Hepatosis of the liver

Among liver diseases, hepatoses occupy a special place. They are not associated with inflammation in the hepatic cells( or it is very weakly expressed), with the effect of infection, oncological degeneration. This group of diseases is characterized by a marked disruption of metabolic processes in hepatocytes, followed by dystrophy and death.

What are the forms of hepatosis?

Behind the common name are 3 different variants of the disease. They differ in the predominant type of metabolic disorder, morphological features. They are classified as fatty, cholestatic and pigmented.

The causes of each disease are different, so to know how to treat the disease, you need to find out the mechanism of violations. All can manifest themselves in acute and chronic form. The most common fatty degeneration of the liver( steatosis).

In obese people with a body mass index of 30 or more, as well as in chronic alcoholics, fatty hepatosis is detected in 95% of morphological studies. Steatosis is common in 25% of all cases of diagnostic punctures.

Changes in liver cells develop immediately in the entire body. But some authors identify the focal form of steatohepatosis. They consider it possible to form local deposits of fat in the portal vein branching zone.

What are the similarities and differences of hepatoses?

The defeat of the liver in hepatosis develops under the influence of external( exogenous) and internal( endogenous factors).Exogenous is the toxic effect of any toxic substances. Acute hepatosis often causes poisoning with arsenic compounds, fluoride, poisonous fungi, large doses of alcohol and surrogates, and certain medications.

For the chronic course, long-term alcoholism, eating disorders( lack of protein and vitamins), exposure to carbon tetrachloride, organophosphorus compounds are more typical. Endogenous factors arise within the body against a background of various diseases( thyroid gland, endocrine obesity, diabetes, and Itenko-Cushing syndrome).

Acute form can become a complication of sepsis, viral hepatitis, avitaminosis. With endogenous lesion, the liver perceives a violation of the general metabolism in the body, changes become secondary to the underlying disease.

Fatty hepatosis

A variant of hepatosis due to the fatty type of dystrophy of the hepatic cells. It develops with such a violation of metabolism, when in the cells either fatty inclusions are accumulated because of massive intake of fatty acids, carbohydrates, or hepatocytes have defects that can not cope with fats.

For the main reason distinguish:

• alcoholic liver infiltration with fat, followed by a transition to alcoholic steatohepatitis and cirrhosis;
• non-alcoholic fatty infiltration( 9% of all morphological studies of the liver), respectively, non-alcoholic steatohepatitis most often accompanies endocrine disorders, insulin resistance with hyperinsulinemia, cardiovascular diseases.

Both forms cause changes in the body, called metabolic syndrome. But there are possible causes of hepatic steatosis, not related to alcohol and metabolic disorders. This applies:

• to the adverse effects of stomach and bowel surgery on obesity;
• hereditary metabolic disorders;
• the effect of infection;
• to the outcome of the course of chronic illnesses that drain the patient's body.

The biochemical criterion for the fatty form of hepatosis is the level of triglycerides in the liver more than 1/10 of the dry mass. Studies show that fatty inclusions have a diffuse spread, when the fat content in the liver reaches 25%.

Cholestatic hepatosis

Cholestasis can be caused by medications( from the group of testosterone, Aminazine, hormonal tablets prescribed for the treatment of infertility).He is helped by a long uncontrolled use of drugs. The accumulation of bile acids causes a violation of the formation of bile and its outflow into the intestine.

Pigmented hepatosis

Disease of the liver is of a dystrophic nature caused by genetic abnormalities in the production of enzymes( enzymes) required for the process of intrahepatic bilirubin metabolism. Accompanied by temporary or chronic jaundice.

Distinguish between bilirubin and pigmental metabolism disorders:

• caused by unconjugated bilirubin( Kriegler-Nayyar Syndromes, Lucy-Driscola, Gilbert's Disease);
• because of unconjugated and conjugated bilirubin( syndromes of Dubinin-Johnson, Rotor).

The prevalence of hereditary manifestations is 2-5% of the total population. For example, we will analyze the most common Gilbert syndrome( other names: simple family cholemia, idiopathic unconjugated hyperbilirubinemia, constitutional hyperbilirubinemia, familial non-hemolytic jaundice).

Form of pigmentary hepatosis, for which a typically unstable increase in the blood content of indirect bilirubin. The reason for the disrupted intracellular transport of pigment molecules and its attachment to glucuronic acid

. What changes occur in the liver?

With fatty form of hepatosis, the mechanisms of fat accumulation during liver overload are:

• in excess intake from the food of fats and carbohydrates, which are converted to fatty acids;
• depletion of glycogen stores, which causes the release of fats from the depot and increased deposition in the liver;
• growth of production of growth hormone pituitary, it is he who mobilizes fat from the depot;
• action of alcohol by increasing the synthesis of catecholamines, a violation of the biological fat oxidation reaction.

The removal of fat from the liver is reduced due to: a decrease in the concentration of low density lipoproteins, increased synthesis of triglycerides, inhibition of the decomposition of fatty acids in hepatocytes due to disruption of the phosphorylation process, a hereditary deficiency of enzymes that affect the regulation of fat in the liver.

In cholestatic hepatosis, cholesterol and bile acid metabolism in the liver cells is primarily affected. It is important, in addition to the influence of the harmful factor on the liver cells, a pronounced toxic-allergic reaction.

Pigmented hepatosis causes accumulation in the hepatocytes of bilirubin. The significance is:

• an increase in the blood content of the unconjugated form of the pigment due to the increased decay( hemolysis) of the erythrocytes;
• decreased ability of hepatocytes to capture unconjugated bilirubin;
• disruption of conjugation of bilirubin inside the liver;
• damage to the hepatocyte and the release of the pigment directly into the blood;
• obstructed the transition of bile from the hepatocyte into the capillary passage of the biliary tract;
• inhibition of free circulation of bile in the intrahepatic and extrahepatic ways.

Manifestations of

The general symptoms of hepatic liver show the extent of impairment of organ functions. At the initial stage of fatty degeneration, they are minimal, then the hepatic insufficiency gradually increases. Symptoms of the disease can manifest right after birth( with enzyme pathology) or years later.

Chronic course of the disease is accompanied by the appearance of:

• dyspeptic disorders( nausea, vomiting, stool disorders);
• unclear fatigue and weakness;
• decreased appetite;
• by weight loss;
• blunt pains or a feeling of heaviness in the hypochondrium right;
• in connection with the breakdown of the synthesis of sex hormones, women often turn to a doctor for infertility, and men are treated for impotence.

Over time, changes in brain functions are manifested: attention, sleep, character changes. The course of the chronic form of hepatosis is more favorable, it is impossible to get rid of the disease, but there is time to support and compensate for lost liver function.

Symptoms of acute development develop rapidly. The patient is diagnosed with severe intoxication, jaundice, vomiting and nausea. The development of acute hepatic insufficiency can lead to hemorrhagic manifestations and hepatic coma with a fatal outcome.

When examined palpation, the attending physician discovers a dense edge of the liver protruding from beneath the costal arch. The leading clinical sign is hepatomegaly( enlargement of the liver), smooth, moderately painful to the touch. The enlargement of the spleen is not typical.

Cholestatic hepatosis is manifested by symptoms of bile stasis( cholestasis syndrome), characterized by jaundice of sclera and skin, painful itching, dark urine, discolored gray feces, fever. The cholestatic form of hepatosis is faster than the others in hepatitis due to the pronounced response of the stroma of the hepatic tissue.

Gilbert syndrome manifests itself usually at the age of puberty. In childhood, it is possible to periodically jaundice the skin after a physical strain or a transferred infection. Symptoms stimulate prolonged hunger, compliance with a low-calorie diet.

sclera. Pigmentation may have the form of stained spots on the skin, xantelasm of the eyelids, a small icteric sclera. Pain in the right hypochondrium is not intensive, nausea, upset of the chair. Rare forms of pigmentary hepatosis are manifested:

• Lucy-Driscola syndrome - yellowing of breast milk, terminates after transferring the child to nutritional formula;
• by Dubin-Johnson syndrome - a violation of bile synthesis, icteric sclera, typically augmentation after taking contraceptives, against the background of pregnancy.

Diagnostics of

For fatty hepatosis, changes in biochemical blood tests are typical:

• moderately increased activity of alanine and aspartic aminotransferase, alkaline phosphatase, fructose-1-phosphataldolase, urokinase;
• for severe flow indicates a decrease in potassium concentration, an increase in ESR;
• on the violation of fat metabolism is judged by the level of cholesterol, triglycerides and β-lipoproteins;
• on ultrasound show: an increase in liver size, increased echogenicity of the parenchyma, an unclear "blurred" vascular pattern, the appearance of "granularity" indicates the onset of hepatitis;
• computed tomography and nuclear magnetic resonance imaging detect a decrease in the tissue absorption coefficient, sometimes limited areas of fat infiltration around which a healthy tissue surrounds;
• radioisotope reveals the slowing or complete cessation of hepatic cell function;
• in the morphological study of the biopsy specimen shows fat deposits in the central hepatic lobules.

With cholestatic hepatosis, a high level of bilirubin, a significantly increased activity of alkaline phosphatase and leucine aminopeptidase are detected in the blood, an increased cholesterol index, high ESR is detected.

To exclude pigmentary hepatosis, special diagnostic tests are done: when fasting, the serum bilirubin concentration is increased 2 times, after taking Phenobarbital - the bilirubin level decreases, for intramuscular injection of nicotinic acid - after five hours, the bilirubin content is increased by 25%.

How is the degree of liver damage different?

The study of the liver biopsy material of different people led to the classification of the development of hepatoses in degrees:

• Initial - small fat drops appear in individual hepatocytes. Clinical signs are absent.
• 1 degree - fat drops become large, accumulate in separate areas. The course of the disease is sluggish and it is practically impossible to detect it at this stage.
• 2 degree - Cell obesity is mixed, present in the entire liver tissue. The patient complains of pain in the hypochondrium to the right, a feeling of heaviness, possibly augmentation of the liver.
• 3 degree - obesity diffusely covers the entire body, fatty inclusions are located and extracellularly, form fatty cysts, there is an increased proliferation of connective tissue.

What is dangerous for hepatosis?

In modern conditions of life and production a person constantly meets with toxic toxic substances. If the symptoms of liver damage are not manifested everywhere, this does not mean the absence of morphological changes at the level of 1-2 degrees.

Progression of the process is recorded when clinical manifestations appear. A liver biopsy is performed only if there are serious suspicions of pathology. Over time, hepatosis changes into non-viral hepatitis. Further development is cirrhosis. Experts believe that in the next 3 decades, hepatoses will be the main reason for liver transplantation.

is affected. Methods for treating hepatosis

Treatment of hepatic liver requires: strict adherence to a diet that restricts the intake of fats and carbohydrates with food, the proper selection of exercises and physical exertion to "burn" fat, correct hormonal disorders, usedrugs group hepatoprotectors, choleretics and cholekinetics, with severe obesity - bariatric surgery.

Power features of

Patients are shown the menu of Table No. 5 according to Pevsner's classification. Contraindicated animal fats( beef meat, pork, butter, culinary fat, sour cream, lard, smoked meat and fish products, fatty cottage cheese, sweets and cooking products), hot sauces, strong tea and coffee.

Only boiled, stewed dishes are included in the menu, it is allowed to steam, bake. Increased protein content is provided by the dishes of their low-fat meat and fish, low-fat cottage cheese, kefir, porridges. To compensate for the loss of vitamins and electrolytes, vegetables and fruits are recommended.

The approximate composition of a daily diet includes:

• proteins - 110 g;
• fats - 80 g;
• carbohydrates - up to 300 g.

Caloric value - 3200-3500 kcal. The disease can be cured in the initial stage, if you stop the effect on the liver of toxic factors. Especially important is the refusal of alcohol. If after the course of treatment the patient has again drunk, then the process can not be stopped.

Use of

Drugs In acute toxic hepatosis, the patient is shown hospitalization and elimination of pathology caused by poisoning. To remove intoxication, solutions of Hemodeza, Polyglukin, salt electrolyte preparations are introduced. Panangin helps to restore the content of potassium in the blood.

With hemorrhagic manifestations, you may need platelet mass, corticosteroids. To restore normal fat metabolism, vitamins, especially group B, folic acid are needed. For the treatment of chronic fatty hepatosis,

• is used for medicinal treatment with drugs blocking lipase( Orlistat) that increase insulin sensitivity( Metformin), they contribute to a decrease in the level of triglycerides;
• antioxidants( vitamin E, betaine, S-adenosylmethionine, and N-acetylcysteine) lower the level of transaminases;
• from the hepatoprotector group uses essential phospholipids, Silybin, Silymarin, herbal remedies Legalon, lipoic acid, Ursosan is a drug of ursodeoxycholic acid.

Care should be taken with regard to preparations from liver tissue( Sirepard, Progepar).They give allergic reactions.

In case of cholestatic hepatosis, preparations stimulating the production of bile( Allochol, Holenzyme) and cholekinetics( Holosas, Flamin, Sorbitol, Mannitol) are used, which promote bile through the ducts, starting with interlobular ones.

Patients with pigmentary hepatosis show symptomatic therapy with progression of the process. If there are signs of inflammation of the gallbladder, then prescribe antibacterial drugs. People with genetic disorders are not recommended to have a sanatorium treatment.

Forecast

To the question: "Can liver hepatosis be cured?" - the doctor is able to respond after a full examination of the patient. Most often, complete elimination of the pathogenic factor contributes to non-alcoholic hepatosis in a favorable course.

If the patient is over 50 years old, the body mass index is more than 30, there is a high level of alanine transaminase and triglycerides, cholesterol and glucose, then a favorable situation for early fibrosis of the hepatic tissue develops, which increases the risk of cirrhosis.

Hepatoses are far from harmless diseases. They seriously worsen the patient's life, require constant restrictions in nutrition. Timely correction of diet and exercise, regular cleansing of the liver with a tendency to obesity helps to keep the body in a working state.