Symptoms of cirrhosis of the liver: from the initial to the last stage

Cirrhosis of the liver is more common in men. Symptoms of cirrhosis of the liver differ in the variety of manifestations.

According to research data, 60% of patients have pronounced symptoms, in 20% of patients cirrhosis of the liver is latent and is detected accidentally during a survey for another disease, in 20% of patients the diagnosis of cirrhosis is established only after death.

The main symptoms of cirrhosis are as follows:

• pain in the right side and right upper quadrant and epigastric region, intensifying after eating (especially after taking acute, fatty foods), physical activity. The pains are due to the enlargement of the liver and the dilatation of its capsule, concomitant chronic gastritis, chronic pancreatitis, cholecystitis, dyskinesia of bile ducts. With hyperkinetic dyskinesia of the biliary tract, pain in the right hypochondrium is characterized by colic, with hypokinetic dyskinesia they are usually non-intensive, pulling, often disturbing the feeling of heaviness in the right hypochondrium;
• nausea, sometimes vomiting (bloody vomiting is possible with bleeding from varicose veins of the esophagus and stomach);
• feeling of bitterness and dry mouth;
• itching of the skin (prihostestaz and accumulation of a large number of bile acids in the blood);
• fatigue, irritability;
• frequent loose stools (especially after eating fatty foods);
• bloating;
• weight loss;
• sexual weakness (in men), menstrual cycle (in women).

Survey of patients reveals the following characteristic symptoms of liver cirrhosis:

• weight loss, in severe cases, even exhaustion;
• pronounced muscular atrophy and a significant decrease in muscle tone and strength;
• lag in growth, physical and sexual development (if cirrhosis develops in childhood);
• dry, scaly yellow-pale skin. Intensive jaundice is observed in the final stage of cirrhosis of the liver, with biliary cirrhosis, as well as with the adherence of acute hepatitis. Jaundice first appears on sclera, the lower surface of the tongue, the sky, then on the face, palms, soles and, finally, all the skin is stained. Jaundice has different shades depending on the duration of its existence. At first the skin is orange-yellow, then it acquires a greenish-yellow color, a very prolonged jaundice causes skin coloring in a brownish-bronze color (for example, with primary biliary cirrhosis of the liver). Jaundice is caused by a violation of the ability of hepatocytes to metabolize bilirubin. In rare cases, with severe necrosis of the hepatic parenchyma, jaundice may be absent;
• xantelasms (yellow lipid spots in the upper eyelid) are more often detected with primary biliary cirrhosis;
• fingers in the form of tympanic sticks with flushing of the skin at the nail holes;
• swelling of the joints and adjacent bones (mainly with biliary cirrhosis - "biliary rheumatism");
• the expansion of the veins of the abdominal wall due to the difficulty of blood flow in the liver due to the development of pronounced fibrosis in it. The dilated veins of the anterior abdominal wall are collateral, roundabout ways for the outflow of blood. In severe cases, this collateral venous network resembles the head of a jellyfish ("caput medusae"). Sometimes (with the development of collaterals through the umbilical veins) there is a venous noise on the anterior abdominal wall. Especially pronounced noise in the navel with cirrhosis of the liver in combination with the nebulization of the umbilical vein (Cruevel-Baumgarten syndrome);

It is extremely important to identify when examining small signs of liver cirrhosis:

• appearance on the skin of the upper half of the trunk of "vascular asterisks" - telangiectasias in the form of spiders. It is characteristic that the "vascular asterisks" are never located below the navel, they are most pronounced with exacerbation of cirrhosis; during the period of remission, their reverse development is possible;
• Angiomas at the edge of the nose, in the corner of the eyes (they can bleed);
• erythema of the palms - bright red cowberry coloring of warm palms spilled or in the area of thenar or hypothenar, as well as in the area of the pads of the fingers ("liver palms", "hands of beer lovers") (Weber); rarely such erythema occurs on the soles of the feet;
• lacquered, edematous, uneducated tongue of cowberry-red;
• carmine-red coloration of the mucous membrane of the mouth and lips;
• gynecomastia in men;
• atrophy of genital organs;
• decrease in the severity of secondary sexual characteristics (decreased severity of hair in the armpits, in the pubic area).

The appearance of "small signs" of cirrhosis is explained by most authors by hyperestrogenemia (cirrhotically altered liver is poorly involved in the metabolism of estrogens), besides, the amplification of the peripheral conversion of androgens to estrogens is important;

• in the expressed cases of cirrhosis of the liver, the appearance of ascites is characteristic.

All the above symptoms cause an extremely characteristic type of patients with cirrhosis of the liver:

• emaciated face, unhealthy sub-bacterial skin color, bright lips, prominent cheekbones, erythema of the zygomatic area, widening of facial capillaries; muscular atrophy (limbs thin);
• enlarged abdomen (due to ascites);
• the expansion of the veins of the abdominal and thoracic walls, edema of the lower limbs;
• in many patients, the phenomena of hemorrhagic diathesis are revealed, caused by liver damage with impaired production of blood coagulation factors.

On the skin you can see hemorrhagic rashes of various types, often there are nosebleeds, as well as bleeding of other localizations (this is also promoted by the development of portal hypertension).

In the study of internal organs, there are pronounced functional and dystrophic changes. Distro raphy infarction is manifested palpitations, enlargement of the heart to the left border, deafness tone, shortness of breath, the ECG - ST decrease interval, T-wave variation (reduction, dvufaznost, in severe cases - inversion). Often a hyperkinetic type of hemodynamics is detected (an increase in the minute volume of blood, pulse pressure, fast, full pulse ).

[1], [2], [3], [4], [5], [6], [7]

Hepatorenal Syndrome

Large changes can undergo kidneys (hepatorenal syndrome). A peculiar disturbance of kidney function develops: preservation of functions of the renal epithelium and violation of the filtration function of the glomeruli without pronounced anatomical changes. Many people explain this by a violation of blood supply to the kidneys, an increase in blood flow through the medulla of the kidneys, and bypassing the glomerular capillaries, and the idea of a general increase in vascular resistance in the kidneys is also expressed.

In severe cases of renal dysfunction, kidney failure may develop. Its appearance can be accelerated by factors such as bleeding from the enlarged veins of the esophagus, stomach, repeated punctures in ascites, the use of diuretics, and intercurrent infections.

Symptoms of the hepatorenal syndrome have a number of peculiarities: the specific gravity of urine and its oscillations differ little from the norm, the protein is not always found in a small amount, the pathological sediment (erythrocytes, cylinders) is not always expressed. Most often, the partial functions of the kidneys change, in particular, the glomerular filtration decreases. In very severe cases, especially with severe hepatic insufficiency, blood pressure may rise , oliguria develop, azotemia develop, clinical signs of renal insufficiency. The development of azotemia in liver cirrhosis is considered as a sign of severe liver damage and a near fatal outcome.

Syndrome of hypersplenism

In many patients with cirrhosis of the liver, there is an increase in the spleen and hypersplenism, which manifests itself in the syndrome of pancytopenia (anemia, leukopenia, thrombocytopenia).

Symptoms of enlarged spleen are explained by venous stasis in it, pulp fibrosis, the appearance of a large number of arteriovenous shunts, proliferation of reticulohistiocytic cells. Syndrome of hypersplenism is caused by inhibition of bone marrow hemopoiesis, the formation of antibodies to the formed elements of the blood, increased destruction of erythrocytes in the spleen.

The hypersplenism syndrome is manifested not only by pancytopenia in the peripheral blood, but also by a decrease in the number of myeloid cells in the bone marrow.

Disturbance of the digestive system with cirrhosis of the liver

Often with cirrhosis, reflux esophagitis is determined . Its main symptoms are belching with air, stomach contents, heartburn, burning sensation behind the sternum. Reflux-esophagitis is caused by increased intra-abdominal pressure due to ascites and the transfer of contents from the stomach into the esophagus. Chronic esophagitis can be accompanied by erosion and ulceration of the mucous membrane of the lower third of the esophagus and the cardiac part of the stomach.

Very often symptoms develop liver cirrhosis a chronic gastritis and (usually superficial and hypertrophic). It manifests itself with blunt epigastric pains that appear after eating, nausea, a feeling of fullness and heaviness in the epigastric region, eructations, a decrease in appetite.

In 10-18% of patients with liver cirrhosis, symptoms of stomach ulcers and 12 duodenal ulcers are detected. A characteristic feature of these ulcers is the absence or weak severity of the pain syndrome. Often, these ulcers for the first time appear symptomatic of bleeding. One of the reasons for the development of ulcers is the high content of histamine in the blood. Histamine passes the liver in the development of porto-caval anastomoses and, therefore, is not rendered harmless in it. It stimulates excessive secretion of hydrochloric acid by the glands of the stomach, which contributes to the formation of ulcers. Also important is the hypergastrinemia, which is often observed with cirrhosis of the liver.

The defeat of the pancreas is manifested by symptoms of chronic pancreatitis with exocrine insufficiency, intestinal damage - symptoms of chronic enteritis with impaired absorption capacity ( malabsorption syndrome ).

[8], [9], [10], [11]

Disturbance of the endocrine system with cirrhosis of the liver

Great changes in cirrhosis of the liver undergoes the endocrine system:

• In 50% of patients, symptoms of a violation of carbohydrate metabolism in the form of reduced tolerance to carbohydrates are detected, which is accompanied by an increased content of insulin in the blood . These changes indicate a relative insulin insufficiency, which is caused by hyperproduction of the contrinsular hormones ( glucagon, somatotropin ) and a decrease in the sensitivity of peripheral tissues to insulin. In 10-12% of patients approximately 5-7 years after the appearance of obvious symptoms of cirrhosis the liver develops clinically expressed diabetes mellitus. It is possible that cirrhosis translates the genetic predisposition to diabetes mellitus into a clinically manifested form of the disease;
• mainly in decompensated liver cirrhosis, the functional state of the sexual glands in men is disrupted, which is manifested in a decrease in the content of testosterone in the blood , an increase in estrogens, proletin, globulin, which binds sex hormones. Hyperestrogenemia is caused by reduced degradation of estrogens in the liver, as well as increased peripheral conversion of androgens to estrogens. Clinically, these changes are manifested in hypogonadism (atrophy of the testes, penis, decrease in the expression of secondary sexual characteristics, sexual weakness), gynecomastia, feminization. In women, the pathology of the reproductive system is expressed in violation of the menstrual cycle; atrophy of the mammary glands, decreased sexual desire;
• the violation of the functional state of the adrenal glands is expressed in symptoms of hyperaldosteronism, which contributes to the development of ascites in patients with cirrhosis of the liver.

[12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22], [23]

The defeat of the central nervous system

The defeat of the central nervous system manifests itself as symptoms of toxic encephalopathy. It is characterized by asthenia, sleep disturbance (sleepiness during the day, sleeplessness at night), memory loss, headaches, paresthesias in hands and feet, trembling of fingers, apathy, indifference to others. The extreme manifestation of hepatic encephalopathy is the hepatic coma.

The liver is defined by an enlarged, dense, often bumpy, with a sharp edge. Significantly impaired the functional capacity of the liver, especially in late, final phases of the disease.

Hepatic cell insufficiency

The general condition of patients and the prognosis for cirrhosis of the liver is determined by the syndromes of hepatic-cell insufficiency and portal hypertension.

At the heart of hepatocellular hypertension is always damage to hepatocytes (dystrophy and necrosis) and the development of cytolytic, cholestatic, excretory-biliary syndromes.

Symptoms of hepatic-cellular hypertension:

• malnutrition syndrome (decreased appetite, nausea, intolerance to alcohol, tobacco, belching, flatulence, abdominal pain, stool disorders, thinning, dry flaky skin, manifestations of hypovitaminosis);
• fever due to autolysis processes in the liver and the entry into the blood of toxic products and pyrogenic steroid - etiocholanolone (its inactivation in the liver is disrupted);
• jaundice;
• skin changes small signs of cirrhosis);
• symptoms of endocrine changes.
• hepatic odor from the mouth (appears with severe hepatic insufficiency and resembles the sweetish smell of raw liver);
• hemorrhagic diathesis (due to a violation of the synthesis in the liver of clotting factors and thrombocytopenia).

Distinguish the following stages of hepatic-cell insufficiency:

The compensated (initial) stage is characterized by the following symptoms:

• the general condition is satisfactory;
• moderately severe pain in the liver and epigastrium, bitterness in the mouth, bloating;
• weight loss and jaundice;
• the liver is enlarged, dense, its surface is uneven, the edge is sharp;
• can be enlarged spleen;
• the indicators of the functional state of the liver have changed insignificantly;
• there are no clinically significant manifestations of hepatic insufficiency.

The subcompensated stage has the following symptoms:

• expressed subjective manifestations of the disease (weakness, pain in the right hypochondrium, flatulence, nausea, vomiting, bitter taste in the mouth, diarrhea, decreased appetite, nosebleeds, bleeding gums, itching, headaches, insomnia);
• decreased body weight;
• jaundice;
• "Small symptoms" of liver cirrhosis;
• hepatomegaly, splenomegaly;
• initial manifestations of hypersplenism: mild anemia, leukopenia, thrombocytopenia;
• changes in indicators of the functional capacity of the liver: the level of bilirubin in the blood was increased 2.5 times, alanine aminotransferase increased 1.5 to 2 times as compared with the norm, the thymol test was increased to 10 units, the albumin content in the blood was reduced to 40%, the sulem test to 1.4 ml .

The stage of severe decompensation (the last stage) is  characterized by the following symptoms and laboratory manifestations:

• severe weakness;
• significant weight loss;
• jaundice;
• itching;
• hemorrhagic syndrome;
• edema, ascites;
• hepatic odor from the mouth;
• symptoms of hepatic encephalopathy;
• changes in indicators of the functional capacity of the liver: blood levels of bilirubin increased by 3 or more times, alanine aminotransferase - more than 2-3 times compared with the norm; the level of prothrombin is less than 60%, the total protein is less than 65 g / l, albumin is below 40-30%, cholesterol is less than 2.9 μmol / l.

Syndrome of portal hypertension

The syndrome of portal hypertension is an important symptom of cirrhosis and consists in increasing the pressure in the portal of the portal vein.

Portal hypertension in liver cirrhosis occurs due to reduction of blood flow through sinusoids. This is due to the following factors:

• compression of small hepatic veins by sites of regenerating hepatocytes;
• Reduction of the final and larger branches of the portal vein and hepatic artery as a result of the inflammatory process in the liver;
• narrowing of the lumen of sinusoids by proliferating endothelial cells and inflammatory infiltrates. In connection with the reduction of blood flow, portal pressure begins to increase and anastomoses develop between the portal vein and the hollow veins.

The most important are the following port-caval anastomoses:

• in the cardiac part of the stomach and abdominal part of the esophagus, connecting the vessels of the portal and the superior vena cava via the unpaired vein system;
• upper hemorrhoidal veins with middle and lower hemorrhoidal veins, connecting the basins of the portal and lower hollow veins;
• between the branches of the portal vein and the veins of the anterior abdominal wall and diaphragm;
• between veins of the organs of the gastrointestinal tract, retroperitoneal and mediastinal veins, these anastomoses connect the gates and the inferior vena cava.

The greatest clinical importance is the anastomosis in the cardiac region of the stomach and esophagus, since at very high pressure they may experience severe bleeding, which can cause death.

With the increase in venous pressure in the portal vein is associated with the appearance of ascites.

The main symptoms of portal hypertension are:

• persistent dispeptic phenomena, especially after eating;
• bloating and a feeling of a full stomach after taking any food ("wind before rain");
• a feeling of constantly overcrowded intestines;
• progressive weight loss and signs of polyhypovitaminosis with sufficient nutrition;
• periodic diarrhea without pain and fever, after which the state of health improves;
• splenomegaly;
• ascites;
• oliguria;
• caput medusae;
• varicose veins of the esophagus and stomach, revealed by X-rays of the stomach and FEGS;
• gastric and hemorrhoidal hemorrhages;
• increased pressure in the splenic vein (recognized by splenoportometry). Characteristically, after bleeding, the pressure in the splenic vein decreases, and the spleen may contract.

Distinguish the following stages of portal hypertension:

The compensated stage is characterized by the following main symptoms:

• severe flatulence;
• frequent loose stool, after which the flatulence does not decrease;
• anterior wall of the abdominal wall;
• increased pressure in the portal and hepatic veins (determined by catheterization of these veins, the catheterization of the hepatic veins also allows you to judge the sinusoidal pressure);
• an increase in the diameter of the portal vein and a lack of expansion during inspiration (determined by ultrasound).

Initial decompensation of portal hypertension has the following symptoms:

• varicose veins of the lower third of the esophagus (determined by X-rays of the stomach and PEGS);
• often expressed hypersplenism;
• The remaining symptoms are the same as in the first stage.

Decompensated (complicated) stage of portal hypertension is characterized by significant hypersplenism; hemorrhagic syndrome; a pronounced expansion of the veins of the lower third of the esophagus and stomach and bleeding from them, edema and ascites; porto-caval encephalopathy.

Spontaneous bacterial peritonitis

In the case of decompensated liver cirrhosis in the presence of ascites, the development of spontaneous bacterial peritonitis is possible (in 2-4% of patients). The most frequent causative agent is E. Coli.

The main symptoms of spontaneous bacterial peritonitis:

• acute onset with fever, chills, abdominal pain;
• muscle tension of the anterior abdominal wall;
• weakening of intestinal peristaltic noise;
• lowering blood pressure;
• aggravation of the symptoms of hepatic encephalopathy, in severe cases - the development of hepatic coma;
• leukocytosis in peripheral blood with a shift to the left;
• intraperitoneal fluid is turbid, rich in cellular elements (more than 300 cells per mm2, neutrophilic leukocytes predominate among the cells); poor protein (less than 20 g / l); in most cases an infectious agent is released from the liquid;
• the mortality rate is 80-90%.

Mesenchymal-inflammatory syndrome (immune inflammation syndrome)

Mesenchymal-inflammatory syndrome (MVS) is an expression of the processes of sensitization of cells of the immunocompetent system and activation of RES. AIM determines the activity of the pathological process.

The main symptoms of AIM:

• increased body temperature;
• enlarged spleen;
• leukocytosis;
• acceleration of ESR;
• eosinophilia;
• an increase in thymol assay;
• reduction of the test sample
• hyper alpha-2 and y-globulinemia;
• hydroxyprolinuria;
• increased serotonin levels in platelets;
• the appearance of C-reactive protein;
• possible immunological manifestations: the appearance of antibodies to liver tissue, LE-cells, etc.

The course of cirrhosis of the liver

The course of cirrhosis of the liver is chronic, progressive, with exacerbations and remissions and is determined by the activity of the pathological process in the liver, the severity of hepatic-cell failure syndromes and portal hypertension. In the period of the active process, the symptoms of liver cirrhosis and the severity of hepatic insufficiency and portal hypertension are aggravated.

An important indicator of liver cirrhosis activity is the high intensity of the mesenchymal inflammatory process, it indicates the continuing progression of the pathological process. The active phase of liver cirrhosis is characterized by an increase in body temperature, hypergammaglobulinemia, hypoalbuminemia, increased ESR, Ig content of all classes, high blood levels of alanine and asparagine aminotransferases, sensitization of T-lymphocytes to a specific liver lipoprotein, confirming participation in the progression of the autoimmune mechanisms.

Depending on the severity of laboratory indicators, moderate and pronounced activity of liver cirrhosis is isolated.

Degrees of cirrhosis activity

Indicators of blood serum	Moderate degree of activity of liver cirrhosis	Severe activity of liver cirrhosis
A2-Globulins	Up to 13%	T more than 13%
Gamma globulins	Up to 27-30%	T more than 27-30%
Timole sample	Up to 8-9%	Tolshche 8-9 OD
ALT	In 1,5-2 times	3-4 times or more
Sulim sample	From 1.8 to 1.2 ml	Less than 1.2 ml

An active pathological process is also characterized by clinical symptoms: deterioration of health, pain in the liver, weight loss, jaundice, fever, the emergence of new stellate telangiectasias. The histologically active phase is manifested by the proliferation of Kupffer cells, inflammatory cell infiltration inside the hepatic lobules, the appearance of a large number of hepatocyte step necrosis, the increase of fibrogenesis.

The manifestations of the active phase of viral cirrhosis and chronic replicative hepatitis B are very similar and can be combined. In this regard, many hepatologists offer to allocate "cirrhosis of the liver with active hepatitis" or "chronic active hepatitis in the phase of cirrhosis of the liver." (HBV-XAG-cirrhosis). Some scientists believe that liver cirrhosis develops predominantly in chronic hepatitis B, induced by mutant strains lacking the ability to synthesize HBeAg.

With the long-term cirrhosis of the liver, there may be no signs of activity of the inflammatory process (the active process has already ended, according to the figurative expression of SN Sorinson, cirrhosis is "burned out"), and decompensation and indications of portal hypertension are pronounced.

Viral cirrhosis of the liver

Viral cirrhosis of the liver has the following clinical and laboratory features, which must be taken into account in its diagnosis.

1. The most common viral liver cirrhosis is observed in young and middle age, and more often in men.
2. It is possible to establish a clear link between the development of liver cirrhosis and acute viral hepatitis. There are two variants of viral cirrhosis of the liver: early, developing during the first year after acute hepatitis B, and late, developing during a long latent period. Hepatitis D and C viruses have expressed cirrhotic properties. Chronic hepatitis caused by these viruses is often transformed into cirrhosis of the liver. Chronic hepatitis C can persistently proceed clinically rather benignly and nevertheless naturally leads to the development of cirrhosis of the liver.
3. Viral cirrhosis of the liver is most often macronodular.
4. Symptoms of cirrhosis of the liver resemble the acute phase of viral hepatitis and also manifested pronounced asthenovegetative, dyspeptic syndromes, jaundice, fever.
5. Functional liver failure with viral form of cirrhosis appears early enough (usually during periods of exacerbation of the disease).
6. In the stage of the formed cirrhosis of the liver, varicose veins of the esophagus and stomach, hemorrhagic syndrome in the viral etiology of cirrhosis are observed more often than with alcoholic cirrhosis.
7. Ascites with viral cirrhosis of the liver appears much later and is observed less often than in the alcoholic.
8. The indices of thymol test in viral cirrhosis reach the highest values in comparison with alcoholic cirrhosis of the liver.
9. Viral cirrhosis is characterized by the detection of serological markers of viral infection.

Alcoholic cirrhosis of the liver

Alcoholic cirrhosis of the liver develops in 1/3 of persons suffering from alcoholism, in terms of 5 to 20 years. Characteristic for alcoholic cirrhosis of the liver are the following clinical and laboratory features:

1. Anamnestic indications of long-term alcohol abuse (however, most patients, as a rule, hide this).
2. A characteristic "image of an alcoholic": a puffy face with reddened skin, small telangiectasias, a crimson nose; tremor of hands, eyelids, lips, tongue; edematic cyanotic eyelids; slightly bulging eyes with injected sclera; euphoric manner of behavior; swelling in the parotid glands.
3. Other manifestations of chronic alcoholism (peripheral polyneuropathy, encephalopathy, myocardial dystrophy, pancreatitis, gastritis).
4. Severe dyspeptic syndrome (loss of appetite, nausea, vomiting, diarrhea) in the developed stage of alcoholic cirrhosis due to concomitant alcoholic gastritis and pancreatitis.
5. Telangiectasias and Dupuytren's contracture (in the area of the palm tendons), as well as testicular atrophy, hair loss are more characteristic of alcoholic cirrhosis than in other etiologic forms of cirrhosis.
6. Portal hypertension (including one of its most important manifestations - ascites) develops much earlier than with viral cirrhosis of the liver.
7. The spleen increases significantly later than with viral cirrhosis, in a significant number of patients splenomegaly is absent even in the advanced stage of the disease.
8. Leukocytosis (up to 10-12x10 ⁷ l) with a stab shift, sometimes until the appearance of myelocytes and promyelocytes (leukemoid reaction of the myeloid type), anemia, an increase in ESR. The causes of anemia are the blood loss caused by erosive gastritis, the toxic effect of alcohol on the bone marrow; infringement of absorption and an alimentary deficiency of folic acid (it can cause megaloblastide type of a hemopoiesis); impaired metabolism of pyrvdoxin and insufficiency of heme synthesis (this causes the development of sidero-anhrestonic anemia); sometimes hemolysis of red blood cells.
9. Characterized by a high content of IgA in blood, as well as an increase in blood activity of y-glutamyltranspeptidase - 1.5-2 times (normal for men 15-106 ED / l, for women - 10-66 VD / L).

A high blood level of y-glutamyltranspeptidase usually indicates long-term alcohol abuse, alcoholic liver damage and many authors are considered as a biochemical marker of alcoholism. The test can be used to screen alcoholics and control during abstinence (only after 3 weeks of stopping alcohol intake enzyme activity is reduced by half). However, it should be borne in mind that the activity of y-glutamyltranspeptidase can be increased in diabetes mellitus, myocardial infarction, uremia, pancreatic tumors, pancreatitis, cytotoxic drugs, anti-epidemic drugs, barbiturates, and indirect anticoagulants. In chronic alcoholism, the blood content of acetaldehyde (a product of alcohol metabolism, more toxic than alcohol itself) is increased, and urinary excretion of salsolin (an acetaldehyde and dopamine condensation product) is increased. Often with alcoholic cirrhosis, the blood content of uric acid is increased.

10. In hepatic biopsy specimens the following symptoms are revealed:

• Mallory's body (accumulation of alcoholic galin in the hepatic lobule);
• accumulation of neutrophilic leukocytes around hepatocytes;
• fatty degeneration of hepatocytes; pericellular fibrosis;
• relative safety of portal tracts.

11. The cessation of alcohol consumption leads to remission or stabilization of the pathological process in the liver. With continued use of alcohol, cirrhosis progresses steadily.

[24], [25], [26], [27], [28], [29], [30]

"Stagnant liver" and cardiac cirrhosis of the liver

Stagnant liver - liver damage caused by stagnation of blood in it due to high pressure in the right atrium. Stagnant liver is one of the main symptoms of congestive heart failure.

The most common causes are mitral heart defects, tricuspid valve insufficiency, chronic pulmonary heart, constrictive pericarditis, right atrial myxoma, myocardiosclerosis of various genesis. The main mechanisms for the development of "stagnant liver" are:

• blood overflow of the central veins, the central part of the hepatic lobules (development of central portal hypertension);
• development of local central hypoxia in the liver lobules;
• dystrophic, atrophic changes and necrosis of hepatocytes;
• active synthesis of collagen, development of fibrosis.

With the progression of stagnant phenomena in the liver, the connective tissue develops further, connective tissue strands connect the central veins of neighboring lobules, the hepatic architecture of the liver is broken, cardiac cirrhosis of the liver develops.

The characteristic symptoms of liver cirrhosis in a "stagnant liver" are:

• hepatomegaly, the surface of the liver is smooth. In the initial stage of circulatory insufficiency the consistency of the liver is soft, its edge is rounded, later the liver becomes dense, and its edge is sharp;
• pain of the liver during palpation;
• a positive Plesche symptom or a hepatouhygular "reflex" - pressing on the area of an enlarged liver strengthens the swelling of the cervical veins;
• variability of liver size depending on the state of central hemodynamics and the effectiveness of treatment (positive results of treatment of congestive heart failure are accompanied by a decrease in liver size);
• slight severity of jaundice and its decrease or even disappearance with successful therapy of congestive heart failure.

In severe form of congestive heart failure, edematous-ascitic syndrome develops, in this case there is a need for differential diagnosis with cirrhosis of the liver with ascites.

With the development of cardiac cirrhosis, the liver becomes dense, its edge sharp, its dimensions remain constant and do not depend on the effectiveness of treatment of heart failure. When diagnosing cardiac cirrhosis, the main disease that caused heart failure, the absence of signs of chronic alcohol abuse and markers of the viral infection are taken into account.

Assessment of the severity of liver cirrhosis

Clinical evaluation of the stage and severity of liver cirrhosis is based on the severity of portal hypertension and hepatic-cell insufficiency. The degree of severity of liver cirrhosis can also be assessed using the Child-Pugh diagnostic complex, which includes an evaluation of the serum levels of bilirubin, albumin, prothrombin, and the severity of hepatic encephalopathy and ascites.

The severity of liver cirrhosis by Child-Pugh is highly correlated with the survival rates of patients and the results of liver transplantation, the lifespan of patients belonging to class A is on average 6-7 years, to class C - 2 months.

The most important task of clinical and laboratory examination of a patient is the timely recognition of complications of cirrhosis of the liver.

The most important complications of cirrhosis:

• encephalopathy with the development of hepatic coma;
• profuse bleeding from varicose veins of the esophagus and stomach;
• bleeding from a varicose dilated lower hemorrhoidal vein;
• thrombosis of the portal vein;
• attachment of a secondary bacterial infection (pneumonia, sepsis, peritonitis);
• progressive hepatic-renal failure);
• transformation of cirrhosis of the liver into cirrhosis.

[31], [32], [33], [34], [35], [36], [37]