Cytolysis treatment. Cytolysis (cytolysis syndrome). Lipid metabolism disorder

M. G. Ipatova 1, 2 To. m. n., YU. G. Mukhina 1 d. m. n. Professor, P. IN. Shumilov 1 d. m. n., Professor

1 RussianNationalresearchmedicaluniversitythem. N. AND. Pirogov
MOHRF, Moscow

2 Children'sUrbanClinicalHospital№ 13 them. N. F. Filatova, Moscow

Key words : liver, syndrome cytolysis, alanine aminotransferase, aspartate amino- transferase, hepatoprotective drugs

The article describes biochemical laboratory parameters and their clinical significance in liver diseases occurring with cytolysis syndrome. Special attention is paid to the mechanisms of action of hepatoprotective drugs used for cytolytic syndrome.

Rice. 1. The role of the liver in metabolism.

Abbreviations: HDL - high density lipoproteins; VLDL - very low density lipoproteins; RESreticuloendothelial system; NAD - nicotinamide adenine dinucleotide; FAD - flavin adenine dinucleotide.

The liver is the central organ of chemical homeostasis in the body, where a single metabolic and energy pool is created for the metabolism of almost all classes of substances. The main functions of the liver include: metabolic, storage, barrier, excretory, homeostatic and detoxifying. The liver can neutralize both foreign exogenous substances that have toxic properties and those synthesized endogenously.

Table 2. Causespromotionlevelaminotransferases

Hepaticcauses

Extrahepaticcauses

Viral hepatitis (B, C, CMV, etc.)

Non-alcoholic steatohepatitis

Autoimmune liver diseases

Alcohol abuse

Taking medications
(statins, some antibiotics, antifungals, nonsteroidal
anti-inflammatory drugs,
glucocorticosteroids, others)

Metabolic liver diseases
(galactosemia, fructosemia, glycogenosis,
alpha1-antitrypsin deficiency,
aminoacidopathy, urea cycle disorder, fatty acid oxidation disorder, mitochondrial hepatopathy, some lysosomal diseases (disease
Gaucher disease, Niemann-Pick disease, acid lipase deficiency, etc.), cystic fibrosis, Shwachman-Diamond syndrome, hemochromatosis, Wilson's disease, etc.)

congenital and acquired defects
vessels of the portal vein system (disease
Badda-Chiari, etc.)

Cirrhosis of the liver

Liver tumors

Heart pathology (acute myocardial infarction)
myocardium, myocarditis)

Hereditary muscle disorders
metabolism

Acquired muscle diseases

Trauma and muscle necrosis

Celiac disease

Hyperthyroidism

Severe burns

Hemolysis of red blood cells

Acid-base imbalance

Sepsis

Located between the portal and systemic circulation, the liver acts as a large biofilter. More than 70% of the blood enters it through the portal vein, the rest of the blood enters through the hepatic artery. Most of the substances absorbed in the digestive tract (except for lipids, the transport of which is mainly carried out through the lymphatic system) enters the liver through the portal vein. Thus, the liver functions as the primary regulator of the content of substances in the blood that enter the body with food (Figure 1).

The wide variety of functions of hepatocytes leads to the fact that in pathological conditions of the liver, biochemical constants are disrupted, reflecting changes in many types of metabolism. Therefore, a standard biochemical blood test includes the determination of various parameters that reflect the state of protein, carbohydrate, lipid and mineral metabolism, as well as the activity of some key enzymes.

The concentration of enzymes in cells is much higher than in blood plasma; Normally, only a very small part is detected in the blood. The most common causes of increased enzyme levels in the blood serum are: direct damage to cell membranes, in particular viruses and chemical compounds, hypoxia and tissue ischemia. Sometimes enzyme activity increases as a result of their increased synthesis in tissues. Determining the activity of certain enzymes in blood serum allows one to judge the nature and depth of damage to various components of hepatocytes.

Enzymes, depending on their location, can be divided into several groups:

1) universally distributed enzymes, the activity of which is found not only in the liver, but also in other organs - amino transferases, fructose-1-6-diphosphate aldolase;

2) liver-specific (organ-specific) enzymes; their activity is exclusively or most highly detected in the liver. These include cholinesterase, ornithine carbamyltransferase, sorbitol dehydrogenase, etc.;

3) cell-specific liver enzymes are attributed predominantly to hepatocytes,
Kupffer cells or bile canaliculi (5-nucleotidase, adenosine triphosphatase);

4) organelle-specific enzymes are markers of certain organelles
hepatocyte: mitochondrial (glutamate dehydrogenase, succinate dehydrogenase, cytochrome oxidase), lysosomal (acid phosphatase, deoxyribonuclease, ribonuclease), microsomal (glucose-6-phosphatase).

The specificity of the enzymes and their diagnostic value are presented in Table 1.

Based on the above, it follows that in most cases, deviations in serum enzyme activity from the “norm” are nonspecific and can be caused by various reasons. Therefore, one must be very careful when interpreting these deviations, comparing them with the clinical picture of the disease and data from other laboratory and instrumental research methods.

In connection with the use in clinical laboratories of different methods for studying enzymes and units of measurement of their activity, it is advisable each time, having received the results of the analysis, to clarify by what method and in what units the enzyme activity was measured, and compare the obtained value with the “norm” adopted in this laboratory .

A special place is occupied by macroenzymemia - a rare and extremely difficult condition for differential diagnosis, in which the molecules of one or another enzyme are complexed with immunoglobulins or non-protein substances. Clinical observations of macro-CPK-emia, macro-LDH-emia, macro-AST-emia, macro-GGT-emia, macroamylasemia are described. Macroenzymemia is difficult to diagnose and differentially diagnose and leads to invasive examination methods and unnecessary treatment.

The detection of macroenzymemia is based on identifying the differences between the macroenzyme molecule and the ordinary enzyme molecule. Some of these methods are direct, that is, those that directly determine the presence in the blood of an enzyme complex that has a much higher molecular weight than a normal enzyme molecule. The direct method is based on the separation of whey proteins by molecular weight. Other methods are indirect, since the detection of a macroenzyme in the blood is not carried out by identifying the enzyme complex itself, but is based on identifying any of the properties of the macroenzyme. Direct tests have greater diagnostic value and involve fewer technical and diagnostic errors.

In some situations, the increase in enzymes is physiological: the level of alkaline phosphatase is increased in adolescents during the period of traction (period of accelerated growth), in healthy women during the third trimester of pregnancy (due to the placenta). However, very high alkaline phosphatase activity is observed in women with preeclampsia, which is associated with impaired blood circulation in the placenta.

In case of liver pathology, a biochemical blood test identifies 4 syndromes:

Cytolysis syndrome

Cholestasis syndrome

Hepatocellular failure syndrome

Mesenchial-inflammatory syndrome.
In this article we will look in detail at
indicators characteristic of cytolysis syndrome.

Cytolysis syndrome is a syndrome caused by impaired permeability of cell membranes, disintegration of membrane structures or necrosis of hepatocytes with the release of enzymes (ALT, AST, LDH, aldolase, etc.) into the plasma.

AMINOTRANSFERASES:aspartate aminotransferase and alanine aminotransferase

Reference values: for newborns up to 1 month. – less than 80 U/l; from 2 months up to 12 months - less than 70 U/l, from 1 year to 14 years - less than 45 U/l, in women - less than 35 U/l, in men -less than 50 U/l.

In clinical practice, simultaneous determination of the level of two transaminases - aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in blood serum is widely used.

The enzymes ALT and AST are found in almost all cells of the human body. However, the highest level of the ALT enzyme is found in the liver, so the level of this enzyme serves as a specific marker of liver damage. In turn, AST, in addition to the liver (in order of decreasing concentration), is found in cardiac and skeletal muscles, kidneys, pancreas, lungs, leukocytes and red blood cells.

In the liver, ALT is present only in the cytoplasm of hepatocytes, and AST is present in the cytoplasm and mitochondria. More than 80% of hepatic AST is represented by the mitochondrial fraction.

Normally, the constancy of the concentration of trans-aminases in the blood plasma reflects the balance between their release due to physiological apoptosis of aged hepatocytes and elimination. The ratio of AST/ALT synthesis in the liver is 2.5/1. However, during normal hepatocyte turnover, the levels of AST and ALT in the blood plasma are almost the same (30–40 U/L) due to the shorter half-life of AST (18 hours versus 36 hours for ALT).

In liver diseases, ALT activity increases first and most significantly compared to AST. For example, in acute hepatitis, regardless of its etiology, the activity of aminotransferases increases in all patients, but the level of ALT contained in the cytoplasm predominates due to its rapid exit from the cell and entry into the bloodstream. Thus, the biochemical activity of liver disease is judged by the level of ALT. An increase of 1.5–5 times from the upper limit of normal indicates low activity of the process, 6–10 times – moderate and more than 10 times – high biochemical activity. Increased transaminase activity for more than 6 months is a biochemical sign of chronic hepatitis.

Some drugs (for example, valproic acid) are metabolized in the mitochondria of hepatocytes, so only an isolated increase in AST may be an early laboratory marker of hepatotoxicity.

In addition to liver pathology, AST serves as one of the early markers of damage to the heart muscle (increases in 93–98% of patients with myocardial infarction to 2–20 norms); its specificity is not high. The level of AST in the blood serum increases 6–8 hours after the onset of a painful attack, the peak occurs at 18–24 hours, and activity decreases to normal values on days 4–5. An increase in enzyme activity over time may indicate an expansion of the focus of necrosis and the involvement of other organs and tissues, for example, the liver, in the pathological process.

Intense and excessive muscle exercise may also cause a transient increase in serum AST levels. Myopathies, dermatomyositis and other diseases of muscle tissue cause an increase in transaminases, mainly due to AST.

A moderate increase in AST activity (2–5 times the upper limit of normal) is observed in acute pancreatitis and hemolytic anemia.

In latent forms of liver cirrhosis, increases in enzyme activity are usually not observed. In active forms of cirrhosis, a persistent slight increase in aminotransferases is detected in 74–77% of cases, and, as a rule, the activity of AST prevails over ALT by two or more times.

A decrease in the activity of ALT and AST occurs with pyridoxine (vitamin B6) deficiency, with renal failure, and pregnancy.

Below are hepatic and extrahepatic causes of increased aminotransferase activity in the blood serum (Table 2).

In addition to assessing transaminase levels, the de Ritis coefficient, the ratio of AST to ALT (AST/ALT), is widely used in clinical practice. Normally, the value of this coefficient is 0.8–1.33. It should be noted that calculating the de Ritis coefficient is advisable only when AST and/or ALT exceed the reference values.

In newborns, the AST/ALT ratio usually exceeds 3.0, but by the fifth day of life it decreases to 2.0 or lower.

With liver damage with destruction of hepatocytes, ALT predominantly increases, the de Ritis coefficient decreases to 0.2–0.5. In cardiac pathology, the AST level predominates, and the de Ritis coefficient increases. However, this coefficient is not suitable for accurate differential diagnosis, since often with alcoholic liver damage, non-alcoholic steatohepatitis, and liver cirrhosis, an increase in AST also predominates and the de Ritis coefficient is 2.0–4.0 or more. The value of this coefficient above normal is often observed in obstructive jaundice, cholecystitis, when the absolute values of ALT and AST are small.

Thus:

1. In acute viral and chronic hepatitis, especially in the early stages, ALT activity is higher than AST (de Ritis coefficient less than 1.0). Severe damage to the liver parenchyma may change this ratio.

2. In alcoholic hepatitis and cirrhosis, AST activity is often higher than ALT (de Ritis coefficient is more than 1.0).

3. In acute MI, AST activity is higher than ALT (de Ritis coefficient greater than 1.5).

LACTATE DEHYDROGENASE

Reference LDH values for newbornsdaily - up to 600 U/l, in children from 1 year to 12 yearsLDH activity – 115 – 300 U/l, for children over 12 years of age and in adults the LDH norm is up to230 U/l.

Lactate dehydrogenase (LDH)– a glycolytic zinc-containing enzyme that reversibly catalyzes the oxidation of L-lactate to pyruvate, widely distributed in the human body. The highest LDH activity is found in the kidneys, cardiac muscle, skeletal muscle and liver. LDH is contained not only in serum, but also in significant quantities in red blood cells, so the serum for research must be free of traces of hemolysis.

With electrophoresis or chromatography, it is possible to detect 5 isoenzymes of LDH, differing in their physicochemical properties. The two isoenzymes that are most important are LDH1 and LDH5. The LDH1 fraction more actively catalyzes the reverse reaction of converting lactate into pyruvate. It is mostly localized in the heart muscle and some other tissues that normally function under aerobic conditions. In this regard, myocardial cells, which have a rich mitochondrial system, oxidize in the tricarboxylic acid cycle not only pyruvate, which is formed as a result of the glycolysis process occurring in them, but also lactate, which is formed in other tissues. The LDH5 fraction more effectively catalyzes the direct reaction of pyruvate reduction to lactate. It is localized mainly in the liver and skeletal muscles. The latter are often forced to function in anaerobic conditions (with significant physical exertion and rapid fatigue). The resulting lactate enters the bloodstream into the liver, where it is used for the process of gluconeogenesis (resynthesis of glucose), as well as into the heart and other tissues, where it is converted into pyruvate and involved in the tricarboxylic acid cycle (Krebs cycle). Any damage to tissue cells containing large amounts of LDH (heart, skeletal muscle, liver, red blood cells) leads to an increase in the activity of LDH and its isoenzymes in the blood serum. The most common causes of increased LDH activity are:

1. Heart damage (acute myocardial infarction, myocarditis, congestive heart failure); in these cases, an increase in the activity of LDH1 and/or LDH2 usually predominates.

2. Liver damage (acute and chronic hepatitis, liver cirrhosis, tumors and liver metastases), when the isoenzyme LDH5, LDH2, LDH4 predominantly increases.

3. Skeletal muscle damage, inflammatory and degenerative diseases
skeletal muscles (mainly an increase in the isoenzyme LDH1, LDH2, LDH3).

4. Blood diseases accompanied by the breakdown of blood cells: acute leukemia, hemolytic anemia, B12-deficiency anemia, sickle cell anemia, as well as diseases and pathological conditions accompanied by the destruction of platelets (massive blood transfusion, pulmonary embolism, shock, etc.). In these cases, an increase in the activity of LDH2 and LDH3 may predominate.

5. Acute pancreatitis.

6. Lung diseases (pneumonia, etc.)

7. Kidney infarction.

8. Tumors (increased levels of LDH are observed in 27% of cases of tumors in stage I and in 55% of metastatic seminomas).

It should be remembered that many diseases of the heart, skeletal muscles, liver and blood can be accompanied by an increase in the activity of total LDH in the blood serum without a clear predominance of any of its isoenzymes.

Table 3. Efficiencyhepatoprotectorsatsyndromecytolysis (ByWITH. IN. MorozovWithco-author., 2011 G. AndN. B. Gubergritz, 2012 G.)

Note: (+) – positive therapeutic effect; (±) – relative therapeutic effect;

Increased activity of LDH under physiological conditions is observed in pregnant women, newborns, after blood transfusion, and in persons after intense physical exertion.

GLUTAMATE DEHYDROGENASE

Reference values for GLDG activity in blood serum are less than 4 IU/l.

Glutamate dehydrogenase (GlDH) is a mitochondrial enzyme that catalyzes the conversion of glutamate to alpha-ketoglutaric acid. The enzyme is found in nerve cells, myocardium, and skeletal muscles, but the largest amount is found in liver cells - hepatocytes.

Elevated serum GLDG levels indicate liver damage. Since the enzyme is mitochondrial, the degree of increase in its activity reflects the depth and severity of the pathological process.

In viral hepatitis, GLDG activity increases in the blood on the first day of the icteric period. The degree of its increase depends on the severity of viral hepatitis; especially high values are detected with the development of liver failure.

High GLDG activity is observed in patients with primary and metastatic liver cancer. During exacerbation of chronic persistent hepatitis, the increase in GLDG activity is either absent or insignificant. In liver cirrhosis in the stage of decompensation, the increase in GLDG activity can be significant, and high enzyme activity is considered as an unfavorable sign.

Alcohol intoxication is also accompanied by a significant increase in GLDG activity in the blood serum.

To establish the etiology of increased transaminase levels, it is recommended to carry out additional laboratory tests (markers of cholestasis, viral hepatitis, autoimmune diseases, blood lipidogram, determination of the level of alpha1-antitrypsin, ceruloplasmin, ferritin, etc.), and instrumental examination methods (ultrasound, computer and magnetic resonance imaging of the abdominal cavity, puncture biopsy of the liver followed by histological examination of the biopsy).

Long-term increased destruction of hepatocytes, accompanied by an inflammatory response and cytolysis, ultimately leads to the development of fibrosis and cirrhosis.

Treatment of liver diseases should be comprehensive and include etiotropic therapy (after diagnosis) and pathogenetic therapy (from the moment cytolysis is detected).

In order to increase the liver's resistance to pathological influences, drugs belonging to the group of hepatoprotectors are used.

Hepatoprotective drugs used for cytolysis syndrome are presented in Table 3.

MECHANISMS OF ACTIONHEPATOPROTECTIVEDRUGS FOR SYNDROMECYTOLYSIS

Essential phospholipids (EPL)

are a purified mixture of polyunsaturated phospholipids (mainly phosphatidylcholine), which are obtained from soybeans. EPLs correspond in their chemical structure to endogenous phospholipids. EPL restores the deficiency of the pool of phospholipids in the body, which serve as a building material for cell membranes, maintaining their fluidity, and are also a target for lipid peroxidation products, reducing the manifestations of oxidative stress.

Side effect: Gastric discomfort, diarrhea, allergic reactions.

Contraindications: hypersensitivity to phosphatidylcholine or other auxiliary ingredients of the drug; children under 3 years of age.

Silymarin is the common name for chemically related flavonolignan isomers from milk thistle fruits. The main bioflavonoids in silymarin are: silibinin, silydianin, silicristin, isosilibinin, among which silibinin has the greatest biological activity.

Silymarin neutralizes free radicals in the liver and prevents the destruction of cellular structures. Specifically stimulates RNA polymerase and activates the synthesis of structural and functional proteins and phospholipids in damaged hepatocytes. Stabilizes cell membranes, accelerates the regeneration of liver cells. Silymarin is a specific antidote for poisoning by toadstool (prevents the penetration of toadstool poisons into the cell: phalloidin and amanitin).

Side effect: Laxative effect.

Contraindications: hypersensitivity to the components of the drug.

Ademetionine– an active sulfur-containing metabolite of methionine, a natural antioxidant and antidepressant, formed in the liver from methionine and adenosine in amounts up to 8 g/day. and present in all tissues and fluids of the body, but most of all in the places of its formation and consumption: in the liver and brain.

Ademetionine plays a central role in intermediate metabolism and is second only to ATP in its versatility in participating in a variety of biochemical reactions. The S-adenosyl-L-methionine molecule donates a methyl group in the methylation reactions of phospholipids of cell membranes of proteins, hormones, neurotransmitters, etc. (transmethylation). It is a precursor of physiological thiol compounds - cysteine, taurine, glutathione (provides a redox mechanism of cellular detoxification), CoA, etc. in transsulfation reactions. After decarboxylation, it participates in aminopropylation processes as a precursor of polyamines - putrescine (stimulator of cell regeneration and hepatocyte proliferation), spermidine and spermine, which are part of the ribosome structure. It has been shown to be effective for hepatopathies caused by taking hepatotoxic drugs (paracetamol, cytostatic drugs, etc.).

Side effects: gastralgia; dyspepsia; heartburn; insomnia, allergic reactions.

Contraindications: hypersensitivity to the components of the drug; genetic disorders affecting the methionine cycle and/or causing homocystinuria and/or hyperhomocysteinemia (cystathionine beta synthase deficiency, impaired metabolism of vitamin B 12); I and II trimester of pregnancy; lactation period (breastfeeding); age under 18 years due to lack of studies on effectiveness and safety.

If there is a clinical need for prescribing ademetionine in pediatric practice, the issue is resolved through a consultation or with the permission of the local ethics committee with the informed consent of the parents. Our clinical observations of children showed a positive effect from the use of ade-methionine in the form of a decrease in alkaline phosphatase, GGT, normalization of ALT and AST. None of the patients we observed reported any side effects. Children up to 10 kg are prescribed 50–100 mg/day, from 10 to 20 kg – 100–200 mg/day, over 20 kg – 200–400 mg/day.

Ursodeoxycholic acid (UDCA) is a non-toxic, tertiary, hydrophilic bile acid.

The membrane-stabilizing effect of UDCA is due to the ability of the drug to modulate the structure and composition of mixed micelles rich in phospholipids in bile. UDCA conjugates protect cholangiocytes from the damaging effects of FAs by stimulating basolateral secretion and reducing the cholangiocellular concentration of hydrophobic FAs. While taking the drug, the enterohepatic circulation of hydrophobic bile acids is reduced, their toxic effect on the membranes of hepatocytes and the epithelium of the bile ducts is prevented.

UDCA, through activation of epidermal growth factor receptors (epidermal growth receptor) and MARK (mitogen-activated protein kinases), induces signals in hepatocytes aimed at cell survival, thus causing an anti-apoptotic effect.

UDCA therapy reduces the risk of developing oncological processes, in particular hepatocellular carcinoma (HCC) and chronic viral hepatitis C in patients who have not responded to antiviral therapy. It also has an immunomodulatory effect, affects immunological reactions in the liver: it reduces the expression of certain antigens on the hepatocyte membrane, affects the number of T-lymphocytes, the formation of interleukin-2, and reduces the number of eosinophils. UDCA is indicated in the treatment of autoimmune liver diseases.

In severe cytolysis syndrome, the most pronounced positive effect is observed with simultaneous administration of ademetionine (parenterally) with UDCA.

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Cytolysis syndrome (ICD code K71) is a dangerous condition that provokes the development of various pathological processes in the body, leading to coma and death. It can be diagnosed both in a child immediately after birth and in an adult. There are a lot of reasons for this. And it is important to promptly identify and eliminate them in order to prevent further progression of the pathology and the appearance of irreversible consequences against its background.

What it is?

Liver cells (hepatocytes) synthesize special substances that have an antitoxic effect and provide a number of vital reactions in the body. The influence of negative factors on them leads to a violation of the integrity of the shell and their further death. As a result, active enzymes begin to be released into the blood, provoking the development of necrosis and degeneration of the organ parenchyma.

This condition disables the functioning of the gland (endocrine and exocrine dysfunction is observed) and the entire organism as a whole. Due to the loss of the ability to cope with toxins, harmful substances begin to accumulate in it, causing various disorders in other organs. All this leads to the occurrence of serious pathologies (for example, cirrhosis) or conditions that threaten human life (hemorrhage, intoxication, etc.).

There are several types of syndrome - congenital and acquired. In the first case, genetic and hereditary factors most often play the main role, in the second - exposure to alcohol, long-term use of certain drugs, untimely treatment of other diseases, etc.

The main causes of cytolysis

Damage to hepatocyte membranes occurs against the background of:

Genetic and hereditary predisposition.
Alcohol addiction.
Incorrect or prolonged use of medications.
Excessive consumption of fried, fatty and spicy foods.
Helminthiasis.
Oncological diseases.
Immunodeficiency.

These factors are the most common provocateurs of the syndrome. And often untimely elimination of their influence leads to irreversible processes in the liver, as a result of which it is not possible to completely cure the disease and the risks of complications are always present. Although cytolysis is easily treatable in the early stages, unfortunately, it is not always possible to diagnose it.

Alcoholism is the main cause of the syndrome

Absolutely all alcoholic drinks contain ethanol, which has a toxic effect on liver cells. If alcohol consumption occurs in moderation, the gland copes with the task quite well, despite the fact that during this a small number of hepatocytes are also damaged, since it has the ability to self-heal.

When the organ is constantly exposed to ethanol, and even in large quantities, the liver becomes overloaded and ceases to function fully. Because of this, there is a metabolic disorder, a change in its structural elements (they are deformed), their destruction and the appearance of symptoms of cytolysis.

The speed of these processes is also influenced by the surrogates present in alcoholic beverages (they also have a strong toxic effect), and directly by the quality of the alcohol consumed by a person. When signs of cytolysis appear against the background of addiction, no viruses are detected during the examination, but a significant increase in the level of bilirubin in the blood and the presence of fibrillar protein and Mallory bodies are detected during a biopsy.

Liver cells have a high rate of self-healing. Therefore, if the occurrence of the syndrome is directly related to the abuse of alcoholic products, then stopping it at the initial stages of the disease can lead to a complete recovery and restoration of the functionality of the organ.

Taking medications destroys hepatocytes

There are certain groups of drugs that have a toxic effect on gland tissue. Therefore, their improper use with violation of dosages and duration of treatment can easily lead to cytolysis. If this happens, then the only solution to the problem is to stop taking medications. And since this is not always possible, it is necessary to know exactly which medications can provoke the appearance of the syndrome in order to take preventive measures when using them. And these include:

NSAIDs (non-steroidal anti-inflammatory drugs).
Antimetabolites.
Glucosteroids.
Anticonvulsants.
Antibiotics.
Sedatives.

It should be noted that oral contraceptives can also lead to cytolysis, since they contribute to blood thickening and poor circulation in the liver, thereby slowing down the process of removing toxic substances from the body and increasing the risk of thrombosis.

In addition, these medications have a hepatotoxic effect, which, in combination with other factors affecting the body, significantly increases the likelihood of the syndrome occurring. These include:

Pregnancy.
Simultaneous use of 3 or more drugs.
Existing liver pathologies.
Poor nutrition.
Age-related changes in the body.
Bad ecology.
Frequent use of household chemicals.

In children, cytolysis is most often recorded immediately after birth when the woman took various medications during pregnancy. Their active components affect not only the body of the expectant mother, but also the child. They quickly penetrate the placenta through the blood, affecting the fetal liver cells, damaging them and causing various abnormalities.

It is for this reason that pregnancy is a frequent contraindication for drugs. Therefore, taking any medications during this period of a woman’s life should occur under the strict supervision of a doctor, not exceeding the prescribed dosage and duration of treatment. This reduces the risk of developing the syndrome in a child.

Hepatitis is a disease that affects hepatocytes

There is a certain category of viruses that, upon penetrating the body, cause an inadequate reaction in liver cells in the form of inflammation, followed by their death, intoxication and the occurrence of cytolysis. These include hepatitis pathogens belonging to taxa A, B, C and E.

The most common routes of transmission of the virus are nutritional and vertical modes of infection. In this case, the pathology may not manifest itself at all for a long time, slowly destroying liver cells and disabling the functioning of the organ. And here comes a double blow to the body. Not only is the death of hepatocytes accompanied by saturation of the blood with toxic substances, but also the vital activity of harmful agents causes severe intoxication, which leads to the development of cytolysis, for the treatment of which special antiviral agents are used.

Autoimmune disorders are another risk factor

Destruction of liver cells and further development of cytolysis can occur against the background of congenital disorders of the immune system. As a rule, this phenomenon is observed in newborns. The danger of cytolysis in this case lies in its rapid development. An organ transplant and constant use of immunosuppressants can save the little patient’s life.

However, it is not only children who experience autoimmune disorders. They can also be diagnosed in an adult as a result of exposure to various factors on the body (radiation, taking certain medications, etc.). They are identified based on the results of biochemistry and biopsy.

Helminthiasis is a common cause of the development of the syndrome in children and adults

There are several types of helminths that affect the liver and provoke further development of the syndrome:

Echinococcus.
Giardia.
Amoebas.
Roundworms.

Clinical manifestations of the syndrome

At the initial phase of its development, cytolysis does not manifest itself in any way. As a rule, it is discovered accidentally during a biochemical blood test, which shows an increase in the indicator enzymes contained in the test material.

The first signs of the syndrome appear only when massive damage to the hepotocytes has already occurred. They are expressed as follows:

Weight loss.
Feeling of heaviness in the stomach.
Bitterness in the mouth.
Periodic attacks of nausea.
Belching.
Yellowness of the sclera of the eyes and skin.
The appearance of age spots.
Increased liver volume (observed upon palpation).
Pain in the right hypochondrium.

These are the main signs of the development of cytolysis. But since various factors act as its provocateurs, the clinical picture may be supplemented by other symptoms, for example:

Change in color of urine and feces.
Redness of the palms.
An increase in temperature (observed when acute course of the disease or the development of complications).
The appearance of spider veins on the body.
Enlarged lymph nodes, etc.

Diagnosis of cytolysis

To make an accurate diagnosis and identify the cause that provoked the development of the syndrome, a comprehensive examination is carried out. It includes various diagnostic methods, but the most informative of them is blood biochemistry. As the syndrome progresses, this test shows an increase in serum:

Bilirubin.
LDH-5.
ALT AND AST.
OCT.
Glutamate dehydrogenase.
Fructose monophosphate aldolase.

It should be noted that a characteristic feature of cytolysis is a simultaneous increase in both direct and total bilirubin, which is caused by impaired liver functionality and the progression of parenchymal jaundice. In parallel with this, there is a decrease in the level of:

Albuminov.
Cholinesterase.
Proteins that support platelet functionality, which indicates a blood clotting disorder.

An equally informative method for diagnosing cytolysis is histological examination, which reveals existing changes in the liver and the rate of their progression.

Therapeutic actions

All therapeutic measures for cytolysis are prescribed strictly on an individual basis, depending on the degree of damage to hepatocytes and complications that have developed against the background of the disease. First of all, doctors are faced with the goal of eliminating the factor that caused the syndrome and reducing the level of intoxication.

In cases where the development of the syndrome is associated with alcohol dependence, the patient will need to undergo a full course of treatment at a drug treatment clinic. If liver damage was caused by medications, it is recommended to discontinue them and take more gentle medications.

To restore the functionality of hepatocytes, the following are used:

Hepatoprotectors – “Sirepar”, “Karsil”, “Hepa-merz”.
Sorbents – “Polyphepan”, “Enterosgel”.
Choleretic drugs – “Allohol”, “Hofitol”.

It is also mandatory to take ascorbic acid and B vitamins, as they:

Restores protein productivity.
Bile is removed.
Normalize carbohydrate metabolism.
Synthesize transaminase.
Improves blood circulation.
Increases the body's defenses.

No less important in the treatment of cytolysis is maintaining a special diet that reduces the load on the liver, thereby enhancing the process of regeneration of damaged cells. The patient needs to exclude from the diet:

Fatty, spicy , fried and smoked dishes.
Coffee Tea.
Citrus fruit.
Fresh baked goods.
Alcohol.

You will also need to limit your intake of salt, chocolate and confectionery and strictly follow your daily routine. Meals should be taken at intervals of 3 hours and in small portions. You should drink at least 2 liters of water during the day. You can replace it with mineral water without gases, for example, Borjomi or Essentuki.

It is necessary to understand that cytolysis is a dangerous condition that can lead to death. However, if the necessary measures are taken, then a person has every chance to stop further progression of the disease and avoid negative consequences.

The liver is a huge organ without nerve endings, so we are the last to learn about its diseases. Diseases of this organ also include liver cytolysis.

Hepatocyte: 1 - hepatocyte cytoplasm: 1.1 - glycogen granules; 2 - core

The main feature of cytolysis is that with this syndrome the permeability of the cell membranes of hepatocytes increases. These can be either minor violations of the integrity of the liver cell membrane or their serious destruction.

According to ICD 10 revision, liver cytolysis syndrome is classified as either chronic unspecified hepatitis (K 73.9) or inflammatory unspecified liver disease, that is, K 75.9. This disease is also called nonspecific hepatitis.

With cytolysis syndrome, the activity in the blood of liver enzymes such as aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase and others increases. Also, during cytolysis, the content of vitamin B12 and iron in the blood increases. In this case, not only the membranes of hepatocytes change, but also their organelles. The components of hepatocytes exit into the body, and water and sodium enter the cells themselves.

Causes of occurrence

A process such as cytolysis can be triggered due to a variety of pathological factors. Here are the most common ones.

Alcohol

Everyone knows that ethanol is a powerful hepatropic poison. Destruction of cell membranes can begin at a dose of 40-80 ml. pure ethanol. It also all depends on the dose per day and frequency of drinking ethanol-containing drinks, gender and the amount of enzymes in the body that process alcohol.

It is important to know: liver damage caused by ethanol abuse is reversible if you stop drinking alcohol and undergo restorative treatment of the organ.

amoeba;

(adults and larvae);

schistosomes;

Medicines

Unfortunately, some of them are hepatoxic. The only way to stop the destruction of organ cells when taking such medications is to stop taking medications. In total, more than a thousand drugs are known that damage one of the largest organs of our body.

Among them:

fungal medicines;

some types of antibiotics (for example, tetracycline);

non-steroidal anti-inflammatory drugs;

some laxatives;

psychotropic drugs and neuroleptics;

antimetabolites;

antidepressants;

anticonvulsants;

tamoxifen;

anti-tuberculosis drugs;

glucocorticoids;

ceftriaxone;

sex hormones (steroids).

The risk of cell damage increases with concomitant liver diseases, use of three or more drugs at the same time, during pregnancy and in old age.

Lipid metabolism disorder

Risk factors here may include excess weight, metabolic syndrome, diabetes, dyslipidemia and hypertension.

Autoimmune liver damage

Often causes cytolysis in young children.

Also to blame for cytolysis may be viruses, poor nutrition, fasting, tumors in the organ and metastases, shock, etc.

Symptoms

Like most liver diseases, cytolysis makes itself felt late. Usually the symptoms are not very pronounced. First of all, you need to pay attention to the yellowed whites of the eyes and skin (the release of bilirubin and jaundice are to blame).

Digestive disorders are also typical, including dyspepsia, increased acidity and heaviness in the stomach, bitterness in the mouth after eating or on an empty stomach.

Asthenia, endocrine disorders (especially related to the genital area), hemorrhagic diathesis, skin problems and hair growth disorders, and edema may also be observed.

It is important to know: during blood tests, not only bilirubin is found in it, but also iron, aldolase, and an increased amount of albumin. Also, during cytolysis, coagulability decreases.

This video will tell you about the symptoms of liver damage.

Diagnostics

The study for symptoms of cytolysis should be comprehensive. This is a general blood test, in which attention is paid to markers of hepatocyte destruction (LDH, AlAt, AsAt). The norm for LDH is no more than 260 units per liter, as well as 41 g/l in men and 31 in women. The amount of iron and bilirubin in the blood is also studied.

Traditional treatment

Gastroenterologists and therapists are involved in the treatment of cytolytic syndrome. It is important to understand here that cytolysis is not so much a disease as a process caused by other liver ailments or destructive factors. The first thing to do is to eliminate the disease or factor that provoked cytolysis. So, treatment can begin with eliminating alcohol, medications or diet.

Among the drugs for cytolysis, the most popular are hepatoprotectors or cytoprotectors. These include essential phospholipids, ursodeoxycholic acid, silymarin, admetionine.

It is also possible to prescribe drugs L-ornithine-L-aspartate, pentoxyphylline, etc.

Additionally, detox medications can be used. But essential phospholipids, for example, Essentiale, are recognized as the standard for treatment. The most important thing, as in the treatment of other ailments, is not to prescribe medications to yourself.

Prevention

Proper nutrition

Hepatocytes are destroyed not only by alcohol, but also by fatty foods, spicy foods, sweets, fried and fatty foods. Let your diet always include plant foods and dishes with minimal heat treatment. Fats are also necessary for cell membranes, but let it be fatty sea fish, milk and fermented milk products. Fruits and slow carbohydrates are no less necessary.

Liver cleansing

Alcohol restriction

Of course, be careful with alcohol, especially low-quality alcohol. If a little wine or even beer is good for the nerves, blood and stomach, then large doses weaken the largest organ of the body, and even the membranes of its cells. It is equally important to monitor the sterility of all medical and cosmetic procedures you perform, as well as monitor your personal hygiene.

Hepatic cytolysis- this is the destruction of gland cells under the influence of endogenous and exogenous factors.

Damage to cell membranes leads to the death of hepatocytes, necrosis and degeneration of the parenchyma, and, in general, to dysfunction of the organ. If not treated in a timely manner, the destructive process becomes irreversible and leads to severe complications such as cirrhosis, internal hemorrhages, and coma. In some cases, cytolysis provokes the death of the patient.

Reasons for the development of liver cytolysis

The permeability of cell membranes is disrupted under the influence of the following factors:

Cytolysis often occurs due to taking medications in the wrong dosage or without taking into account contraindications. Thus, the following drugs have a detrimental effect on liver cells:

antibiotics;
antidepressants;
antifungal medications;
glucocorticoids;
non-steroidal anti-inflammatory drugs;
drugs for convulsions;
antimetabolites (used in chemotherapy).

Also, long-term use of oral contraceptives is harmful to the liver, as they thicken the blood, can provoke thrombosis, disrupt blood flow in the liver, causing stagnation and slowing down the removal of toxins.

The use of these medications must be agreed with your doctor and be sure to carefully study the instructions for use.

Important! At an early stage, cytolysis is reversible, because you can stop cell destruction and stimulate parenchyma regeneration.

If necrotic processes have begun, it is impossible to heal the organ and completely restore its functions.

Symptoms of cytolysis

As with many liver diseases, the early stages of cytolytic syndrome are characterized by the absence of clear clinical symptoms. Sometimes pathology is detected by the results of a biochemical blood test, which shows elevated levels of indicator enzymes.

When the process of cell destruction is started and fibrotic foci appear, manifestations characteristic of cytolysis occur:

skin pigmentation;
icteric color of the skin and eye sclera, indicating bilirubin intoxication;
dyspeptic syndrome: nausea, bitterness in the mouth, belching, heaviness in the stomach;
“liver palms” - redness of the skin on them;
hemorrhagic syndrome (increased bleeding of the skin and mucous membranes);
increase in liver size;
pain in the right hypochondrium.

The severity of symptoms depends on the degree of organ damage.

Diagnosis of the pathological process

To establish the stage and causes of the development of cytolysis, a comprehensive examination of the patient is carried out. First of all, this is laboratory diagnostics. First of all, it is aimed at studying cytolysis cells in a general blood test. A blood chemistry test is also performed to check the levels of the following liver enzymes:

ALT and AST - their increase becomes the first signal of cell damage;
lactate dehydrogenase (LDH-5);
fructose monophosphate aldolase (FMPA);
gamma-glutamyl transpeptidase (GlDH);
ornithine carbamyltransferases (OCT and GGT).

An increased concentration of these proteins indicates damage to hepatocytes and organ intoxication.

The bilirubin content is also determined: during cytolysis, the concentration of this pigment increases and leads to jaundice.

During cytolysis, the following biochemical blood parameters drop:

albumin - due to the destruction of cells in the liver, less simple proteins are formed;
cholinesterase - indicates severe destruction.

A coagulogram is performed to assess hemostasis. During cytolysis, it shows a disturbance in blood clotting processes due to a lack of proteins important for platelets.

In severe cases, the patient may be prescribed a puncture biopsy with histological examination to determine the extent of damage to the gland and the causes of cell destruction.

Therapy is selected depending on the degree of parenchymal damage, symptoms and the presence of concomitant diseases. First of all, the factors that provoke cell destruction are eliminated. For this purpose, detoxification agents and hepatoprotectors are prescribed, which help restore hepatocytes and support the functions of the organ.

The effectiveness of treatment depends on the severity of the disease.

Treatment of cytolysis is aimed at eliminating the provoking factors of the disease:

If the cells are destroyed by taking medications, they need to be stopped, and if this is not possible, replaced with others or the dose adjusted.
With alcoholic cytolysis, complete abstinence from alcohol is required. If necessary, a rehabilitation course for drug addiction is prescribed.
If there are signs of autoimmune processes, immunosuppressive therapy is prescribed, which is aimed at reducing the production of antibodies.

Complex therapy also involves following a diet. Nutrition should be complete, balanced, but easy on the liver.

Basic rules of diet for cytolysis:

fried, smoked, spicy foods should be excluded;
salt, sugar, chocolate must be limited;
Avoid coffee, tea, fresh pastries and citrus fruits that increase acidity.
It is useful to drink compotes, fruit drinks, herbal teas;
you need to drink at least 2 liters of water, including mineral water without gas, per day;
meals are divided, with intervals between meals of no more than 3 hours.

Prevention of cytolytic syndrome

Cytolysis is the first sign of liver dysfunction. If detected at an early stage, the process is reversible, and complete restoration of normal organ function is possible. In the absence of proper treatment and continued exposure to negative factors, the destruction progresses to the stage of necrosis until liver failure.

Doctors often identify cytolysis syndrome when they carry out diagnostic measures to detect a specific disease (screening, physical examination). A person may not experience obvious symptoms, which complicates the process of interpreting research results.

Basic facts about the liver and its functions

The liver is considered the largest gland in the human body. The organ is involved in the activity of the digestive tract, and also supports metabolic processes and neutralizes toxic substances.

Attention! The liver has one essential property: when the disease develops in this area, at the initial stage, pronounced symptoms do not occur. Therefore, any organ pathology is diagnosed at a late stage.

This can be explained by the absence of nerve endings in it, which causes unmanifested pain. For many years, a person does not even suspect that the disease is developing - until significant damage to hepatocytes occurs.

The liver performs many tasks, which are divided into 2 groups: digestive and non-digestive. Regarding the non-digestive functions of iron:

The digestive activity of the gland is carried out due to the bile produced in it. So, liver:

breaks down physiologically active compounds;
produces uric acid, urea from any toxic compound;
regulates carbohydrate metabolism in the body;
regulates lipid metabolism;
synthesizes proteins;
forms bile.

What is cytolysis syndrome

Liver cytolysis is primarily characterized by an increase in the level of permeability of the cell membranes of the organ - hepatocytes. Both minor violations of their integrity and serious pathological conditions are equally diagnosed.

According to the International Classification of Diseases, 10th revision (ICD-10 code), the disease is assigned code K 73.9 (chronic unspecified hepatitis) and K 75.9 (inflammatory unspecified liver disease).

Hepatic cytolysis is characterized by an increase in the activity of the liver enzymes aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. There is an increase in the content of iron and vitamin B12 in the bloodstream. The cell (hepatocyte), that is, its shell, and its organelle are modified. The constituent cells of the organ enter the body, and water and sodium penetrate into their cavity.

Cytolysis syndrome in infants

The consequence of cytolytic syndrome is cholestasis, which can be intrahepatic and extrahepatic. The first form of the disease is characterized by stagnation of bile fluid in the main ducts of the gland, and the second - in nearby organs.

Cytolytic syndrome in infants occurs with symptoms characterizing the primary disease. To establish a diagnosis, a number of measures are carried out, based on the results of which effective treatment is prescribed. Therapy for intrahepatic cholestasis caused by cytolysis involves only surgery.

Symptoms

In most cases, the pathological condition is asymptomatic in the initial stages. The disease can be detected only during diagnostic procedures (laboratory). Among the characteristic manifestations of cytolysis:

feeling of bitterness in the mouth;
heaviness in the right hypochondrium (the clinical symptom increases in intensity as the number of affected cells increases);
nausea and vomiting syndrome;
flatulence and bloating;
constipation and diarrhea.

The child begins to complain of general malaise. Adults and children develop jaundice, a disease characterized by a change in the color shade of the epidermis and sclera. The stool also becomes discolored and the urine darkens. Cholestasis of the liver, which develops with an increase in its size, is accompanied by pain that occurs after eating and during movement.

Reasons for development

Experts associate the formation of liver cytolysis syndrome with the following predisposing factors:

abuse of alcoholic products (the ethanol they contain negatively affects not only the gland, but also all other organs);
therapy with drugs with hepatotoxic effects;
ongoing viral infection, for example, hepatitis type A, B, C;
non-alcoholic organ disease with toxic effects of lipids;
the presence of helminthic infestations in the organ;
genetic background;
enzyme deficiency;
autoimmune processes.

Pregnancy is a period during which many diseases can worsen and begin to develop under the influence of hormones.

It is important to know! Cytolysis and cholestasis are some of the common pathologies occurring in pregnant women.

Possible complications

An advanced condition can cause life-threatening complications. Among the negative consequences of cytolytic syndrome:

It is important to know! Due to a malfunction of the gland, a general intoxication syndrome occurs and metabolic processes slow down.

Diagnostic procedures

First of all, the doctor finds out what liver diseases are developing in a person or have been cured previously, and whether there are symptoms from the organ. Next, laboratory diagnostics are prescribed, and this includes mandatory biochemistry and a general blood test. Based on the research results, bilirubin, alkaline phosphatase, liver enzymes, and proteins are determined in quantitative ratios to the norm.

The condition of the organ can be visualized using instrumental diagnostics. Ultrasound, computed tomography or magnetic resonance imaging are prescribed. A gland biopsy followed by histological analysis may be required.

Treatment tactics

How to treat cytolysis syndrome depends on the cause that caused it. Laboratory blood tests and instrumental diagnostic results are taken into account.

Excluding the cause of development

First of all, the fight against the syndrome begins with identifying the source of pathological changes in the organ. To eliminate the cause of cytolysis, it is recommended to follow the following rules:

Drug therapy

After the final diagnosis has been established, drug treatment is prescribed aimed at combating the underlying pathology, as well as accelerating the regeneration of hepatocytes. The syndrome can be treated using the following means:

hepatoprotectors, which contain synthetic or plant components;
detoxification solutions;
sorbents that block the absorption of toxic substances;
vitamin complexes;
drugs that have a stimulating effect on the outflow of bile fluid.

Diet

Treatment of pathology with diet therapy helps reduce the load on gland cells and facilitate their functioning. The recommendations are as follows:

exclude fatty and fried foods, pickles, smoked meats, and marinades from the diet;
it is necessary to switch to fractional meals;
reduce the consumption of salt, baked goods, cream products, chocolate;
exclude foods that increase acidity, as well as coffee.

Preventive measures

Prevention of cytolytic syndrome is maintaining proper nutrition, weight correction, and limiting alcohol consumption. Another recommendation is to exclude long-term drug therapy, because 90% of them negatively affect the condition of the liver.

Cytolysis of the gland is not yet an indicator that a person is hopelessly ill. In any case, it is necessary to undergo follow-up examinations in order to detect the disease in time and begin appropriate therapy.

Cytolysis syndrome is a set of signs indicating a disruption in liver function due to damage to the integrity of the membranes of hepatocytes with subsequent death. As a result of damage by endogenous and exogenous factors, gland cells lose the ability to function normally, which leads to disruption of the organ as a whole.

The destructive process in hepatocytes is accompanied by the release of active enzymes into the blood, leading to necrosis and degeneration of the liver parenchyma. If the root of the problem is not identified in time and treatment is not started, the pathology progresses, becomes irreversible, and becomes the basis for the development of severe complications: cirrhosis, hemorrhages, coma and death.

Causes

Damage to the cell membranes of hepatocytes develops under the influence of provoking factors. Most often, the permeability of the liver cell membrane is affected due to:

In the early stages, the disease can be treated, destructive processes can be stopped, and damaged cells can be restored. In advanced cases, with the development of tissue necrosis, the disease cannot be completely cured.

Alcohol addiction

Ethanol is the basis of all alcoholic beverages. It is a toxic substance for the liver, since alcohol is broken down into water and carbon in the gland. But with excessive alcohol consumption, the organ cannot cope with its assigned task, metabolic processes are disrupted, the structural elements of the cells are deformed and destroyed over time, which leads to lysis of the parenchyma.

The degree of liver damage is determined by the regular dosage and type of alcohol, as well as the individual characteristics of the activity of enzymes that process alcohol. The quality of the product also plays an important role; surrogates have a toxic effect, additionally poisoning the body with decay products.

In people with alcohol dependence, when diagnosing the disease, viruses are not detected, but symptoms of alcohol intoxication are detected. An increase in total bilirubin is detected in the blood; when examining a biopsy, Mallory bodies, a fibrillar protein synthesized under the influence of ethanol, are present.

Hepatocytes have a high ability to regenerate, so pathological changes disappear with abstinence from alcohol and concomitant treatment. Particularly successful and rapid results are observed in the initial stage of changes in liver cells.

Medicines

The danger of developing cytolysis comes from uncontrolled use of medications in violation of the dosage and without taking into account the contraindications specified in the instructions. The only way to avoid side effects of medications is to stop taking them, but this is not always possible, so you should know which medications can cause liver damage and carefully follow the instructions for use:

non-steroidal anti-inflammatory drugs;
antimycotics;
antibiotics;
antimetabolites – antitumor chemotherapeutic agents;
antidepressants;
anticonvulsants;
glucosteroid hormones.

Long-term use of hormonal contraception increases the risk of developing thrombosis by thickening the blood, disrupting blood flow in the gland and slowing down the elimination of toxins.

The hepatotoxic effects of drugs are enhanced by risk factors. These include the simultaneous use of more than three drugs, the presence of liver pathologies with impaired blood flow and insufficiency of hepatocytes, unbalanced nutrition, pregnancy, and old age. The condition of the organ is worsened by unfavorable ecology and excessive use of household chemicals.

It is important for pregnant women to remember that many medications cross the placenta and enter the fetal liver, damaging the organ and causing congenital anomalies.

Viruses that cause hepatitis

The causative agents of hepatitis are infectious viruses belonging to taxa A and E, B, C, delta infection D, which are characterized by inflammation of liver tissue, death of hepatocytes and disruption of the detoxification process.

The method of entry into the human body depends on the type of infection. Hepatitis caused by pathogens A and E is acute and is transmitted through nutrition or contact if hygiene rules are not observed (rarely washing hands or eating contaminated fruits and vegetables).

Infection with viruses B, C and D occurs through the blood and biological fluids of the patient. There are also known cases of the vertical route, when a baby is infected from a sick mother at the time of birth if the child has lesions on the skin. Often the pathology occurs chronically, without pronounced symptoms, so it is not possible to diagnose the disease immediately, and prolonged exposure to viruses on the liver leads to its destruction.

Liver syndromes are observed in severe acute forms of hepatitis and in its chronic course. The process of cell death can be stopped with antiviral drugs and restorative therapy.

The causative agents of hepatitis include cytomegalovirus, herpesvirus, rubella, TTV, SEN, and AIDS viruses.

Autoimmune disorders

In some cases, under the influence of a congenital disorder in the immune system, hepatocytes are destroyed. The situation is usually observed in infants; cytolysis syndrome in children develops with the progression of autoimmune diseases, or for unexplained reasons, their own antibodies affect organ cells. In this case, the gallbladder is without pathology, not enlarged, and no changes are detected in the bile ducts.

The anomaly develops quickly; only a liver transplant can save the patient’s life; to improve the condition, therapy is carried out with immunosuppressants that inhibit the activity of the immune system.

Autoimmune disorders in an adult can be suspected if, when cytolysis is diagnosed, the patient does not drink alcohol, has not previously had a blood transfusion, there are no markers of viral damage, but biochemical changes in the composition of the blood and biopsy are detected.

Lipids

Sometimes cytolysis progresses due to a lipid metabolism disorder. Disorders usually occur after age 50. Changes develop due to excess weight, the formation of type 2 diabetes, and obesity.

As a result of the loss of cell sensitivity to insulin, triglycerides accumulate in the gland tissues. But due to problems in the processes of oxidation and reduced excretion of fat molecules, destruction of cellular structures occurs, replacement of hepatocytes with lipids and the development of fatty hepatosis.

Main signs of the disease

In the initial stage of the formation of cytolytic syndrome, there are no clinical manifestations. Sometimes pathology is detected by chance during examination of blood biochemistry, expressed in a slight increase in indicator enzymes.

With partial and total damage to the organ, clinical symptoms of cytolysis appear, which are characterized by the following signs:

weight loss;
dyspepsia and increased acidity: heaviness in the stomach, nausea, belching, bitterness in the mouth;
skin pigmentation;
hemorrhagic diathesis;
"liver palms";
yellowness of the skin and sclera of the eyes, which indicates a disorder of metabolic processes and the release of bilirubin into the blood;
the appearance of pain in the hypochondrium, enlarged liver.

Since damage to the gland is caused by multifactorial mechanisms, syndromes for liver diseases appear in aggregate, depending on the stage of damage and the pathology that caused cytolysis.

To identify cytolysis and establish the causes of its development, a comprehensive examination of the patient is carried out. Laboratory tests are an informative method for identifying the disease and the degree of pathology activity. To detect markers of the cytolytic process, biochemical blood testing is performed.

Biochemical syndromes of liver damage are bilirubin and indicator enzymes:

serum transaminases: ALT and AST – the first signal about the onset of hepatocyte damage;
lactate dehydrogenase (LDH-5);
fructose monophosphate aldolase;
glutamate dehydrogenase;
ornithine carbamyl transferase (OCT);
gamma-glutamyl transpeptidase.

Direct and total bilirubin is detected, with cytolysis syndrome an increase in pigment is detected, which indicates the development of parenchymal jaundice.

The analyzes also determine a decrease in the following indicators:

albumin, since the gland synthesizes fewer protein fractions;
cholinesterase enzyme levels, which indicates a severe course of the disease;
blood clotting (the results indicate a violation of the production of proteins responsible for the normal functioning of platelets; testing is carried out using a coagulogram).

Histological examination of the liver is considered the most productive way to diagnose changes in the gland. A puncture biopsy is prescribed in difficult cases by a council of doctors. The procedure is carried out to clarify the cause of the pathological process, the stage of development and the degree of damage to the organ.

Treatment

The treatment regimen for liver cell cytolysis is determined by the stage of the pathology, the presence of provoking factors and concomitant pathologies. The purpose of the measures is, first of all, to eliminate disease factors, reduce intoxication, restore the structure of hepatocytes and liver functions.

Eliminating the cause

The effectiveness of treatment measures depends on the duration of the pathological process. In relation to the type of hepatotoxic effect, the following measures are indicated:

Restoration of organ functions

To stop the progression of liver cytolysis syndrome and restore normal functioning of the gland, the following medications are prescribed:

Hepatoprotectors. Medicines of plant or synthetic origin, phospholipids, derivatives of animal fats and amino acids (Karsil, Sirepar, Phosphogliv, Hepa-merz) are recommended. A long course of taking drugs allows you to remove toxins, strengthen the membranes of hepatocytes, stimulate their regeneration and facilitate the functioning of the gland.
Sorbents. The prescription of drugs is due to endotoxicosis; sorbents absorb harmful substances in the gastrointestinal tract and remove them from the body (Polyphepan, Enterosgel).
Choleretic drugs. Used in the absence of stone formation (“Allohol”, “Hofitol”).

B vitamins and ascorbic acid are used to regulate protein synthesis, activate bile flow, improve energy and carbohydrate metabolism and transaminase synthesis, normalize hematopoietic functions, and restore immunity.

Diet therapy

Diet for liver cytolysis is an integral part of the treatment of pathology. Properly organized nutritious nutrition helps reduce the load on the cellular structures of the organ and facilitate the performance of functions by hepatocytes. Rules to follow:

exclude fats, fried, smoked and spicy foods from the diet;
limit the consumption of salt, sweets, chocolate;
give up foods that increase acidity - coffee, citrus fruits, alcohol and tea, fresh baked goods.

Food should be taken in small portions at intervals of no more than three hours, and water should be drunk (at least 2 liters). Herbal tea, compotes and fruit drinks are allowed. Mineral water is chosen without gas; Essentuki or Borjomi are suitable.

Table 2. Causes promotion level aminotransferases

Hepatic causes

Extrahepatic causes