Cirrhosis of the liver


Liver cirrhosis is a common process characterized by fibrosis and abnormal liver structure due to the replacement of liver cells with connective tissue cells. Cirrhosis is accompanied by a transformation of the normal structure of the liver, leads to the formation of nodes and is the final stage of a number of chronic liver diseases. Replacement of liver cells with connective tissue cells leads to the development of liver failure.

In patients with cirrhosis of the liver, a variety of symptoms can be recorded, which depend on the etiology, stage of the disease and the activity of the process. Approximately 20% of patients have cirrhosis latently or under the guise of another gastroenterological disease. In 20% of cases, liver cirrhosis is detected only on histological examination.

In the initial stage, as a rule, it proceeds with minimal symptoms. The patient has moderate pain in the right hypochondrium and “under the spoon”, “causeless” nosebleeds, transient jaundice of the sclera and skin. Periodic there is a slight itching of the skin, low-grade fever, weakness, insomnia, decreased appetite. Intestinal upset, bitter taste in the mouth, heartburn, nausea, and fat and alcohol intolerance may also occur. An objective examination can determine an increase in the size of the liver. Characteristic “liver” stars are formed on the skin, palms turn red.

In the stage of pronounced clinical manifestations, all of the listed symptoms increase. Additionally, gastrointestinal disorders appear, weight loss – sometimes bloody vomiting, anemia (decrease in hemoglobin and red blood cells), hepatolienal syndrome with symptoms of hypersplenism (enlargement of the spleen) or without them, persistent flatulence (abdominal distension).

In the terminal stage, a progressive weight loss of the patient is observed, up to cachexia (extreme exhaustion), the phenomenon of encephalopathy (disruption of the brain), ascites appears and progressively nars , up to the development of anasarca (generalized edema of the whole body), bleeding increases and becomes life-threatening (from varicose veins of the esophagus and stomach), a skin hemorrhagic rash appears (small punctate hemorrhages), in men gynecomastia develops (an increase in the size of the mammary glands).


Liver cirrhosis is classified according to:

  • Morphological structure.
  • Etiological factor.
  • Stages of liver failure.
  • The degree of portal hypertension (increased pressure in the intrahepatic vein) and the activity of the process.

There are the following stages of liver failure:

  • The compensated (initial) stage is characterized by the following symptoms: moderate pain in the liver and epigastrium , bitterness in the mouth, bloating; weight loss and no jaundice; the liver is enlarged, dense, its surface is uneven, the edge is sharp; the spleen may be enlarged.
  • Subcompensated stage: severe subjective manifestations of the disease (weakness, pain in the right hypochondrium, flatulence, nausea, vomiting, bitterness in the mouth, diarrhea, decreased appetite, bleeding gums, itching, headaches, insomnia), weight loss, jaundice, hepatomegaly , splenomegaly, moderate anemia, leukopenia, thrombocytopenia, the level of bilirubin in the blood is increased 2.5 times, ALT is 1.5-2 times higher than the norm, the albumin level in the blood is reduced to 40%.
  • Stage of severe decompensation: weakness, significant drop in body weight, jaundice, pruritus, hemorrhagic syndrome, edema, ascites, hepatic odor from the mouth, symptoms of hepatic encephalopathy, changes in indicators of the functional ability of the liver: the content of bilirubin in the blood is increased by 3 or more times, ALT – more than 2-3 times compared to the norm; the level of prothrombin is less than 60%, total protein is less than 65 g / l, albumin is less than 40-30%, cholesterol is less than 2.9 μmol / l.

The reasons

The main reasons for the development of liver cirrhosis in 50% of patients are considered to be a combination of several factors:

  • Medicines and toxins that lead to the development of fulminant (fulminant) hepatic failure: alcohol, methotrexate, isoniazid, vitamin A, amiodarone, perhexiline , α- methyldopa , oxyphenisatin , halothane , paracetamol, erythromycin, chlorpromazine.
  • Infectious diseases (parasitic and infectious diseases): chronic hepatitis B, C, D, brucellosis (systemic bacterial infection), echinococcosis, opisthorchiasis (helminthiasis), toxoplasmosis).
  • Autoimmune diseases: autoimmune hepatitis (type 1 and 2).
  • Vascular diseases: chronic venous congestion, hereditary hemorrhagic telangiectasia ( Randu-Osler disease ).
  • Metabolic and genetic disorders: Wilson-Konovalov disease, hereditary hemochromatosis , deficiency of alpha-1-antitrypsin, impaired carbohydrate metabolism (glycogenosis I, II, IV types), impaired lipid metabolism, impaired urea metabolism, porphyria, impaired amino acid metabolism, impaired bile metabolism acids.
  • Biliary obstruction (diseases of the hepatobiliary system: primary biliary cirrhosis, secondary biliary cirrhosis (in the outcome of primary sclerosing cholangitis, cystic fibrosis, biliary atresia / neonatal hepatitis, congenital biliary cysts).
  • Syndrome , Budd-Chiari syndrome : hepatic vein thrombosis occurring at the level of the confluence of the inferior vena cava with impaired blood outflow from the liver (cirrhosis develops due to the progressive narrowing or closing the hepatic vein).
  • Liver cirrhosis of unclear etiology (idiopathic, cryptogenic): the frequency may be 20-30% (more often found in women).

Most often, liver cirrhosis develops as an outcome of chronic hepatitis B, chronic hepatitis C, chronic hepatitis D and as a result of alcoholic liver disease.


Diagnosis of liver cirrhosis is carried out by a gastroenterologist or hepatologist on the basis of anamnesis, clinical examination, collection of complaints, the use of laboratory and instrumental examination methods. Diagnostics is aimed at determining the degree of liver damage, assessing the severity of the condition and emerging complications.

The diagnosis of liver cirrhosis at the initial stage is difficult, since the development of cirrhosis occurs gradually and at the beginning of the expressed symptoms may not be. An important biochemical sign of the transition of hepatitis to cirrhosis is a drop in the activity of transaminases after a long period of their increase, which reflects the death of most of the hepatocytes . For the same reason, there is a decrease in the level of albumin in the blood. Such patients are diagnosed with liver ultrasound, CT and MPT. A puncture liver biopsy is performed to confirm the diagnosis.

From the anamnesis, one can find out the presence of viral hepatitis B, C and D, alcohol abuse, the presence of hereditary diseases ( hemochromatosis , Wilson-Konovalov disease, cystic fibrosis, alpha-1-antitrypsin deficiency, galactosemia , glycogenosis), the presence of heart failure, contact with industrial poisons in production, long-term use of a number of drugs (methotrexate, isoniazid, etc.).

An objective examination reveals symptoms characteristic of liver diseases – “liver signs”, ascites, palmar erythema, jaundice of the skin (jaundice of a bright color with a dirty gray tinge), encephalopathy, venous collaterals on the anterior abdominal wall. Varicose veins of the esophagus, cardia of the stomach, rectum are found in 90% of patients with cirrhosis.

The patient loses weight and loses weight by reducing adipose tissue and muscle atrophy. There is a deformation of the terminal phalanges of the fingers like “drumsticks”, nails like “watch glasses”, trophic disorders appear, an increase in the size of the liver and spleen. “Medusa’s head” (dilated vessels in the abdomen) and umbilical hernia appear in the presence of portal hypertension.

When more than 1.5 liters of fluid accumulate in the abdominal cavity, a dull sound is determined by percussion over the place of accumulation. With tense ascites, palpation of internal organs is difficult, the liver and spleen can run (fail). In the later stages of cirrhosis of the liver in men, gynecomastia and testicular atrophy (decrease in the testicles), female-pattern hairiness are observed .

In the clinical analysis of blood, signs of anemia, leukocytopenia and thrombocytopenia are found. When examining a coagulogram, a decrease in the prothrombin index is found.

In a biochemical blood test, an increase in the activity of transaminases – AST and ALT (by 1.5 – 3 times, depending on the degree of decompensation, normal indicators are possible) is determined to a significantly lesser extent than in viral hepatitis, an increase in the activity of alkaline phosphatase is determined. An increase in the content of bilirubin (total and direct fraction), a decrease in the content of urea, creatinine, sodium and albumin are recorded.

Biochemical indicators of an unfavorable prognosis are: bilirubin more than 300 μmol / l, albumin less than 20 g / l, prothrombin index more than 60%.

To find out a possible etiological factor in the development of cirrhosis, serological and PCR diagnostics of viral hepatitis B, C and delta are carried out. Determination of alpha- fetoprotein in serum is prescribed to diagnose the possible development of liver cancer.

To assess the severity of liver fibrosis may conduct noninvasive biochemical tests that are alternative to histological examination of liver tissue: FibroTest ( FibroTest ) and FibroMaks .

With the development of spontaneous bacterial peritonitis, a study of ascitic fluid is performed. Neutrophilia and positive bacterial culture are recorded .

To detect bacterial infection in liver cirrhosis, the content of C-reactive protein and procalcitonin is determined .

Confirmation of the diagnosis and the possibility of establishing the causes of the development of cirrhosis is carried out with a histological study of liver tissue obtained during its biopsy.

The main methods of instrumental diagnostics of liver cirrhosis include ultrasound of the liver, spleen, biliary tract, CT and MRI studies. Esophagogastroduodenofibroscopy is recognized as the standard for diagnosing esophageal varicose veins and predicting the risk of bleeding. Also, dopplerographic examination of the vessels of the liver and spleen, radionuclide scanning of the liver, and indirect elastography of the liver are prescribed .

The main laboratory tests used:

  • Clinical blood test: hemoglobin, erythrocytes, platelets and leukocytes are reduced;
  • Biochemical blood test (liver function tests): ALT – an increase in activity, AST – an increase in activity, alkaline phosphatase – an increase in activity, creatinine, urea, albumin, sodium, cholesterol – a decrease.
  • Coagulogram: prothrombin time – increase.
  • Antibodies to mitochondria (AMA-M2) – primary biliary cirrhosis.
  • Antibodies Sp100, PML, gp210 – primary biliary cirrhosis).
  • FibroTest ( FibroTest ) and FibroMaks – evaluation of the degree of severity of hepatic fibrosis.
  • Diagnostics of viral hepatitis (B, C, D) – serological tests, PCR diagnostics (anti-HCV; PCR RNA Hepatitis C virus; HBsAg surface antigen of hepatitis B virus; HBe- antigen of hepatitis B virus; PCR-hepatitis D, anti-HDV ).
  • Study of ascitic fluid: neutrophilia , bacterial culture – positive, with the development of spontaneous bacterial peritonitis.
  • Histological examination of liver biopsy material.

Additional laboratory tests used:

  • Alpha- fetoprotein (AFP) – diagnostics of liver cancer or hepatocellular carcinoma.
  • C-reactive protein.
  • Procalcitonin .
  • Serum iron.
  • Ceruloplasmin .
  • Serum immunoglobulins – IgG , IgA , IgM .

The main instrumental studies used:

  • CT or MRI of the abdominal organs with intravenous contrast enhancement.
  • Ultrasound of the pelvic organs (liver, spleen, pancreas, bile ducts, kidneys).
  • Esophagogastroduodenoscopy .

Additional instrumental studies used

  • Doppler study of the vessels of the liver and spleen;
  • Radionuclide liver scan;
  • Indirect liver elastography .


With cirrhosis, there are no radical treatments. Therapy is symptomatic, and therefore the choice of drugs depends entirely on the clinical manifestations of the disease. Definitely, it is necessary to exclude the influence of factors destroying the liver.

Prescribe hepatoprotective drugs ( silymarin , ademetionine ). If the liver stops performing its cleansing function, periodic plasmapheresis is prescribed . Nitrosorbide is prescribed to reduce portal pressure . With the development of edematous syndrome, diuretics are prescribed. If autoimmune disorders are identified, glucocorticoid drugs are prescribed. With a decrease in blood protein, anabolic steroids, albumin are prescribed. With severe edema, the intake of fluid is limited, salt is excluded, and diuretics are given.

It is important to follow a diet: refusal of fatty, fried foods, alcoholic drinks. In the case of the development of ascites, it is necessary to reduce or completely eliminate salt intake.

The average life expectancy with developed decompensated cirrhosis of the liver, as a rule, is no more than 3 years.

In some cases, liver transplantation is performed.


The prognosis of the life of patients with liver cirrhosis largely depends on the development of its complications, among which the most important are hepatic encephalopathy, bleeding from varicose veins of the esophagus and stomach, ascites (with or without infection of ascitic fluid), hepatolienal syndrome, hyponatremia (decrease in sodium in the blood), infectious complications.

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