripheral neuropathy, seizures).
  • Portal hypertension syndrome (varicose veins - gastroesophageal, anorectal, retroperitoneal, "head of the jellyfish"; 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 initial stage 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, ending in death.

2. Rapidly progressing (active) cirrhosis.

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

3. Slowly progressive (active) cirrhosis.

A weak 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, the morphological manifestations of activity are moderately expressed. Portal hypertension develops slowly, and 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 hepatic failure do not develop. In the majority of patients, this form of liver cirrhosis does not negatively affect life expectancy.

Complications

  • Bleeding from varicose veins of the digestive tract.
  • Hepatorenal syndrome (malaise, thirst, dryness and decreased skin turgor, decreased urine formation, arterial hypotension).
  • Ascites.
  • Bacterial peritonitis.
  • Portal vein thrombosis.
  • Hepatopulmonary syndrome.
  • Attachment of a secondary infection (most often with the occurrence of pneumonia).
  • Formation of stones in gallbladder and ducts in primary biliary cirrhosis.
  • Transformation into cirrhosis-cancer.
  • Liver failure.

Diagnostics

Among the laboratory and clinical indicators to detect liver cirrhosis, the following studies must be carried out: hemogram, coagulogram, proteinogram, liver function tests, immunogram, as well as determination of autoantibodies ANA, AMA, SMA, determination of the level of α 1 -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 cytolysis syndromes, cholestasis, synthetic inferiority of liver function, as well as the occurrence of regeneration syndrome and tumor growth.

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

A study of liver fibrosis markers is being conducted, however, these markers do not reflect excessive protein deposition in the extracellular matrix, but tissue metabolism as a whole, and individually do not have specificity for liver tissue. The presence of other inflammatory foci in the body 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 assessed for markers of viral hepatitis B, C, D, which helps in establishing the severity and 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 for various autoimmune diseases The liver is characterized by certain combinations of autoantibodies.

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

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

As part of elucidating the etiology of liver cirrhosis differential diagnosis must 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 nodules form or fibrosis develops (nodular regenerative hyperplasia, non-cirrhotic liver fibrosis, schistosomiasis, echinococcosis, opisthorchiasis, tuberculosis, syphilis, brucellosis); malignant neoplasms different organs with liver metastases.

The final diagnosis is established using histological examination, which identifies regeneration nodes.

Treatment

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

General principles of treatment include strict lifelong abstinence from alcohol in the presence of alcoholic cirrhosis of the liver, the use of antiviral pharmaceuticals (INF-α and pegylated INF-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, and spontaneous bacterial peritonitis.

Traditionally, patients with liver cirrhosis are prescribed drugs with hepatoprotective properties - essential phospholipids, drugs of silymarin, ademetionine, 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 epithelial cells bile ducts, which stimulate fibrogenesis through the release of profibrinogenic agents.

The effect of hepatocyte transplantation on liver function and the reverse development of fibrosis is being studied.

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

Forecast

The prognosis for all types of liver cirrhosis is determined by the degree of morphological changes in the liver, the tendency to progression and the absence effective methods 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 and complete treatment of viral hepatitis; avoiding the consumption of alcoholic beverages, minimizing the influence of hepatotoxic substances.

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 intercourse, manipulation of blood and other possible methods of infection. Sometimes they remember alcoholic liver disease, cirrhosis and other conditions that are combined general symptoms and principles of treatment.

General information

But it turns out that sometimes there is no need to be in a risk group, use drugs, or visit questionable nail salons and consume alcohol substitutes to develop hepatitis. Sometimes it occurs without any connection with alcohol intake or viral infection. This disease is called autoimmune hepatitis.

For the first time, cases of unknown liver damage began to be recorded in the early 1950s, mainly in women young. They suffered chronic hepatitis, but at the same time their blood levels of gamma globulins were increased. Characteristic feature This condition responded well to the use of hormones.

Then, when improving methods laboratory research, 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 an era of intensive research into this disease. In the following decades, diagnostic criteria were developed and many drugs were tested. 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 made significant progress - it was in this pathology that for the first time, correctly selected treatment 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 UC (nonspecific ulcerative colitis). Despite complete information and understanding of the mechanisms of pathogenesis, the world situation (especially in relation to the first) is very far from favorable. What is this pathology from a modern point of view?

Definition

Currently, there is no generally accepted definition of the disease. Therefore, the most correct, “combined” definition can be formulated as follows: autoimmune hepatitis is chronic process inflammation and necrosis in the liver, occurring for unknown reasons, with the circulation in the blood of a significant amount of autoantibodies to tissues, an increase in the level of gamma globulins, and 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, and against the background of alcoholic liver damage. Even in the European Union countries, with a perfect level of diagnostics, the prevalence does not exceed two cases per 10 thousand people. Women suffer from autoimmune hepatitis three times more often than men.

This may be due to the fact that women are generally more prone to developing autoimmune pathologies than men. Such “major” diseases as systemic scleroderma, systemic lupus erythematosus, and rheumatoid arthritis are more common in women. After all, reproductive function involves bearing an organism that is genetically different from the mother’s. This requires both a high intensity of the immune background and its tolerance to foreign (paternal) genetic material.

The chances of developing autoimmune hepatitis are high in two periods of life: both in young (25 years) and in old (60 years) age, although in Lately these peaks “level out”, and there is a tendency to increase incidence in both men and women in all periods 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 defense, and intoxication (alcohol and drugs). All this adversely affects the function immune system and liver.

About classification

Two variants of hepatitis development 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 characteristic of a disease such as primary sclerosing cholangitis (it is also classified as a disease connective tissue). The antigen in this situation is liver-specific protein;
  • the second type of hepatitis is characterized by the presence of antibodies to liver and kidney microsomes. 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 enzyme P 450 - 2 D. 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 occurrence of autoimmune hepatitis, is the so-called cross-antigenic reactivation, or molecular mimicry. This means that if at the time of “learning” of T-lymphocytes in the thymus gland some proteins of the body are not studied and identified by them, then in the future they may encounter a foreign antigen similar to them. And later, having encountered proteins of their body that have appeared on the surface of the membrane, similar to enemies, T - lymphocytes successfully organize an attack on them without recognizing their own.

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

  1. Genetic predetermination (with type 1 hepatitis).

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

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, herpetic infection);
  2. Expression of “false” antigens on the surface of hepatocytes;
  3. Lymphocytes (T and B) are activated and respond to these decoys;
  4. There is an accumulation of gamma globulins, or autoantibodies, and a pool of inflammatory mediators (cytokines, arachidonic acid metabolites) is formed;
  5. Development of alteration (damage) to liver tissue;
  6. The emergence of the clinic of autoimmune hepatitis.

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

Clinical manifestations

How does autoimmune hepatitis manifest? Are there any differences in the course of this hepatitis that would suggest the presence of immune inflammation of the liver?

Debut

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

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

Typical clinical manifestations occur: jaundice, intoxication, laboratory symptom complexes of cytolysis and necrosis of liver tissue. Weakness, loss of appetite, darkening of urine, and discoloration of feces occur. ALT and AST (liver aminotransferases) increase tenfold or higher. 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 an 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 itself as a pronounced articular syndrome: polyarthritis occurs, vascular disorders, a hemorrhagic rash may appear. These patients unsuccessfully visit doctors: treatment does not help them, and only after 4–6 months do symptoms appear, such as icterus of the sclera, 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”, “suspicious tuberculosis” and a host of other diagnoses. Naturally, no treatment is carried out, or, on the contrary, they treat “everything” and “for 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 to 60 mmh and above;
  • arthralgia – pain in the joints (large ones in the arms and legs);
  • hemorrhagic hemorrhages in the skin, or recurrent purpura;
  • sometimes – psoriasis, symptoms of focal scleroderma;
  • endocrinopathies – amenorrhea, stretch marks on the thighs and abdomen, hirsutism occurs;
  • jaundice intermittently, weakening during remission and increasing during exacerbation;
  • the liver enlarges and thickens.

It is surprising that many patients with hepatitis, despite severe symptoms, feel well.

In conclusion, the description of the symptoms 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 suffer from 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

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

The following criteria turned out to be most characteristic of autoimmune hepatitis:

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

To summarize, it should be said that if the patient has:

  • the above clinic;
  • he was not given a blood transfusion;
  • he did not take medications with hepatotoxic effects;
  • did not abuse alcohol;
  • did not suffer from acute or 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 “definite autoimmune hepatitis.”

Principles of treatment

Unlike viral liver diseases, for autoimmune hepatitis the basis of treatment tactics is the administration of corticosteroid hormones. In this case, the main drug is prednisolone. It acts on T lymphocytes, causing their suppression, and inhibits their reaction cycle. As a result, the process of inflammation and necrosis in liver tissue 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.

Cytostatics, such as azathioprine, are also used in treatment. But there are cases when it is possible not to prescribe these drugs, but to observe the patient. This is possible with an asymptomatic course, with low transaminase levels. On the other hand, in case of profound dysfunction of the organ, in the presence of decompensated cirrhosis, anemia, ascites, portal hypertension, treatment is already overdue.

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

Hormones are used in treatment either alone or in combination with azathioprine. Taking the hormone should be long-term - sometimes from 6 months to six months, and some patients are indicated for lifelong therapy. The diagnosis we are talking about is so serious that there are no absolute contraindications to the prescription of hormones.

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

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

Typically, a noticeable improvement occurs already in the first weeks after the prescription of drugs, and normalization of laboratory parameters by the end of the year in 75% of patients with correctly selected therapy. But this is true provided that the level of transferases - ALT and AST - in the peripheral blood decreases. If they are not reduced, then remission cannot be expected. In general, treatment failures occur in every fifth case.

Forecast

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

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

But the total life expectancy of a patient with the occurrence of a similar process in the liver does not exceed 15 years, in as a last resort- 20 years. Therefore, when type 2 disease occurs in children, this diagnosis still sounds like a death 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 pathology may be on the waiting list for liver transplantation for several years, and after liver transplantation, life expectancy is significantly prolonged.

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

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

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

1Mechanism of ascites formation

Ascites is an excessive accumulation of fluid in the peritoneal cavity (physiologically, there is about 150 ml of fluid there). Ascites occurs when the patient collects more than 500 ml of fluid in the abdominal cavity. As a rule, this is a serous fluid. It contains more than 3 g/dL of protein (mostly albumin), as well as sodium, potassium and glucose in the same concentrations as in blood serum. The presence of neutrophils in the fluid may indicate an existing infection. And the presence of red blood cells implies the distribution tumor process in the abdominal cavity.

2Etiology of the disease

The main causes of ascites include:

  • increased venous pressure in the vena cava;
  • obstructed blood flow from the liver (for example, cirrhosis of the liver);
  • obstructed lymph drainage;
  • increased permeability of peritoneal vessels (for example, inflammatory processes of various origins);
  • decrease in plasma oncotic pressure (for example, nephrotic syndrome).

The most common diseases causing abdominal dropsy:

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

Ascites is characterized the following symptoms: increased abdominal circumference, increased body weight, abdominal pain, a feeling of discomfort and pushing outward in the abdominal cavity. More late symptoms- problems with sitting and walking, disorders of the gastrointestinal tract, swelling of the legs and external genitalia.

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 only possible using 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 may feel fluid moving in the abdominal cavity. To recognize ascites, the doctor can tap the patient's abdomen while he is lying on one side, then on the other. Then you can observe the moving fluid in the patient’s peritoneum as his position changes.

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

4 Symptoms and diagnosis of pathology

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

If the volume of collected fluid exceeds 1.5 liters (in very advanced cases), it can lead to a feeling of suffocation. Long-lasting abdominal hydrops can lead to the development of pleural exudate (hydrothorax), i.e. collecting water in pleural cavity, which surrounds the lungs. More often it has right-hand traffic than left-hand traffic. 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 should always be differentiated from pregnancy, enlargement Bladder, ovarian cancer, which can produce similar symptoms.

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

Sometimes necessary additional research eg cytopathology. To distinguish ascites caused by hypertension from ascites due to other causes, fluid obtained through abdominal puncture (paracentesis) is diagnosed. Fluid removal is also carried out in 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.

Progress 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 liquid volume of 50-100 ml is collected, which is then analyzed.

A sample of the liquid is tested for protein concentration and for the presence of possible bacteria. The appearance of the fluid may suggest the cause of ascites. Straw-colored fluid occurs with cirrhosis of the liver (although it may be mixed with bile or clear), also with heart failure or nephrotic syndrome (although in this case it may be milky). Purulent and cloudy fluid 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 hemorrhagic, milky-colored liquid, and in the case of tuberculosis, even transparent).

5Therapeutic measures

Ascites is a symptom various diseases. In 80% of cases it accompanies cirrhosis of the liver. In approximately 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 reasons for the development of ascites.

Treatment of ascites consists mainly of treating the underlying disease that causes it.

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

If treatment with diuretics does not produce 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, a liver transplant is considered.

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

Bleeding from the esophagus is a serious problem that requires immediate medical attention. help. Heavy bleeding in the absence of urgent measures can lead to death. Small and moderate development of chronic blood loss, leading to loss of strength 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;
  • pathologies of the esophagus;
  • varicose veins of the stomach;
  • tumors;
  • burn;
  • cardiovascular diseases;
  • long-term use of medications;
  • alcohol poisoning;
  • long-term negative emotions;
  • hemophilia.

There are cases in medicine that a similar condition is caused by taking medications such as Nise, Aspirin, children are especially susceptible to this. Also due to severe vomiting, which is often provoked by alcohol poisoning, a tear occurs in the longitudinal lining of the esophagus and the development of a dangerous condition.

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

Symptoms of the disease

This condition is a rather rare disease, which sometimes not only patients, but also doctors cannot identify in a timely manner. This is due to the fact that with mild bleeding, blood gradually enters the stomach, which is digested there, without showing any obvious signs. Even if this pathology is accompanied by pain, experts often attribute it to gastritis. Heavy bleeding makes it difficult to identify the source of this condition. However, there are specific symptoms diseases are usually:

  • Vomiting blood. When the pathology is caused by injury, an ulcer, a discharge of scarlet blood is observed. This means that it did not have time to undergo digestion; this phenomenon occurs with heavy bleeding. Minor bleeding causes vomiting, similar to coffee grounds, since the liquid has been processed by gastric juice. If cherry color is released when vomiting, then gastric varicose veins occur.
  • The patient's stool changes; it has a deep black color. This condition occurs when blood passes through the digestive tract.
  • A sharp decrease in blood pressure, manifested by dizziness, nausea, malaise, and weakness.
  • Tachycardia, rapid heartbeat.
  • Increased need for water.
  • Changes in the skin.

The intensity of the symptoms depends on the degree of hemorrhage; with minor damage, the symptoms are sometimes not noticeable. If a person has at least one of the symptoms, then it is necessary to urgently contact a specialist for diagnosis.

Diagnosis of the disease

To make an accurate diagnosis, you must undergo the following examination:

  • how to get rid of varicose veins of the esophagus
  • a general blood test establishes the fact of bleeding, which will show a decrease in hemoglobin and red blood cells;
  • stool analysis will help determine hidden hemorrhage;
  • FGDS is an accurate method that will not only help determine the location of bleeding, but also administer a hemostatic injection and stitch up the burst vessel;
  • Ultrasound will not help accurately determine the location of the pathology, but will determine the condition of the internal organs;
  • MRI, CT will determine the cause of hemorrhage;
  • X-ray with the introduction of a dye will reveal the localization of the pathology.

First aid

In case of bleeding, it is important to call for medical help as soon as possible and provide competent pre-medical intervention. Since applying 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. It must be in a horizontal position, which will not only limit physical activity, but will help control how much blood he lost. Because horizontal position limits its entry into the digestive tract.

It is necessary to create comfort for the patient; unnecessary clothes should be removed from him and covered with a blanket. An important condition is to monitor blood pressure and pulse rate, which should be carried out every 10 minutes. Lower blood pressure increases the heart rate and indicates that a significant amount of blood has been lost. If blood pressure drops below 80 mmHg, and the heart rate increases to 130 beats, then this is an indicator of the possibility of shock.

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 him inhale ammonia. Ice taken orally in small pieces will help relieve 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:

  • insertion of a Blackmore probe, which is located in the esophagus. The probe is then inflated with air, causing the cuff to inflate, pressing against the blood vessels. This cuff also contains a tube that does not increase the vascular lumen; nutrition and medications are supplied through it. This device may remain in the patient’s body for several days until a blood clot forms on the damaged vessel;
  • with the help of surgery performed through laparoscopy, sutures are placed on the damaged vessel or cauterization is performed using electricity or a laser;
  • used together with surgery drug therapy which involves the administration of hemostatic drugs, for example, Vikasol, Calcium chloride. Sometimes it is necessary to replace blood loss with erythromass;
  • if the erosive area suggests infection, then a course of antibiotic therapy, for example, Macrolide or Cephalosporin drugs, may be required.

Patients must be on strict bed rest for a long time. They are not allowed to eat on their own; they receive nutrition by intravenous administration. Once they are allowed to feed themselves, 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 to avoid the development of complications and death.

Version: MedElement Disease Directory

Alcoholic cirrhosis of the liver (K70.3)

Gastroenterology

general information

Short description


Alcoholic liver cirrhosis- chronic liver pathology that develops during chronic alcohol intoxication, with gradual death of hepatocytes, widespread fibrosis and atypical regeneration nodes gradually replacing parenchyma Parenchyma is a set of main functioning elements of an internal organ, limited by 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 liver blood flow, leading to jaundice, portal hypertension and ascites Ascites - accumulation of transudate in the abdominal cavity
. Is a variety alcoholic illness liver.


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

Period of occurrence

Chronic pathology. The course is more favorable when alcohol abuse is stopped.

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 porphyria cutanea tarda (develops with hereditary predisposition To her).

To assess the severity of alcoholic cirrhosis of the liver, the Child-Pugh scale and other classifications can be used (see also the section “Fibrosis and cirrhosis of the liver” - K74).

Etiology and pathogenesis

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

The risk of developing alcoholic liver disease occurs when drinking more than 40 g of pure ethanol per day. Drinking more than 80 g of pure ethanol for 10 years or more increases the risk of liver cirrhosis. There is no direct correlation between the degree of liver damage and the amount of alcohol taken: less than 50% of people who drink alcohol in dangerous doses have severe forms 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 Liver 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

Sign of prevalence: Common

Sex ratio(m/f): 2


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

Risk factors and groups


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

Clinical picture

Clinical diagnostic criteria

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

Symptoms, course


Clinical signs alcoholic illness range from moderate symptoms to a picture of severe liver failure and portal hypertension.

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

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

14. Other symptoms overuse alcohol (see section "Diagnostics").

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

Diagnostics

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

Fact of alcoholism
1. An alcohol history is revealed by interviewing the patient and relatives according to a special questionnaire, which significantly increases the likelihood of diagnosing alcoholism.
2. Most common symptoms(alcohol stigmas detected during examination):
- dilation of blood vessels in 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;
- presence of lesions of other organs and systems ((pancreatitis, dilated cardiomyopathy, peripheral neuropathies).

Instrumental studies

Ultrasound is considered the starting method, and liver biopsy is the “gold standard of diagnosis.”

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 - non-invasive and non-radioactive diagnostic method for analysis of arteries and veins (a combination of Doppler technology with ultrasound imaging)
: identifying the direction of hepatic blood flow, the degree of development 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 nodes.

4. Laparoscopy Laparoscopy (peritoneoscopy) is the study of the abdominal organs by examining them using medical endoscopes inserted into the peritoneal cavity through a puncture of the abdominal wall.
 with a liver biopsy make it possible to describe the surface of the liver, the size of the regeneration nodes and morphologically confirm the diagnosis. These studies are carried out only in the absence of contraindications to them. For example, percutaneous needle biopsy of the liver is often impossible due to contraindications (primarily coagulopathy) and is associated with a large number of diagnostic errors. In such cases, transjugular liver biopsy is recommended.


At needle biopsy of the liver with histological examination they find:
- hepatocyte steatosis is predominantly macrovesicular;
- Mallory bodies Mallory bodies - acidophilic clumps around the nucleus, formed in the cytoplasm (usually 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 the attenuation of X-ray radiation by tissues of different densities.
 And MRI MRI - magnetic resonance imaging
 have sufficient sensitivity and specificity.


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

Laboratory diagnostics

Signs of alcohol abuse:


1. Sharp increase the level of gamma-glutamyltransferase (GGT) in the blood serum and its sharp decrease during abstinence. 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 to detect alcohol abuse. Data on the specificity (82% to 92%) and sensitivity (58% to 69%) of the test for detecting current alcohol abuse vary widely. The test has been proven to be highly informative 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 alcohol abuse, lacks sensitivity (27-52%), but changes become quite sensitive (85-91%) for patients drinking alcohol more than 50 g / day (in the absence of vitamin therapy B12 or folic acid).

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


Signs of liver damage:

1. Increased aminotransferase levels: AST AST - aspartate aminotransferase
(sensitivity - 50%, specificity - 82%) and ALT ALT - alanine aminotransferase
(sensitivity - 35%, specificity - 86%) are increased in all forms of alcoholic liver disease when drinking alcohol more than 50 g / day. "Classical" AST ratio AST - aspartate aminotransferase
/ALT ALT - alanine aminotransferase
for alcoholic liver disease equal to or more than 2.

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

8. Coagulopathy (prothrombin time, INR International normalized ratio (INR) is a laboratory indicator determined to assess the extrinsic pathway of blood coagulation
>1.5) - there is a persistent, long-term increase.

9. Urea and serum 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. Folic acid Serum (folate) levels may be normal or low.
2. Serum ammonia does not always correlate with hepatic encephalopathy, developing in alcoholic cirrhosis of the liver. Thus, its regular, routine determination is impractical.
3. Alpha-1-antitrypsin - differential diagnostic test. In alcoholic cirrhosis of the liver, the content is normal.
4. Serum iron, ferritin, transferrin - test for differential diagnosis with hemochromatosis. In alcoholic cirrhosis of the liver, the content is normal or slightly increased.

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

6. The level of daily copper excretion in urine is a differential diagnostic test for Konovalov-Wilson disease.
7. Antimitochondrial antibodies (AMA) - a differential diagnostic test for primary biliary cirrhosis. In 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 differential diagnostic test for autoimmune hepatitis.

Differential diagnosis


Alcoholic cirrhosis of the liver is differentiated with the following diseases:
- other forms of alcoholic liver disease;
- cirrhosis, fibrosis, sclerosis Sclerosis is a hardening of an organ caused by the replacement of its dead functional elements with connective (usually fibrous) tissue or a homogeneous hyaline-like mass
liver of other etiology;
- storage diseases (for example, hemochromatosis Hemochromatosis (syn. hemomelanosis, bronze diabetes, siderophilia, Troisier-Anaud-Choffard syndrome, pigmentary cirrhosis) -hereditary disease, characterized by impaired metabolism of iron-containing pigments, increased absorption of iron in the intestines and its accumulation in tissues and organs; manifested by signs of liver cirrhosis, diabetes mellitus, skin pigmentation
, Konovalov-Wilson disease Konovalov-Wilson disease (syn. hepato-cerebral dystrophy) is a hereditary human disease characterized by a combination of liver cirrhosis and degenerative processes in the brain; caused by impaired protein metabolism (hypoproteinemia) and copper; inherited in an autosomal recessive manner
);
- obstruction Obstruction - obstruction, blockage
biliary tract;
- chronic inflammatory liver diseases.

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

Complications


It is necessary to distinguish between complications of alcoholic cirrhosis 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 use ingestion of hepatocarcinogens, liver cirrhosis caused by other causes
;
- hepatorenal syndrome Hepatorenal syndrome - pathological condition, sometimes manifested in severe liver damage and manifested by secondary renal dysfunction up to severe renal failure. The development of acute liver and kidney failure is manifested by a combination of jaundice, blood clotting 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 impaired contractility muscle fibers and manifested by muscle weakness, decreased volume active movements, decreased tone, atrophy, sometimes pseudohypertrophy of muscles

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Cirrhosis is a disease in which the parenchymal tissue of the liver is gradually replaced by connective tissue. The organ ceases to perform its functions, which leads to the death of the patient. The process develops over a long period of time, initial stages the clinical picture is erased. With further development, symptoms appear that allow one to suspect pathology. But for a more precise diagnosis, differential diagnosis of liver cirrhosis is necessary.

Flow different types Cirrhosis is different, so several types of classifications are used to make a diagnosis.

According to the form of the processes, they are classified depending on the size of the formed nodes.

  • Small nodular cirrhosis, sizes up to three millimeters in diameter.
  • Large-knot, over three millimeters.
  • Incomplete septal (septal) form.
  • Mixed, with nodes of different diameters.

There are types of cirrhosis based on the causes and conditions of the disease.

  • Viral – caused by viral hepatitis B and C.
  • Alcoholic – caused by prolonged use of alcohol-containing substances.
  • Medicinal – arising after long-term use medicines that destroy the liver.
  • Secondary biliary cirrhosis is associated with impaired functioning of the extrahepatic bile ducts.
  • Congenital – caused by hereditary diseases.
  • Stagnant - provoked by circulatory disorders.
  • Budd-Chiari disease is endophlebitis of the hepatic veins with thrombosis, anomalies of vein development.
  • Metabolic and nutritional – associated with metabolic disorders.
  • Cirrhosis of unknown etiology - this group includes primary biliary, associated with pathology of immunoregulation, cryptogenic, presumably provoked by a nutritional factor, and Indian childhood, possibly caused by high copper content in drinking water.

The third type of classification is used to assess severity. It examines the functioning of liver cells in a patient. Known as Child-Pugh.

According to this table, three groups are determined, depending on the points scored. A – five or six points, B – up to nine, C – over ten.

The role of differential diagnostics in making a diagnosis

Differential diagnosis is a set of measures prescribed by the attending physician to clarify the diagnosis. Used to distinguish between diseases that have similar symptoms. The differential diagnosis of liver cirrhosis is established after the following studies:

  • taking anamnesis;
  • examination of the patient;
  • clinical tests of blood, urine, feces;
  • biochemical blood tests;
  • coagulogram - study of the functioning of blood clotting factors;
  • enzyme tests;
  • examination for hepatitis markers;
  • ultrasound examination;
  • computed tomography or MRI;
  • biopsy with histological examination of tissue;
  • research using radioisotopes;
  • laparoscopic examination.

Differential diagnosis of liver cirrhosis

Differential diagnosis is used in cases where it is necessary to exclude diseases with a similar clinical picture.

What diseases require differential diagnosis?

Primary cancer and cirrhosis cancer. With similar symptoms, it is characterized by rapid development. Blood tests show leukocytosis, increase in ESR, anemia. The patient quickly loses weight and complains of pain. Ascites develops quickly and is not treatable with diuretics. Differential diagnosis helps to determine this type of pathology during laparoscopy, MRI results, and when α-fetoprotein is detected.

Alveolar echinococcosis. An enlarged spleen and functional tests are misleading. Differential diagnosis – ultrasound, MRI, antibodies in the latex agglutination reaction.

Constrictive pericarditis. Symptoms of ascites and liver enlargement, as with cirrhosis. For differentiation, cardiac echography is performed. Accurate data is obtained from x-ray kymography.

Myelofibrosis. In the early stages, the enlargement of the spleen is pronounced. Trephine biopsy, a bone marrow puncture, helps with differential diagnosis.

Amyloidosis, hemochromatosis. Differential diagnosis is based on biopsy results. Wilson-Konovalov disease is distinguished by low serum ceruloplasmin.

Comparative table of pathologies

Diseases Signs
Hepatitis Increase in temperature, yellowness of the skin in an ocher shade. Headache, aches in joints and muscles. Weakness, nausea, vomiting. Dark urine, itchy skin. Pain syndrome. Increased bilirubin, ALT, AST.
Cholangitis Fever with chills. Nausea, vomiting. Weakness. Skin itching, jaundice. Thickening nail phalanges. Point sensitivity in the area of ​​the gallbladder. Increased bilirubin, ALT, AST, amylase. Neutrophilia, lymphocytosis.
Congestive liver Expansion of the boundaries of the organ. Pain syndrome. Weakness, weight loss. Anxiety, poor attention. Edema of the lower extremities. Yellowness of the skin. Shortness of breath and accompanying cough. Inflammation of the lymph nodes. Increased bilirubin, ALT, AST.
Liver cancer Rapid development. Weakness, weight loss, change in stool, dyspepsia, pain in the right hypochondrium. Jaundice, dry skin and mucous membranes, itching. The temperature is subfebrile.
Liver necrosis Dyspepsia, pain syndrome, yellowness of the skin and mucous membranes, fever. Erythema, spider veins, hand tremor. The stool is light, the urine is dark. Pain syndrome. High bilirubin, ALT, AST. Decreased albumin and protein. Monocytopenia, eosinopenia.
Cirrhosis Dyspepsia. Yellowness of the skin and sclera. Weight loss, abdominal enlargement. Pain. Erythema, spider veins, changes in the shape of fingers and nails. Ascites, encephalopathy. Increased bilirubin. Reduced protein in the blood. Neutrophilia.

The symptoms of all pathologies are similar, the differences lie in the details. Only through differential diagnosis is it possible to establish an accurate diagnosis.

Prognosis for cirrhosis

Estimated predictions can be made based on the Child-Pugh score. Patients who receive class A have a life expectancy of about twenty years, and the mortality rate after surgery is 10%. Class B has a shorter lifespan and postoperative mortality reaches 30%. The most severe is class C, 18% survive after surgery, and without surgery they live no more than three years.

Thanks to differential diagnosis, there is a chance to identify cirrhosis in the early stages of development. In such cases, the patient has the opportunity to extend his life for a long time, subject to the doctor’s recommendations.

When making a diagnosis, it is often possible to suspect cirrhosis of the liver based on anamnesis - alcohol abuse, previous 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: telangiectasia in the area of ​​the face and shoulder girdle, erythema of the palmar and digital eminences, blanching of the nails (a sign low level serum albumin), phenomena hemorrhagic diathesis(bleeding of the mucous membrane of the nose and gums, subcutaneous petechiae and hemorrhages, localized or generalized purpura), loss of nutrition and atrophy of skeletal muscles, grayish-pale skin tone or moderate icterus of the sclera, compacted liver with a sharp lower edge, splenomegaly with a tendency to leukothrombocytopenia, endocrine disorders (hair growth disorders, acne, gynecomastia, infertility, etc.). The diagnosis is confirmed by the detection of characteristic biochemical changes: hyperuglobulinemia, hypoalbuminemia, increased aminotransferase activity, hyperbilirubinemia due to the conjugated fraction of pigment, etc.

Ultrasound allows you to obtain information about the condition of the vessels of the portal system. Using computed tomography, changes 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 esophagus can be detected varicose veins veins of the esophagus, which is of paramount importance for the diagnosis. Using a morphological study of a liver biopsy, diffusely widespread pseudolobules surrounded by connective tissue septa are identified. In addition, they install morphological type cirrhosis and the degree of activity of the process.

Recognition of etiological forms of cirrhosis is based on medical history (alcoholism, viral hepatitis, etc.), features of the clinical picture, 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 diagnosing the etiological types of cirrhosis, the greatest difficulty is in distinguishing between primary and secondary biliary cirrhosis of the liver. Distinctive features first - the gradual onset of the disease with itching without pain and fever, late development jaundice, early-onset high alkaline phosphatase activity that does not correspond to the degree of hyperbilirubinemia, antibodies to the mitochondrial fraction and increased IgM content. In secondary biliary cirrhosis, along with the symptoms of cirrhosis, signs of the disease that served as its cause are found. Less common than with primary biliary cirrhosis, melasma, xanthomas and xanthelasmas, and osteoporosis are observed.

The diagnosis of liver cirrhosis with α-antitrypsin deficiency is made by determining the Pi phenotype using immunoelectrophoresis. Congestive cirrhosis that forms in terminal stage, occurs with persistent ascites, hepatosplenomegaly, but unlike other forms of cirrhosis, it is accompanied by severe shortness of breath, swelling of the neck 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, and liver amyloidosis. Due to the fact that cirrhosis develops gradually, a clear distinction between chronic active hepatitis and chronic active hepatitis is impossible in some cases. The transition of hepatitis to cirrhosis is indicated by the presence of signs of portal hypertension (varicose veins of the lower third of the esophagus). 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 architecture of the liver is preserved. Liver cancer is more common acute development illness, pronounced progressive course, exhaustion, fever, pain, leukocytosis, anemia, severe increased ESR. A pathognomonic sign of liver cancer is a positive Abelev-Tatarinov reaction - detection of a-fetoproteins (embryonic serum globulins).

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

Ed. prof. I.N. Bronovets

“Diagnosis of liver cirrhosis, diagnostic signs” article from the section