At the same time, sinusoids are compressed, blood circulation in them worsens; possible death of individual liver cells. The disease leads to the formation of the so-called stellate portal fibrosis of the liver.

Causes of fatty degeneration of the liver

Various causes can lead to fatty degeneration of the liver: alcohol abuse, improper and malnutrition, and especially protein starvation; endocrine disorders (damages of the diencephalic-pituitary system, insular apparatus pancreas), prolonged infections (tuberculosis) and intoxications (phosphorus, chloroform, carbon tetrachloride, etc.), treatment with corticosteroids and antibiotics.

Symptoms and signs of fatty liver

At an early stage, the disease is asymptomatic; possible hepatomegaly without noticeable functional abnormalities. The liver is smooth and soft to the touch. In this still reversible period, the elimination of the cause leads to the normalization of the size of the liver. With the progression of the disease, the liver becomes sensitive, dense. A high level of choline in the blood serum is determined, the activity of acetylcholinesterase increases. The content of total fats in the blood serum is often increased, and the first stage of the polarographic wave shows a tendency to increase. They emphasize the increased sensitivity and vulnerability of the liver in fatty degeneration, a decrease in the content of glycogen in it.

In the terminal period of the disease, severe complications are possible: fat embolism, vascular thrombosis, hemorrhagic diathesis, hepatic coma. There is no convincing evidence that stenosis can lead to cirrhosis in humans.

Diagnosis. One should think about fatty degeneration of the liver in cases of finding an enlarged liver of a soft consistency, in the absence of noticeable functional disorders, especially when it comes to alcoholics, diabetics, ulcerative colitis, tuberculosis or alimentary disorders, etc. The pathology of fat metabolism and the presence of fatty degeneration of the liver are indicated by a high level of choline in the blood serum, increased activity of acetylcholinesterase, a high content of total fats and an increased first step of the polarographic wave. A definite diagnosis can be made by histological examination. biopsy material from the liver.

Fatty degeneration of the liver is differentiated from liver prolapse, chronic hepatitis and compensated inactive cirrhosis.

Treatment of fatty degeneration of the liver

First of all, the cause that led to fatty liver should be eliminated. The diet should be rich in animal proteins, vitamins, lipotropic substances with a limited amount of fat. It is possible to prescribe vitamin B6 due to the unconditional dapotropic action inherent in the drug, as well as choline chloride, lipocaine, folic acid, empirically methionine and choline (the use of the latter in the clinic has been disappointing).

Fatty degeneration of the liver of non-alcoholic etiology

Fatty degeneration of the liver of non-alcoholic etiology is called liver damage of varying severity, histologically resembling alcoholic liver damage, but occurring in those who do not abuse alcohol. It includes the actual fatty degeneration of the liver, damage to hepatocytes, necrosis and fibrosis; cirrhosis of the liver with portal hypertension and other complications, including hepatocellular carcinoma. Life expectancy in fatty liver is lower than in the general population.

In practice, the diagnosis of fatty degeneration of the liver of non-alcoholic etiology is made by the method of exclusion. It should be suspected in a patient with chronic liver disease who does not abuse alcohol, negative results serological studies for viral hepatitis and the absence of congenital or acquired liver diseases.

Associated diseases and conditions

Fatty degeneration of the liver of non-alcoholic etiology is often found in type 2 diabetes mellitus, obesity and dyslipoproteinemia, which, in turn, are closely associated with the presence of metabolic syndrome.

Obesity. It is obesity that most often accompanies fatty degeneration of the liver, not associated with alcohol consumption. The presence of obesity is noted in 40-100% of cases of fatty liver with signs of hepatitis, and fatty liver with signs of hepatitis is detected in 9-36% of obese people. In addition, the type of obesity matters.

Hyperlipoproteinemia(hypertriglyceridemia, hypercholesterolemia, or both) is detected in 20-80% of cases of fatty liver with signs of hepatitis.

As a rule, with fatty liver with signs of hepatitis there are several risk factors.

In addition, risk factors include female gender, rapid weight loss, acute starvation, diverticulosis of the small intestine.

To hereditary diseases in which fatty degeneration of the liver develops, include Wilson's disease, homocystinuria, tyrosinemia, abetalipoproteinemia and hypobetalipoproteinemia, as well as spontaneous Weber-Christian panniculitis.

To fatty degeneration of the liver (especially with signs of hepatitis) can lead surgical interventions eg gastroplasty, jejunoileoanastomosis, biliopancreatic shunting.

Medicines and other substances. Fatty liver can cause a number of drugs and other chemical compounds. These include glucocorticoids, amiodarone, synthetic estrogens, tamoxifen, dietifen (a former cardiovascular drug), isoniazid, methotrexate, perhexilin, tetracycline, puromycin, bleomycin, dichloroethylene, ethionine, hydrazine, hypoglycine A, asparaginase, azacitidine, azauridine, azaserine . Constant contact with petroleum products at work is also a risk factor for fatty liver disease.

Symptoms and signs of liver dystrophy of non-alcoholic etiology

Symptoms. Most often, fatty degeneration of the liver is asymptomatic; sometimes patients complain of weakness, malaise, mild pain.

Physical examination. Almost three-quarters of patients have hepatomegaly, and a quarter have splenomegaly.

Laboratory research. In the absence of signs of hepatitis, laboratory studies are uninformative. In their presence, the main change in the biochemical parameters of liver function is an increase in the activity of ALT and AST. Usually these abnormalities are detected during the next medical examination or when you go to the doctor for another reason. There is no clear relationship between enzyme activity, on the one hand, and histological parameters and the severity of inflammation or fibrosis, on the other. The activity of AlAT is often higher than the activity of AsAT, which distinguishes fatty degeneration of the liver of non-alcoholic etiology from liver damage in alcoholism, when the activity of AsAT is higher than AlAT, and the activity of alkaline phosphatase can be slightly increased; serum bilirubin and albumin levels are usually normal. Elongation of the PV indicates decompensated liver failure. In some patients, a low titer of antinuclear antibodies is determined. However, there are no antimitochondrial antibodies, antibodies to the hepatitis C virus and HBsAg in the blood, and the serum levels of ceruloplasmin and α 1 -antitrypsin do not go beyond the normal range. There is often an increased serum level ferritin and increased transferrin saturation. In men, excess iron in the body is more pronounced than in women. In a third of patients with fatty liver with signs of hepatitis, a homozygous or heterozygous mutation in the HFE gene is detected, leading to the replacement of cysteine ​​in position 282 with tyrosine (a genetic marker of hemochromatosis). Liver fibrosis in the presence of this mutation is usually more pronounced.

Instrumental Research. Various non-invasive imaging modalities are used to diagnose fatty liver disease, including abdominal ultrasound, CT, and abdominal MRI. None of them is sensitive enough to detect liver inflammation and fibrosis. CT and MRI can detect only extrahepatic manifestations of cirrhosis and portal hypertension. Thus, these methods lack both sensitivity and specificity to reliably diagnose fatty liver with signs of hepatitis and determine its severity.

Liver biopsy- a method to confirm the diagnosis of fatty liver, with or without signs of hepatitis, to assess the activity of hepatitis and the degree of fibrosis. It is still unclear whether to perform a biopsy in all patients, since the results do not always affect the treatment. A biopsy is indicated in the presence of metabolic syndrome in patients and with constantly elevated, despite proper treatment, activity of liver enzymes.

Histological picture with fatty degeneration of the liver of alcoholic and non-alcoholic etiology is the same. Histologically, there are 3 stages of fatty degeneration of the liver. The first stage is fatty infiltration of hepatocytes without their inflammation and destruction. At the same time, fat accumulates in large drops in hepatocytes. The second stage is fatty infiltration of hepatocytes with signs of necrosis and inflammation. Fatty degeneration can be diffuse, and can be concentrated in the central zones of the hepatic lobules. There is always inflammation of the parenchyma of one degree or another; the cellular infiltrate in this case consists of neutrophils, macrophages and lymphocytes. Possible necrosis of hepatocytes with areas of devastation of the parenchyma; Mallory and Councilman's bodies may be found.

Iron deposits in hepatocytes are detected in 15-65% of patients. In fatty degeneration with signs of hepatitis in 35-85% of cases, fibrosis is found around individual hepatocytes, around sinusoids and portal tracts. The degree of fibrosis can vary greatly, from mild fibrosis around small veins and cell groups to severe, extensive fibrosis. In 7-16% of patients with fatty degeneration of the liver with signs of hepatitis, cirrhosis of the liver is detected at the first biopsy; histologically, it is indistinguishable from portal cirrhosis.

Causes of liver dystrophy of non-alcoholic etiology

The pathogenesis of fatty degeneration of the liver of non-alcoholic etiology is complex; apparently, it involves not only the liver, but also adipose, muscle and other tissues. Adipose tissue and insulin resistance play a leading role in the pathogenesis of the disease. It is known that fats are stored in the adipose tissue of the internal organs. With excess calorie content of food, the process of normal storage of fats is disrupted, which affects the rate of both lipogenesis and lipolysis and leads to an increased intake of free fats from adipose tissue into the blood. fatty acids. This, in turn, contributes to the accumulation of fats in the liver and striated muscles. At the same time, cytokines are released, which disrupts intracellular signaling when insulin binds to receptors and reduces insulin-mediated glucose uptake into muscles. At the same time, utilization is suppressed and production of glucose in the liver is stimulated. In addition, the availability of fatty acids in the liver stimulates their esterification and de novo lipogenesis. This increases the level of apoprotein B 100l VLDL. All this together leads to the accumulation and oxidation of fats in the liver, stimulates free radical oxidation, release of inflammatory cytokines and activation of Ito cells.

In general, although the specific mechanisms for the development of inflammation and necrosis of hepatocytes in fatty liver are not fully understood, it is most likely that two processes underlie at once: fatty infiltration of the liver, on the one hand, and free radical oxidation and release of pro-inflammatory cytokines, which cause progressive damage. liver, on the other. There is increasing evidence that the second mechanism of pathogenesis of fatty liver is mediated by adipokines released from adipose tissue.

Adiponectin is an adipokine with anti-inflammatory properties. A network of significant associations between low levels of adiponectin and an increase in the amount of fatty tissue in the internal organs, hyperlipoproteinemia and insulin resistance. Another adipokine, leptin, in contrast, has a pro-inflammatory effect. It promotes liver fibrosis by increasing expression of transforming growth factor beta and stimulating Ito cell activation. Pro-inflammatory cytokines produced by adipose tissue of internal organs also include PIO and IL-6. They play a leading role in the development of insulin resistance, as they disrupt intracellular signaling when insulin binds to receptors and promote inflammation. In addition, they have a negative effect on the immune system.

The course and prognosis of liver dystrophy of non-alcoholic etiology

The course of the disease depends on the histological picture. If there is no inflammation and destruction of hepatocytes, the disease usually does not progress, but in the presence of signs of hepatitis, approximately 20% of patients develop cirrhosis over time. In the presence of signs of hepatitis, fatty degeneration of the liver in most cases is considered a stable condition, but in a number of patients it progresses and leads to severe cirrhosis of the liver. Risk factors for cirrhosis are advanced age, the presence of metabolic syndrome, obesity, diabetes mellitus, and a higher activity of AST than ALT.

Treatment of liver dystrophy of non-alcoholic etiology

There is currently no treatment for fatty liver of non-alcoholic etiology; the available methods are aimed at eliminating the factors associated with the development of the disease. Patients are advised to lose weight and refrain from alcohol, correct hyperglycemia and hyperlipoproteinemia, cancel hepatotoxic drugs (glucocorticoids, estrogens, amiodarone, perhexilin). In severe obesity, surgical treatment is indicated. In a number of small, short-term studies, ursodeoxycholic acid, vitamin E, gemfibrozil, betaine (a metabolite of choline), acetylcysteine, and metformin improved liver biochemical parameters and reduced the severity of liver fatty infiltration, but had no significant effect on the activity of inflammation or the severity of fibrosis.

Thiazolidinedione derivatives (pioglitazone and rosiglitazone) increase the sensitivity of fatty and muscle tissue to insulin and improve glucose uptake by their cells.

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Normal life without fat is impossible. After intake with food, breakdown in the intestines, fatty acids are absorbed into the blood through the wall of the gastrointestinal tract and enter the liver for further processing.

The result of physiological restructuring is the formation of cholesterol, phospholipids necessary for the construction of cell membranes, the formation of hormones, participation in biochemical reactions.

Describing what is fatty liver symptoms and treatment, which have specificity, we note violations of the process of natural lipid utilization by hepatocytes with high fat accumulation (over 50%). Cytoplasm, vacuoles and some other intracellular organelles are saturated with fats, therefore they cannot perform their functions. Physiologically, the concentration of fatty acids inside the liver cells does not exceed 5%. With fatty degeneration, depending on the degree, this level is exceeded. The condition is irreversible, since the lack of conversion of lipids into energy or the deposition of excess in the subcutaneous adipose tissue leads to the death and degeneration of the hepatic parenchyma. Morphologically, with this nosology, small clusters (small-droplet form) or large deposits (large-droplet variety) appear inside the lysosomes.

The etiological and pathogenetic mechanisms of the disease have not been established, so it cannot be completely cured. Scientists have identified provoking factors leading to lipid degeneration:

• Alcohol abuse in men disrupts the processes of intracellular fat metabolism. Blocking of biochemical reactions leads to difficulty in the physiological utilization of compounds, and excess cholesterol accumulates in lysosomes;
• Mechanisms of biochemical transformation of lipids are also violated in diabetes mellitus. The cause of the condition is the lack of glucose necessary for metabolic reactions;
• Obesity leads to excess deposits in the lipid depot of subcutaneous adipose tissue. Excessive accumulation leads to a lack of excretion pathways, so intracellular infiltration occurs;
• Metabolic diseases (protein deficiency) disrupt the transport processes between the liver and other tissues;
• Poisoning with hepatotoxic poisons, drugs.

The described provoking mechanisms are the result of practical observations, but the pathogenetic links of nosology have not been proven by scientific research. The need for early treatment is due to the development of cirrhosis, when degeneration leads to the growth of rough cirrhotic scars. The more destruction, the higher the degree liver failure.

The main symptoms of fatty degeneration

Dystrophic syndrome with intrahepatic excess of fatty inclusions against the background of the use of ethyl alcohol has several synonyms "hepatosteatosis", "fatty liver", "steatohepatitis". Varieties reflect the diversity of the pathogenetic mechanisms of the process. Long term use ethanol is accompanied by inflammation, general degenerative changes, blockade of metabolic reactions.

Severe fatty degeneration symptoms, which can be traced clinically, has different morphological manifestations. When examining a biopsy specimen (a piece of tissue), several morphological varieties of dystrophic changes are observed.

In chronic viral and toxic hepatitis, not only lipids, but also proteins accumulate excessively in hepatocytes. Morphological examination reveals hyaline and hydropic granularity. The basis of its appearance is the destruction of the protein-lipid complex, which is part of the organelles.

The clinical symptoms of the form are due to the underlying disease:

• Soreness of the right hypochondrium;
• The appearance of linear expansion of blood vessels in the abdomen;
• Capillary asterisks (telangiectasias) all over the body.

Granular dystrophic changes appear against the background of oxidative phosphorylation, imbalance water-salt metabolism. The state is adaptive; it is compensatory aimed at restoring intracellular disorders that occur under the influence of viruses, bacteria, and the use of hepatotoxic drugs. medicines.

A classic sign of parenchymal fatty degeneration on histochemical examination is a single large vacuole filled with fatty inclusions, pushing the nucleus to the periphery.

On morphological examination, a yellowish, dull tissue is observed. With the degeneration of 50% of the cells, small oval-shaped vacuoles can be traced in some hepatocytes. Gradually, the clusters merge, and the cells die. The formation of fatty "cysts" leads to the formation of the following morphological conditions:

1. Segmental obesity lipid deposits are localized along the peripheral, central departments slices;
2. Disseminated hepatosis fat droplets are located in separate hepatic cells;
3. Diffuse obesity is characterized by the defeat of the entire lobule, but the process is reversible.

In diabetes mellitus, the manifestations of hepatosis are not specific. Fatty degeneration appears due to a violation of glycogen metabolism. The absence of insulin leads to a significant decrease in the reserves of this substance. Compensatory hepatocytes increase in size due to the deposition of glycogen. Empty nuclei are observed in tissue biopsy specimens, the number of vacuoles increases.

In diabetes, ten different types of glycogenosis are distinguished, among which fatty degeneration is not a frequent option, but can be seen in patients with obesity. Histochemical examination of the cells shows the accumulation of specific eosinophilic granules.

The described changes cause symptoms depending on the degree of liver failure. The absence of a clinic in the death of a small number of cells is due to the high restorative functions of the liver tissue. Only with extensive damage does liver failure develop, leading to symptoms:

• Yellowing of the skin and sclera in violation of bile secretion;
• Encephalopathy in case of poisoning with toxins, ammonia;
• Skin rashes, itching, increased concentration of bilirubin;
• Pain syndrome under the ribs on the right, an increase in the size of the liver, cirrhosis.

The extreme degree of insufficiency is hepatic coma, the accumulation of fluid inside the abdomen (ascites). The lack of a detoxifying function leads to a concomitant enlargement of the spleen, the development of renal failure. Any liver symptom is life-threatening if accompanied by an accumulation of toxins in the blood.

Treatment of dystrophic conditions of the liver

Alcoholic steatosis is considered by doctors as a dangerous condition leading to death. Nosology provokes dangerous complications with an average degree of degeneration (about 35% of the tissue).

The initial stages of the disease are stopped by the appointment of medications and the cessation of alcohol consumption, severe ones are characterized by high mortality. Approximately 5% of people die within a month when diagnosed with cirrhosis.

There are no specific drugs, therefore, symptomatic therapy is carried out with essential phospholipids (Essentiale), choleretic agents (ursodeoxycholic acid), ademetionine, silibinin. The rationality of prescribing other hepatoprotectors is low.

In alcoholic hepatitis of viral or bacterial origin, the effectiveness of treatment with hepatoprotective drugs is reduced. Steroidal anti-inflammatory drugs are used to reduce progression. The most common representative of prednisone.

The effectiveness of glucocorticoids in fatty degeneration has not been proven, but in practice the therapeutic effect is observed in the presence of 3 factors:

1. Increased portal pressure;
2. Lack of accumulation of nitrogen in the blood;
3. No stomach bleeding.

In practical literature, there are indications of the need for proper nutrition, which increases the survival of patients.

Principles of treatment of lipid degeneration of hepatocytes

• Elimination of risk factors;
• Medical elimination of complications;
• Long-term use of hepatoprotectors.

The main risk factor for the disease is obesity. Scientific research proved that a decrease in body weight by 10% leads to a decrease in the concentration of cholestasis enzymes (AlAt, AsAt).

European experts point to the need for a gradual reduction in body weight. Optimal balance Weekly elimination of more than one and a half kilograms increases the risk of gallstone disease, so care must be taken when dieting.

Features of diet food:

• Calorie content of the diet is not more than 1200 kcal per day;
• Restriction in food of saturated fatty acids;
• Carbohydrates are not more than 100 grams per day, but nutritionists can reduce this rate.

Daily exercise contributes to better absorption of fats, the accumulation of oxygen inside the muscle fibers, which increases the consumption of triglycerides.

In diabetes, obesity is caused by insulin resistance. The factor promotes the conversion of excess carbohydrates into fats. Correction of insulin tolerance is achieved by pharmacological agents thiazolidinediones, biguanides.

The elimination of elevated triglycerides is achieved by the regular use of medicines containing unsaturated fatty acids. Ursodeoxycholic acid products have been used for ten years and have shown high efficiency. The mechanisms of therapeutic activity have not been proven, but the elimination activity of the drug on the elimination of congestive changes in the gallbladder and intrahepatic ducts has been revealed.

In severe liver failure, the protein content in the diet is limited. The daily content is not more than 50 grams. To cleanse the gastrointestinal tract, laxatives and cleansing enemas are prescribed daily. Dysbacteriosis is eliminated by the introduction of antibiotics through a probe (ampicillin, kanamycin, tetracycline).

To neutralize ammonia, arginine is administered at a dose of 50-75 grams per day.

Psychomotor agitation is stopped by haloperidol.

Therapy of steatohepatitis with folk remedies

The doctor prescribes herbal decoctions. Only a specialist will be able to correctly determine the type of therapy, combination and dose of each agent. If the pathology is detected in a timely manner, choleretic preparations immortelle, milk thistle, rose hips help at an early stage.

Herbal preparations reduce the activity of the chronic process, but only with certain nosologies. Therapeutic effect herbal decoctions and infusions, when compared with medicines, appears later, so the combination of medicines with plants is rational. With low process activity, you can use a pumpkin:

• Choose a ripe fruit, cut off the top edge in a circle. Remove the central part, and add light honey to the resulting cavity. Close the fruit and store for 2 weeks in a dark place. Drain the resulting solution into a jar. For treatment, take 3 tablespoons of the drink three times a day in the morning, afternoon and evening.

The second useful folk recipe for eliminating hepatosis is walnuts. To prepare it, you need to chop the nuts. Pour them into a jar, add honey and alcohol in equal proportions. Infuse the medicine for 1 month in a dark room. Use three times a day for a teaspoon.

Milk thistle is part of the popular hepatoprotectors Karsil, Silibinin. You can use the plant at home. The recipe is prepared by mixing dandelion, nettle, birch leaves and milk thistle. Pour boiling water over 2 teaspoons of the mixture, leave for 15 minutes. Take 2 glasses of medicine daily.

Herbal infusions and decoctions, when compared with tablets, have a mild, gradual effect. To increase efficiency, it is recommended to combine folk remedies with diet, exercise.

Features of the diet for dystrophic damage to hepatocytes:

• Avoid spicy, spicy foods;
• Give up fatty meat, fish, broths;
• Choose your products carefully in the store. They should not contain dyes, stabilizers, fragrances, anti-caking additives;
• Don't take too many medications unnecessarily;
• Useful oatmeal, buckwheat.

European scientists point to the fat-soluble effect of apricot kernels. For steatohepatitis, eat 5 pieces daily (but no more). The central content of the fruit is saturated with vitamin B15, which is involved in the breakdown of lipids.

What actually is liver dystrophy?

Liver dystrophy, steatosis, lipodystrophy or hepatosis - all these terms refer to the same chronic disease in which liver cells are gradually replaced by fat.

It should be noted that this fatty liver is quite well known, as many common factors can trigger the development of this disease. Liver hepatosis - this is the very initial stage of development of the most popular ailment in the modern world - cirrhosis.

Causes of liver dystrophy

Steatosis, as a rule, occurs due to such reasons:

• Intoxication with various hepatotropic poisons (poisonous mushrooms, yellow phosphorus, etc.);
• Diabetes;
• Frequent drinking of alcoholic beverages;
• Abuse of food products that contain a huge amount of preservatives and fats;
• Obesity or prolonged fasting;
• Parenchymal protein dystrophy;
• Uncontrolled use of certain drugs;
• Drug addict;
• Tumors of the pituitary gland.

Classification

First, based on changes in the structure of steatosis, several types of hepatic dystrophy are noted:

• Zonal diffusion. It is characterized by local fatty formations in specific areas of the liver. Clinical manifestations are quite strong.
• Disseminated widespread dystrophy. Fat formations are nearby and significantly compacted in the human liver. Symptoms: general weakness and discomfort in the right hypochondrium.
• Disseminated focal dystrophy. It is characterized by rare, dotted and inconsistently located fatty formations. Symptoms are not expressed.
• diffuse dystrophy. This type of liver dystrophy is characterized by an abundant amount of fatty inclusions, which can be in place of the entire liver or in one of its parts.

In addition, renal dystrophy can be divided into several stages depending on the period of development of the disease:

• Stage one - small fatty formations can be found in the liver cells, which have almost no effect on the functions of hepatocytes;
• Stage two - the beginning of destruction of the liver, that is, hepatocytes, is observed, and small inflammations or cysts can form near the dead cells.
• Stage three - liver changes can no longer be prevented, some parts of the liver die off, as a result, cirrhosis of the liver develops.

What is dangerous liver dystrophy?

Real liver dystrophy serious illness, which in no case can be missed or not paid due attention to specific symptoms.

Therefore, if a person with steatosis does not want to start treatment, then later he can expect:

• Increased risk of cardiovascular disease and diabetes;
• chronic hepatitis;
• Fibrosis;
• cirrhosis;
• Liver necrosis.

To avoid such horrific consequences, you need to listen to your body and be aware of the signs of liver dystrophy.

Symptoms and signs of fatty liver

Patients suffering from metabolic disorders in the liver cells often do not have complaints about their physical condition, since in the initial stages of liver hepatosis proceeds painlessly and outwardly imperceptibly.

The disease goes away over a fairly long period. Over time, the patient begins to experience discomfort in the form of:

• dull pain in the right hypochondrium;
• constant weakness of the body;
• headache;
• rapid exhaustion during activities requiring physical activity;
• dizziness.

The most rare case is liver dystrophy with clearly presented clinical symptoms. Of these, we can distinguish:

• sharp weight loss;
• sharp and unbearable pain;
• bloating.

Methods for diagnosing liver dystrophy

There are two ways to detect lipodystrophy:

• Blood chemistry. This analysis easily indicates an increase in the number of specific types of proteins (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), which have the property of increasing during liver dystrophy.
• Abdominal ultrasound. It immediately detects the echo signs of hematosis and allows you to determine the exact diagnosis.
• liver tests.

Treatment of the disease

Before talking about drugs that help relieve symptoms and cure the disease, it should be noted that without following a certain diet, any medication will not work to its full potential and will not help as we would like. Often, one diet therapy is enough for recovery.

Only in the event that proper nutrition recommended by the doctor does not help get rid of liver dystrophy should medical methods treatment. From a wide selection of medicines in getting rid of hepatosis of the liver, drugs can be used that contribute to:

• breakdown of fats
• removing it from the body.

It should be emphasized that it is necessary to repeat this course of treatment repeatedly, several times a year.

A sick person whose condition is stabilized with the use of drugs also needs:

• vitamin therapy,
• the use of hepatoprotectors and antioxidants that improve the functioning of the liver, perform a protective function in relation to cell membranes,
• immunomodulatory drugs that strengthen the body.

Also, if the patient suffers from this disease simultaneously with obesity, then it is recommended to him:

• gradually reduce weight (about 1-1.5 kilograms per week),
• do gymnastics,
• various exercises aimed at burning excess subcutaneous reserve reserves.

What specific physical activity is worth doing, you must definitely find out from a specialist in the field of medicine.

Diet for sickness

Nutrition for fatty liver must be carefully considered so that the daily diet includes maximum amount useful products rich:

The amount of fat should be reduced to a minimum.

The basic rules of the diet for lipodystrophy:

• Eat at least one hundred grams of protein per day;
• Completely abandon alcoholic beverages;
• 2/3 proteins must be of animal origin;
• Do not eat a large amount of food at a time, that is, eat fractionally;
• Do not consume more than twenty percent of fat from total food per day;
• Reduce consumption of preservatives and purine substances.

It is necessary to consider in more detail the diet and the necessary foods for hepatosis of the liver.

• boiled,
• steamed,
• baked in the oven (for example, fish or meat).

You also need to use, and quite often, cottage cheese and sour cream with a small content:

It is necessary to refuse saturated vegetables or meat broths. It is important to avoid:

• fatty meats and fish,
• mushrooms,
• tomatoes,
• bean products,
• raw onion and garlic
• various smoked and canned food.

It is important to drink at least a liter of fluid per day, for example:

• clean drinking water,
• herbal decoctions,
• milk, etc.

• vegetable salads with olive oil,
• vegetable or milk soups,
• boiled carrots,
• cabbage,
• various cereals (preferably oatmeal, buckwheat, semolina and rice).

Prevention

The most important fact in the prevention of the disease is the observance of proper nutrition, which includes the necessary components that are rich in vitamins and trace elements useful for the liver.

You also need to regularly undergo specific medical checks, which are carried out in the initial periods of the development of fatty hepatosis. This will undoubtedly help prevent the further development of the disease. Especially in the later stages, it is much more difficult to correct the situation, and sometimes it is already impossible.

The question of what liver dystrophy is is of interest to many patients who are faced with a similar diagnosis. As doctors explain, this is a coma that arose as a result of a deep inhibition of the functionality of the liver. Liver dystrophy (LP) is provoked by various diseases with a chronic course, in which the bile-forming gland is damaged.

The liver is unique organ, which plays an important role in lipid metabolism. Triglycerides from food enter the intestines, where they are broken down by enzymes, then they enter the bloodstream. Together with the blood, fats enter the liver, where they are converted into various substances necessary for the normal functioning of the body.

With excessive accumulation of lipids, fatty degeneration occurs, in which the concentration of fats in the organ increases 10 times. The content of triglycerides can reach more than 50% of the total volume of the gland, and normally this figure does not exceed 5%.

Causes of the disease

In most cases, DP occurs due to the fact that the response of hepatocytes (liver cells) to the effects of insulin decreases. Insulin is a hormone that transports glucose to the body's cells. Due to the fact that hepatocytes do not respond to the action of insulin, there is a lack of glucose in the liver. Glucose is very important for the normal functioning of liver cells, therefore, with a deficiency of the substance, they begin to die. Affected cells are replaced by adipose tissue over time. As a result, there are disorders of the functionality of the liver.

Hepatocytes become immune to the effects of insulin due to genetic pathologies or metabolic disorders. The absence of a normal reaction of liver cells may be due to immune aggression in relation to insulin.

Other causes of DP:

• The presence of bad habits (alcohol, smoking).
• Excessive consumption of fatty foods.
• Passive lifestyle.

All these factors negatively affect the state of the liver, provoking irreversible changes.

Take this test and find out if you have liver problems.

Symptoms of liver dystrophy are most often mild, and the patient may simply not pay attention to them. As a rule, patients do not complain of any disturbing phenomena. The pathological process develops slowly, and the clinical picture is not clear.

However, over time, the following symptoms appear:

• dull pain on the right under the ribs;
• hepatomegaly;
• nausea;
• eruption of vomit;
• stool disorders.

In rare cases, dystrophic changes in the gland are accompanied by severe pain in the abdomen, a sharp decrease in weight, itching, yellowing of the skin and mucous membranes.

Usually, the symptoms of DP are divided according to the type of pathology. With toxic liver dystrophy with widespread necrosis (tissue death) of the parenchyma of the organ, an increased growth of hepatocytes is observed, which are located next to the portal vein of the lymph nodes and spleen. DP is manifested by multiple bleeding in the skin, internal and serous membranes. In addition, there are necrotic and dystrophic changes in tissues that affect the heart muscle and pancreas.

Liver lipodystrophy

Fatty degeneration of the liver (fatty hepatosis) occurs due to the replacement of hepatocytes with fat cells. With hepatosis, fatty deposits accumulate, which look like drops on the liver.

The cause of fatty degeneration is the pathology of the gallbladder, its duct or intestinal tract. ZhDP (fatty liver) can provoke the following diseases:

• Severe obesity.
• Diabetes mellitus type 2 malabsorptive and maldigestive syndrome.
• Excessive consumption of alcoholic beverages.
• Taking corticosteroids, tetracyclines, estrogens, NSAIDs.

Lipodystrophy often occurs against the background of hepatitis with a chronic course (especially with type C hepatitis).

A macropreparation characteristic of IDP: hepatomegaly, the surface of the liver is smooth, the consistency is dense or flabby, the front edge of the organ is rounded, clayey, yellow or yellow-brown.

Toxic DP

Toxic liver dystrophy (TDP) is manifested by extensive rapidly developing necrotic processes that affect the structure of the liver. Usually, the pathology has an acute course, but sometimes it becomes chronic, provoking liver dysfunction.

Massive necrosis develops under the influence of toxins that are found in foods, such as mushrooms. Such poisoning occurs under the influence of external factors. Toxic degeneration of the liver may occur due to endotoxicosis. Such conditions include toxicosis in pregnant women, hyperthyroidism (an excess of thyroid hormones). Often TDP occurs against the background of hepatitis, then dystrophy is a symptom of its fulminant form.

Toxic liver dystrophy is accompanied by hepatomegaly, flabbiness or density of liver tissues, the organ turns yellow. If left untreated, the size of the gland decreases, the capsular membrane becomes wrinkled. The organ acquires a gray color and outwardly resembles a clay mass. For 3 weeks, the gland continues to decrease, its color changes to reddish. Over time, the reticular stroma of the liver begins to become exposed, in which dilated, blood-filled capillaries are visible. Liver cells are preserved only in certain areas of the lobules. This is how red dystrophy manifests itself.

Chronic TDP is a rare condition in which the patient is more likely to die due to rapidly progressive liver dysfunction.

Acute hepatic dystrophy

Acute liver dystrophy (ALP) is most often a complication of hepatitis A, which occurs in an unfavorable form. Separately, pathology develops quite rarely.

The disease is little studied, so doctors cannot accurately answer how it develops. It is also not clear whether there is a connection with the strength of the virus or if some other factors influence the pathological progress.

Aggravated parenchymal hepatitis is provoked by the following diseases: brucellosis, tick-borne relapsing fever, syphilis. In addition, the likelihood of complications of the disease during pregnancy or after an abortion increases. These factors adversely affect liver cells, provoking severe dystrophy.

Symptoms of ADP at an early stage resemble those of hepatitis A, so there is a risk of a significant deterioration in the patient's condition. The pathological process affects the nervous system, as a result, brain activity is disturbed. The disease is manifested by delirium, anxiety, convulsions, eruption of vomit. In this case, the patient must be urgently hospitalized in a psychiatric department.

The reverse reaction of the nervous system is also possible: indifference to everything that happens, depression, lowering of vitality, craving for sleep. Symptoms continue to grow, the patient loses consciousness, hepatic coma develops.

Alcoholic dystrophy

This type of dystrophy occurs due to excessive drinking for 10-12 years. Ethyl alcohol penetrates the body and poisons hepatocytes.

Alcoholic liver dystrophy (ALD) can occur against the background of hepatosis, cirrhosis, alcoholic hepatitis. Most often, it is hepatosis that causes gland dystrophy due to excessive drinking. If the patient refuses strong drinks at an early stage of hepatosis, then the condition of the liver improves after 2-4 weeks. In most cases, ADP does not show severe symptoms.

• Enlargement of the parotid salivary glands.
• Flexion contracture of fingers.
• Redness of the palms, and sometimes of the feet.

The easiest way to identify the disease is through laboratory tests and biopsy.

Diffuse dystrophy

Diffuse dystrophic changes in the liver parenchyma is a very dangerous condition. It occurs as a result of the fact that hepatocytes are not able to neutralize the toxins that enter the body. Liver cells cannot cope with large-scale poisoning, as a result, the parenchymal tissue begins to die, and fibrous connective tissue grows in the damaged areas. diffuse changes become more and more pronounced, and this threatens with liver failure. This is how diffuse DP manifests itself.

Degenerative dystrophic changes in the liver most often provoke a similar process in the pancreas. This is due to the fact that these organs are closely related to each other.

Focal dystrophy

Focal liver dystrophy (OLD) is difficult to detect using laboratory tests. This is quite difficult even despite the fact that there are functional disorders of the gland. Symptoms of the disease depend on the causes that provoked it.

With focal transformation, individual parts of the liver are affected

Focal DP, which arose as a result of excessive consumption of alcoholic beverages, is manifested by shortness of breath, loss of appetite, sometimes there is pain on the right under the ribs. These signs become more pronounced when the patient moves.

The most effective methods for detecting pathology are magnetic resonance and computed tomography.

Granular dystrophy

This is the most common type of protein DP. Granular liver dystrophy (GLD) is characterized by a violation of the colloidal properties of the cytoplasm of the cell, in which a grain-like protein appears.

ZDP provoke the following factors:

• Inadequate feeding of the newborn.
• Intoxication.
• Infectious diseases.
• Violation of blood circulation and lymph circulation.
• Causes that provoke oxygen starvation of tissues.

Over time, with ZDP, protein metabolism in cells changes, the cytoplasm becomes cloudy, swells. Due to damage to the liver tissue, the bile-forming gland becomes flabby, its blood supply is disturbed.

It is important to distinguish the signs of PDD from the natural processes of protein synthesis in cells, in which granularity appears in the protein.

This pathology is reversible, but it has a severe course. Therefore, there is a possibility of degeneration of the ZDP into intracellular hyalinosis, dropsy or necrosis.

Protein DP

Protein degeneration of the liver (BDP) develops as a result of protein metabolism disorders and occurs against the background of amyloidosis, hyaline or granular degeneration.

In amyloidosis, amyloid (a protein-polysaccharide complex) is formed and deposited in the tissues.

With BDP, the liver acquires a granular structure, since drop-shaped and granular formations appear in the protoplasm of cells. They combine and fill the intracellular space. Protein structures become denser, the work of gland cells is disrupted, as a result, liver tissues die.

hydropic dystrophy

Hydropic degeneration of the liver (HDP, vacuole degeneration) is accompanied by the appearance of vacuoles (a cavity in the cell cytoplasm), which are filled with cytoplasmic fluid. In pathology, the cells of the parenchyma of the organ increase, which is accompanied by wrinkling or vacuolization of the nucleus.

As the disease progresses, the liver overflows with fluid, and its ultrastructures undergo decomposition. Affected cells look like containers filled with water and are a continuous cavity with a bubble-shaped nucleus. This is how GDP manifests itself.

Changes can only be detected using a microscope, since the liver does not change externally.

Yellow dystrophy of the liver

IDP is often a complication of pregnancy. Pathology occurs as a result of acute poisoning of the body against the background of infectious diseases. Jaundice in a future mother can be provoked by DP, inflammation of the gallbladder, stones in the liver. In addition, the disease can occur independently due to autointoxication of the body (toxicosis).

IDP is a severe degree of toxicosis in expectant mothers. Pathology occurs due to severe poisoning by metabolites. The disease is manifested by yellow staining of the skin and mucous membranes, profuse vomiting, clouding of consciousness, delirium and increased excitability. In addition, there is a possibility of a hemorrhagic rash (hemorrhage under the skin), the volume of urine decreases, it contains cyrosine and lecithin, and hepatic dullness decreases. If left untreated, the patient dies within a few days.

Diagnosis of the disease

Diagnosis of DP is difficult, since traditional laboratory tests are ineffective, despite the dysfunction of the gland.

The disease is usually asymptomatic, the only sign of pathology is hepatomegaly. The echogenicity of the liver during ultrasound remains within the normal range, and sometimes even increases, so it is quite difficult to distinguish DP from cirrhosis or fibrosis. Ultrasound examination reveals areas with increased echogenicity. Areas of low echogenicity can be identified using CT. Computed and magnetic resonance imaging are the most informative methods for recognizing DP. With their help, it is possible to determine focal hepatosis of the liver.

A biopsy is performed to detect pathology. With a pathomorphological examination of tissues, the doctor will determine the excess accumulation of fat.

Treatment Methods

Many patients wonder how to treat DP. Treatment consists in observing the following rules:

• Diet.
• Treatment of concomitant diseases.
• Restoration of the structure of the liver.
• Consolidation of results.

As a rule, doctors prescribe the following medications:

• hepatoprotectors,
• synthetic antioxidants,
• statins.

Hepatoprotectors stabilize cell membranes, restore their integrity. They improve the metabolism of bilirubin, fatty acids, proteins. For this purpose, Karsil, LIV-52, Hofitol, Essentiale, etc. are used.

Choleretic agents improve the secretion of bile, normalize its composition, and reduce congestion. With DP, Allohol, Holosas are prescribed.

Statins correct the lipid profile of the blood. With their help, the penetration of fats into the bloodstream is reduced, and excess cholesterol is excreted from the body.

If hepatic encephalopathy is observed with DP, then the patient is urgently hospitalized. The patient is administered drugs by the parenteral method, limit the amount of proteins. In addition, drugs are prescribed that correct the acid-base state. Acidosis is often manifested in DP; sodium bicarbonate is administered to prevent it. Antibacterial agents suppress the intestinal microflora.

With functional disorders of the liver, extracorporeal enterosorption is prescribed. Glucocorticoids are used to support metabolism.

To reduce the load on the liver and speed up recovery, it is necessary to revise the menu. The diet should include foods containing vitamins, fiber, pectins, carbohydrates. The daily norm of fat is 70 g. It is important to exclude foods that contain cholesterol and limit salt intake.

When treating DP, it is forbidden to drink coffee, tea, soda and alcohol.

Patients are allowed to eat soups with vegetables, cereals or based on skimmed milk. It is recommended to consume fresh, boiled, baked or steamed vegetables. Occasionally, you can enjoy low-fat ham, hard cheese (not spicy), scrambled eggs from proteins or boiled eggs (no more than 1 egg per day). You can also include buckwheat, oatmeal, semolina and rice in your diet. In addition, sour-milk products with a low percentage of fat content are not prohibited.

Preventive measures and prognosis for DP

To prevent the disease, you should avoid the factors that provoke it. It is important to give up bad habits: alcohol, smoking, excessive consumption of food (especially fatty), passive lifestyle.

To maintain a high vitality and prevent the development of pathological processes, you should eat right, limit the use of hot, fried foods, smoked, canned foods. In addition, the patient should constantly monitor the weight and maintain it within the normal range.

In order for the liver to function normally, you should exercise daily: race walking, jogging, swimming, etc.

If DP is not accompanied by other diseases, then the prognosis is favorable. With dystrophy with pronounced complications, immunity decreases, the body becomes vulnerable to infectious diseases. Pathogenic microbes enter the body, as a result, the patient tolerates anesthesia, surgical procedures worse and recovers after them longer.

If the patient leads the wrong way of life and does not engage in treatment, then the pathology progresses. Then the probability of small-nodular cirrhosis, non-alcoholic steatohepatitis increases.

If during the treatment of DP the patient refused alcohol, follows a diet and the doctor's recommendations, then most likely he will be able to maintain his working capacity and improve his general condition.

Based on the foregoing, liver dystrophy is a dangerous disease with a chronic course, which occurs as a result of deep inhibition of the functionality of the gland. In order to prevent dangerous complications, you must be attentive to your health and, if suspicious symptoms occur, contact a hepatologist or gastroenterologist. If necessary, the doctor will prescribe an ultrasound, MRI or CT scan, as well as a biopsy. The patient must strictly follow the recommendations of doctors and lead a healthy lifestyle.

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Hepatosis is a collective name liver diseases, characterized by a violation of metabolic processes in hepatocytes ( liver cells) and, as a result, damage to the structure of cells and intercellular substance, metabolic disorders and organ function ( dystrophy). According to the type of metabolic disorders, fatty and pigmented ( pigment - a substance that gives color to body tissues) hepatosis.

Steatosis is a pathological deviation from the norm) a condition in which fats accumulate in the cells of the body.

Fatty hepatosis () is the most common reversible chronic process, at which in hepatocytes ( liver cells) there is an excessive accumulation of lipids ( fat). Gradually, in the liver, an increasing number of cells are replaced by fat cells, which form adipose tissue. As a result, the liver increases in size, its color changes to yellowish or dark red, cells die, fatty cysts form ( pathological cavities in a tissue or organ with contents), organ functions are impaired. Very often fatty infiltration ( accumulation in tissues of substances that are not normally detected) of the liver goes into fibrosis ( reversible process of replacing normal tissue with coarse scar tissue locally or throughout the organ), and then to cirrhosis ( irreversible progressive liver disease in which healthy tissue is replaced by scar tissue).

Fatty liver is a fairly common disease. On average, it affects from 10% to 25% of the population in different countries, among them 75% - 90% are obese and diabetic people. In Russia, every fourth person suffers from fatty hepatosis.

Liver anatomy

The liver is a vital unpaired organ, the largest gland ( an organ that produces specific chemicals) in the human body. It is located on the right in the upper part of the abdominal cavity under the diaphragm. Sometimes there is also a left-sided location of the liver, which must be taken into account during ultrasound ( ultrasound) organ. The liver has an irregular shape, reddish-brown color, weight 1300 - 1800 grams in an adult. It consists of two lobes - the right lobe ( larger in size) and left ( smaller). To facilitate the determination of the liver zone during surgical and diagnostic procedures The liver is divided into 8 segments. Segment - a pyramidal section of the liver adjacent to the hepatic triad, which consists of a branch of the portal vein, a branch of the proper artery of the liver and a branch of the hepatic duct.

The cells that make up the liver are called hepatocytes. The structural and functional unit of the liver is the hepatic lobule. It has the shape of a prism and consists of liver cells ( hepatocytes), vessels and ducts. In the center of the hepatic lobule is the central vein, and on the periphery of the bile ducts, branches of the hepatic artery and hepatic vein. Hepatocytes produce up to one liter of bile ( liquid consisting of bile acids, water, cholesterol, inorganic compounds and involved in the process of digestion) per day. Bile acids contribute to the breakdown and absorption of fats, stimulating small intestinal motility, as well as the production of gastrointestinal hormones. By intrahepatic small capillaries (channels) bile enters the larger bile ducts, and then into the segmental ducts. The segmental ducts merge into the right ( from the right lobe of the liver) and left ( from the left lobe of the liver) bile ducts, which are combined into a common hepatic duct. This duct joins with the duct of the gallbladder and forms the common bile duct, from which bile enters directly into the lumen of the duodenum.

The liver receives nutrients and oxygen from the blood from its own hepatic artery. But, unlike other organs, venous blood, saturated with carbon dioxide and deprived of oxygen, also enters the liver.

There are two systems of veins in the liver:

• Portal. The portal vein system is formed by branches of the portal ( gate) veins. Portal vein - large vessel, into which blood enters from all unpaired organs of the abdominal cavity ( stomach, small intestine, spleen), and from the portal vein to the liver. In the liver, this blood is cleansed of toxins, waste products and other substances harmful to the body. Blood cannot get out of the digestive tract ( gastrointestinal tract) into the general circulation without being "filtered" by the liver.
• Cavalry. It is formed from the totality of all veins that carry blood from the liver. This venous blood is saturated with carbon dioxide and deprived of oxygen due to the gas exchange between the liver cells and blood cells.

The main functions of the liver are:

• Protein exchange. More than half of the proteins main building material of the body), which are produced in the body per day, are synthesized ( formed) in the liver. The main blood proteins are also synthesized - albumins, blood coagulation factors ( act to stop bleeding). The liver stores amino acids ( main structural components of proteins). In case of insufficient intake or loss of protein, the liver begins to produce ( synthesize) proteins from stocks of amino acids.
• lipid metabolism. The liver plays an important role in fat metabolism. She is responsible for the synthesis production) cholesterol ( ) and bile acids ( prevent fat droplets from sticking together, activate substances that break down fats into simpler components). One of the functions is also the storage of fat. Maintains a balance between the metabolism of fats and carbohydrates. With excess sugar main source of energy The liver converts carbohydrates into fats. In case of insufficient intake of glucose ( Sahara) The liver synthesizes it from proteins and fats.
• carbohydrate metabolism. Glucose in the liver sugar) is converted to glycogen and deposited ( is stocking up). In the event of a lack of glucose, glycogen is converted back to glucose and provides the body with the necessary energy.
• pigment exchange ( pigment - a substance that gives color to tissues and skin). When erythrocytes are destroyed red blood cells) and hemoglobin ( iron-containing protein - oxygen carrier) free bilirubin enters the blood ( bile pigment). Free ( indirect) bilirubin is toxic to the body. In the liver, it is converted to bound ( straight) bilirubin, which has no toxic effects on the body. Then direct bilirubin is excreted from the body, and a small part of it enters the blood again.
• Vitamin exchange. The liver is involved in the synthesis ( development) vitamins and absorption of fat-soluble vitamins ( A, D, E, K). With an excess of these vitamins, the liver stores them in reserve or removes them from the body. With a deficiency, the body receives them from the liver reserves.
• barrier function. Is one of the most important functions liver. Its purpose is to neutralize, detoxify substances that are formed in the body or come from environment.
• digestive function. This function consists in the constant production of bile by hepatocytes ( liver cells). Bile enters the gallbladder and is stored there until needed. During meals, bile enters the intestinal lumen, thereby contributing to the digestion process. Bile acids promote emulsification ( mixing with water) fats, thereby ensuring their digestion and absorption.
• enzymatic function. All biochemical reactions are accelerated by special substances - enzymes. These enzymes are found in the liver. And when the body urgently needs any substances ( e.g. glucose) liver enzymes accelerate the processes of their production.
• immune function. The liver is involved in the maturation of immune cells ( Immunity is the sum total of the body's defenses.), as well as in many allergic reactions.
• excretory function. Together with bile, the liver removes metabolic products, which then enter the intestines and are excreted from the body.

Interesting Facts

• The liver ranks second in mass among all organs ( average weight - 1500 g.).
• 70% consists of water.
• In one hour, about 100 liters of blood passes through the liver and, accordingly, more than 2000 liters per day.
• The liver performs more than 500 functions every day.
• The liver could function up to 300 years due to its unique property - the ability to self-repair.
• More than 25% of liver diseases are caused by alcohol consumption.
• About a million chemical reactions take place in liver cells per minute.
• Currently, more than 50 liver diseases are known.
• ).
• More than 11,000 transplants are performed annually ( transplant surgeries) liver.

Forms and stages of hepatosis

To formulate an accurate diagnosis, describe the degree of liver damage and the prevalence of the pathological process, there are classifications of hepatosteatosis according to various criteria. This provides the doctor with a more detailed understanding of the patient's illness, even if the doctor is not familiar with the patient's history ( medical history).

Steatosis can be:

• Alcoholic- pathological changes in the liver against the background of chronic alcohol intake.
• non-alcoholic(non-alcoholic steatohepatosis - NASH, non-alcoholic fatty disease - NAFLD) - fatty degeneration of the liver, which occurs with the wrong lifestyle, diet, various concomitant diseases.

In fatty hepatosis, there are:

• Stage I - minimal obesity. Droplets of fat accumulate in liver cells without damaging hepatocytes.
• Stage II - moderate obesity. Irreversible processes occur in cells, leading to their destruction and death. Their contents enter the intercellular space. Cysts are formed pathological cavities).
• Stage III - severe obesity. pre-cirrhotic state ( cirrhosis is an irreversible chronic process of replacing liver tissue with scar tissue).

According to the degree of damage to the structure of the liver, there are:

• Focal disseminated - accumulation of small areas of fat in various parts of the liver with an asymptomatic course.
• Expressed disseminated - the accumulation of fatty drops in large quantities in various parts of the liver with the manifestation of symptoms.
• Zonal – location of lipids ( fat) in various parts of the hepatic lobules ( structural and functional units of the liver).
• diffuse - Liver damage, in which the accumulation of fat occurs evenly throughout the entire lobule of the liver with the onset of symptoms.

By etiology(the cause of the disease)steatosis happens:

• Primary- congenital intrauterine metabolic disorder.
• Secondary- a metabolic disorder that appears as a result of concomitant diseases, malnutrition and lifestyle.

According to the microscopic picture of hepatosis, that is, pathological changes in cellular level, allocate:

• Small droplet obesity- simple obesity, in which pathological processes are already occurring, but without damage to the liver cells.
• Large droplet obesity- a more severe course of the disease, in which the structure of hepatocytes ( liver cells) is significantly damaged, which leads to their further death ( necrosis).

Morphologically(structure and shape of cells)allocate:

• 0 degree steatosis- locally in hepatocytes accumulations of fat appear.
• I degree steatosis- accumulations of lipids ( fat) increase in size and merge into foci with damage to liver cells - up to 33% of the affected cells in the field of view.
• II degree steatosis- accumulations of lipids of various sizes, which are distributed over the entire surface of the liver - 33 - 66% of liver cells ( small droplet, large droplet intracellular obesity).
• III degree steatosis- the accumulation of fat occurs not only in the cells, but also outside them with the formation of a cyst ( pathological cavity in the tissue), destruction and death of cells - more than 66% of the affected liver cells in the field of view.

Causes of liver steatosis

Many factors lead to the development of pathological changes in the liver and disruption of its functions. Liver health is affected by lifestyle, diet, medication, heredity, concomitant diseases, viruses. Often, not one specific cause leads to steatosis, but a combination of several. Therefore, to establish the etiology ( causes) of illness, the doctor should ask the patient in detail about his bad habits, diseases, medicines that he has taken or is taking, and so on. A correctly identified cause will allow not only to eliminate the factor itself and its pernicious influence on the health of the liver, but also to prescribe an effective treatment. This will significantly increase the patient's chances of recovery.

The causes of steatohepatosis are combined into two large groups:

• causes of alcoholic steatohepatosis;
• causes of non-alcoholic steatohepatosis.

Causes of alcoholic steatohepatosis

Alcohol intake is the only cause of alcoholic steatosis . The accumulation of fat droplets in the liver cells occurs under the action of ethanol ( pure alcohol, the content of which is indicated as a percentage on alcoholic products) in chronic alcoholism or excessive alcohol consumption. Large doses are considered 30 - 60 grams of ethanol per day. Under the influence of alcohol, liver cells die faster than they are renewed. During this period, excess scar tissue forms in the liver. The supply of oxygen to the cells is significantly reduced, as a result of which they shrivel and die. The formation of protein in hepatocytes is reduced, which leads to their swelling ( due to the accumulation of water in the cells) and hepatomegaly ( abnormal enlargement of the liver). Increase the risk of developing alcoholic steatosis heredity, protein deficiency in food, hepatotropic ( peculiar to the liver) viruses, concomitant diseases, obesity and others.

Causes of non-alcoholic steatohepatosis

In addition to alcohol abuse, a number of other factors can lead to steatosis.

Causes of non-alcoholic steatosis

Risk factors are:

• female;
• age over 45;
• body mass index ( BMI is the ratio of weight in kilograms to the square of height in meters) more than 28 kg/m 2 ;
• hypertonic disease ( high blood pressure);
• diabetes ( a disease caused by a lack of insulin, a pancreatic hormone responsible for lowering blood sugar levels);
• ethnicity - Asians are most susceptible to the disease, and African Americans are at a lower risk;
• burdened hereditary history - the presence of a disease in relatives or factors transmitted genetically.

Symptoms of liver hepatosis

Steatohepatosis can be asymptomatic for a long time. It is detected more often by chance during annual medical examinations and diagnostic procedures for other diseases. In the initial stages of hepatosis, the patient does not present any complaints. With the progression and involvement of an increasing area of ​​the liver in the pathological process, the functions and structure of the organ begin to be disturbed. This is what causes the symptoms.

Symptoms of hepatosis

Stage of steatohepatosis	Symptom	Development mechanism	Manifestation
I stage	Asymptomatic	–	–
II stage	Pain syndrome (constellation of symptoms)	The liver has no pain receptors ( proteins that receive information from the stimulus and transmit it to the analyzer center). Pain occurs when the liver increases in size and stretches its capsule ( membrane that covers the liver).	Discomfort, heaviness in the right hypochondrium, appearing regardless of food intake. Feeling of squeezing of organs, pain when probing the liver.
	Weakness	Weakness and malaise are caused by a lack of energy due to a disturbance in nutrient metabolism.	Body aches, constant feeling of fatigue.
	Nausea (persistent or paroxysmal)	It develops due to indigestion associated with a lack of bile-forming liver function. With a lack of bile, the process of digesting fats is disrupted, as a result of which food can stagnate in the digestive tract, which leads to nausea.	Discomfort, discomfort in the stomach and esophagus. Aversion to food, smells. Increased salivation.
	Decreased appetite	Many functions of the liver associated with metabolism are disturbed, which leads to an incorrect assessment of the body's supply of nutrients and the need for them, stagnation of food in the gastrointestinal tract. Also, appetite decreases with nausea.	Lack of hunger, a decrease in the number of meals and its volume.
	Decreased immunity (the body's defenses)	The liver plays an important role in maintaining immunity. Her disease leads to a violation of this function.	Frequent colds, exacerbation chronic diseases, viral infections, inflammatory processes.
III stage	Jaundice of the skin and visible mucous membranes	An increase in the blood of bilirubin, a yellow pigment, as a result of the inability of the liver to bind it and remove it from the body.	Skin, mucous membranes of the oral cavity, sclera of the eyes ( tough outer shell) acquire a yellow color of varying intensity.
	Itching	With impaired liver function, bile acids are not excreted in the bile, but enter the bloodstream. This leads to irritation of the nerve endings on the skin and the appearance of itching.	Severe burning of the skin. Intense itching, more common at night.
	Skin rashes	The detoxification function of the liver is impaired. Under the influence of toxins and waste products of the body, a rash appears. Impaired hemostasis ( a complex biosystem that maintains blood in a liquid state under normal conditions, and in case of violation of the integrity of the blood vessel, it contributes to stopping bleeding), increased vascular fragility.	Small spots on the skin all over the body. Hemorrhagic rash ( small hemorrhages).
	Manifestations of dyslipidemia (lipid metabolism disorder)	As a result of lipid metabolism disorders,	xanthomas - a disease that appears when there is a violation of fat metabolism and is manifested by focal skin formations consisting of cells with fatty inclusions. xanthelasma - flat xanthomas that appear on the eyelids. Lipoid corneal arch - circular deposition of fat in the outer shell of the eye.

Diagnosis of hepatosis

To determine the type, stage, form of steatosis, it is necessary to conduct a series of examinations. The doctor will select the optimal diagnostic methods individually for each patient.

Diagnosis of the disease includes:

• history taking ( information about the patient's life, medical history and other);
• inspection;
• laboratory examination methods ( complete blood count and biochemical blood test);
• instrumental examination methods ( ultrasound examination, computed tomography, magnetic resonance imaging, liver biopsy, elastography).

Collection of anamnesis

The collection of anamnesis is basic in the diagnosis of the disease. The interview with the patient is the first stage of the examination. The more detailed the history is collected, the easier it will be for the doctor to identify the cause of the disease, choose the treatment, diet and give correct recommendations on lifestyle changes.

At the appointment, the doctor will analyze:

• Patient complaints- complaints of pain, discomfort, heaviness in the right hypochondrium, the presence of vomiting, nausea.
• History of present illness- the time when the first symptoms appeared, how they manifested themselves, how the disease developed.
• Anamnesis of life- what concomitant diseases the patient has, what lifestyle he leads, what surgical interventions he underwent, what medications he took or is taking and for what period.
• Family history What diseases did the next of kin suffer from?
• Anamnesis of the patient's diet- what foods the patient prefers, how often he eats, what kind of diet he follows, whether there is an allergy to foods, whether alcohol is taken ( threshold - 20 g/day for women and 30 g/day for men).

Inspection

After collecting an anamnesis, the doctor proceeds to examine the patient, during which he tries to identify various signs of liver disease.

During the examination of the patient:

• The skin and visible mucous membranes are carefully examined, the yellowness of the skin, mucous membranes and its intensity, the presence of scratching, rashes are assessed.
• Percussion is performed tapping) and palpation ( probing) abdomen to determine the size and tenderness of the liver.
• Alcohol dependence is also determined - etilism ( chronic alcohol use). With alcoholism, the patient will have a swollen face, tremor ( jitter) hands, untidy appearance, the smell of alcohol.
• The degree of obesity is determined. To do this, use all sorts of formulas for calculating the normal weight of a person, depending on gender, age, body type, and determine the degree of obesity from the tables.

To determine the degree of obesity are used:

• Body mass index ( BMI). This is an objective factor that evaluates the conformity of a person's height and weight. The calculation formula is very simple - BMI \u003d m / h 2, that is, this is the ratio of a person's weight in kilograms and height in m 2. If the index is 25 - 30 kg / m 2 - the patient is overweight ( preobesity), if the BMI is greater than 30, the patient is obese.
• Calculation of ideal body weight ( BMI). This formula also takes into account the gender of the patient and determines his optimal weight, which should be followed. It is calculated according to the formulas - BMI \u003d 50 + 2.3 x ( 0.394 x height in cm - 60) - for men and BMI = 45.5 + 2.3 x ( 0.394 x height in cm - 60) - for women.
• Measuring waist circumference with a measuring tape. Used to predict complications and disease risk. If a woman has a waist circumference of more than 80 centimeters, and a man has more than 94 centimeters, then the risk of diabetes and hypertension increases ( high blood pressure) and grows with every additional centimeter.
• Ratio of waist circumference to hip circumference. For women, the ratio of the waist circumference to the hip circumference is less than 0.85, for men it is less than 1.0. Studies have shown that people with an apple body type ( waist wider than hips) are more prone to various diseases than people with a pear-shaped body type ( hips wider than waist).

General blood analysis

The procedure consists in taking blood from a vein and analyzing it on special laboratory devices.

To receive you need to reliable results, the following rules must be followed. :

• blood sampling is carried out in the morning on an empty stomach ( not earlier than 12 hours after eating);
• dinner the day before should be light and early, without coffee and strong tea;
• for 2 - 3 days alcohol, fatty foods, some medications are excluded;
• physical activity, sauna visits are excluded per day;
• tests are given before x-ray examination, massage.

A general blood test can reveal:

• Possible anemia ( anemia). Anemia causes a decrease in the number of red blood cells ( red blood cells) - less than 4.0 x 10 12 /l in men and less than 3.7 x 10 12 /l in women. It also reduces the amount of hemoglobin ( oxygen carrier protein) - less than 130 g/l in men and less than 120 g/l in women.
• Signs of possible inflammation. The number of leukocytes in the blood increases white blood cells) - more than 9.0 x 10 9 /l, ESR increases ( erythrocyte sedimentation rate) - more than 10 mm/hour in men and more than 15 mm/hour in women.

Blood chemistry

The procedure for taking blood biochemical analysis identical to the procedure for taking blood for a general analysis. Only the lack of dinner the day before is added to the restrictions ( more than 12 hours of fasting), cancellation of lipid-lowering ( blood lipid lowering) drugs two weeks prior to analysis.

A biochemical blood test can reveal:

• Increased activity of transaminases ( ). Aspartate aminotransferase levels rise ACT) more than 31 u/l in women and more than 41 u/l in men and alanine aminotransferase ( ALT) more than 34 u/l in women and more than 45 u/l in men. An increase in their concentration in the blood indicates the process of destruction of liver cells.
• Dyslipidemia ( violation of protein metabolism). An increase in cholesterol levels fat-like component of all cells) more than 5.2 mmol/l. Decreased concentration of HDL lipoproteins - complexes of proteins and high-density fats, "good cholesterol") less than 1.42 mmol/l in women and less than 1.68 mmol/l in men. An increase in the concentration of LDL low density lipoproteins, "bad cholesterol") more than 3.9 mmol / l.
• Violation of carbohydrate metabolism. There is hyperglycemia ( increase in blood sugar) more than 5.5 mmol/l.
• hepatocellular insufficiency ( decreased function). Decreased albumin concentration major blood protein) less than 35 g/l, blood coagulation factors. This indicates the inability of the liver to produce proteins and provide hemostasis ( hemostasis is a complex biosystem that maintains blood in a liquid state under normal conditions, and in case of violation of the integrity of the blood vessel, it helps to stop bleeding).

Ultrasonography ( ultrasound)

Ultrasonography ( ultrasound) – non-invasive ( without penetration into the human body and violation of the integrity of the skin, tissues, blood vessels) research method. The essence of the method is to apply ultrasonic waves to the human body. These waves are reflected from the organs and captured by a special sensor, followed by displaying the picture on the monitor. The denser the structure of an organ or medium, the fewer waves pass through them and more are reflected. On the screen, such tissues and organs appear brighter and lighter. A special gel is applied to the patient on the right in the area of ​​​​the liver to facilitate the sliding of the sensor. Then an image of the liver is obtained on the screen. The doctor conducts a description of the results. This is an absolutely painless and harmless procedure, so there are no contraindications to ultrasound.

Indications for ultrasound of the liver are:

• an increase in the size of the liver when probing;
• tenderness of the liver on palpation probing);
• changes in the biochemical analysis of blood.

Ultrasound of the liver can reveal:

• Hyperechogenicity ( increased reflection of waves from tissues) liver- this indicates the compaction of the tissues of the organ.
• Enlargement of the liver in size ( hepatomegaly) - as a result of inflammatory processes and the accumulation of fatty deposits in the liver.
• fatty infiltration ( accumulation in tissues of substances that are not normally present) more than 30% of the liver- all changes in the liver are detected by ultrasound only with fatty degeneration of more than 30% of the organ area.
• Alternating areas of hyperechoic ( with increased reflection of waves from tissues) and hypoechoic ( with reduced reflection of waves from tissues) - dense areas reflect rays, less dense ones absorb them, which indicates the heterogeneity of liver damage.

CT scan ( CT)

CT scan ( CT) – non-invasive ( without penetration into the human body and violation of the integrity of the skin, tissues and blood vessels) examination method. This method is based on the passage of X-rays through the human body from various points and under different angle, which allows you to create a three-dimensional and layered image of organs on the monitor.

For the examination, the patient must remove all clothing, jewelry, removable dentures and put on a special gown. Then he is placed on a bed with a scanning system that looks like a circle. This system is placed in the area of ​​the liver, after which the scanning probe rotates, passing x-rays through the patient's body. To improve the quality of imaging, the doctor can do a CT scan with a contrast agent, which will more clearly display the structures of the organ on the screen.

Computed tomography is shown:

• with focal ( local a) liver damage;
• with unsatisfactory results of ultrasound ( ultrasound);
• if necessary, in a more detailed, layered image;
• in the presence of formations, cysts ( pathological cavities in tissue).

Carrying out computed tomography(CT)contraindicated:

• with mental illness;
• with inappropriate behavior of the patient;
• with a patient's body weight of more than 150 kilograms;
• during pregnancy.

With liver steatosis, computed tomography can reveal:

• decrease in the x-ray density of the liver due to the accumulation of fats;
• thickening of the liver vessels in comparison with its tissue;
• focal accumulations of fat.

Magnetic resonance imaging ( MRI)

Magnetic resonance imaging is also a non-invasive method. Its essence is as follows. When a human body is placed in a strong electromagnetic field, hydrogen nuclei in its tissues begin to radiate a special energy. This energy is captured by special sensors and displayed on a computer monitor.

For the procedure, the patient must remove all clothing, jewelry, removable dentures and anything that contains metal. He is placed on a bed that slides into the MRI machine. After the procedure, an image of the organ appears on the monitor, which the doctor can examine in detail in all positions, sections and at different angles.

Indications for magnetic resonance imaging are:

• the need for more detailed visualization of liver structures;
• the presence of cysts, neoplasms;
• greater accuracy in tissue imaging, compared to computed tomography, which is more suitable for studying bone structures.

Contraindications to magnetic resonance imaging are:

• mental illness;
• inadequacy of the patient;
• having a pacemaker apparatus in the heart that helps control the heartbeat);
• the presence of metal implants ( dental or bone implants);
• claustrophobia ( fear of closed, cramped spaces);
• the presence of tattoos containing iron in the paint;
• the patient's weight is more than 160 kilograms.

With fatty infiltration of the liver, MRI can detect:

• hardening of the liver;
• enlargement of the liver in size;
• cysts and neoplasms, determine their size and location;
• heterogeneity of the liver structure;
• focal or diffuse accumulations of fat.

Liver biopsy

Biopsy ( excision of a portion of an organ for further examination under a microscope) liver is an invasive method of examination, that is, with a violation of the integrity of the skin, organs, blood vessels. For the procedure, the patient is placed on the examination table. He undergoes an ultrasound examination of the liver to determine the site from which tissue will be taken for study. After the doctor determines the required area for the biopsy, the procedure itself begins. The skin area in the liver area is treated with an antiseptic ( disinfectant). Necessarily in the puncture area, anesthesia of the skin is carried out. The doctor will explain how you will need to breathe during the procedure. Then a special biopsy needle is inserted into the liver area under ultrasound control ( ultrasound) and excised a small area of ​​tissue of the organ. incised area ( biopsy) are sent to the laboratory for examination under a microscope.

After the biopsy, the patient must be monitored by medical staff for four hours. He is strictly forbidden to get up. A cold compress is applied to the puncture area. For some time this place will feel slight discomfort. A day later, repeat the ultrasound ( ultrasonography) liver, general and biochemical blood tests.

Indications for a biopsy(excision of a part of the organ for its further study under a microscope)liver are:

• Destruction of hepatocytes ( liver cells) for an unknown reason, detected in a biochemical blood test in patients older than 45 years.
• The need to determine the stage and degree of fatty liver hepatosis.
• Differential Diagnosis ( exclusion of other diseases) steatosis and other associated liver diseases.
• The need for a detailed study of the structure of cells.
• Fibrosis is suspected reversible replacement of normal organ tissue with scar tissue) or cirrhosis ( irreversible replacement of organ tissue with scar tissue).
• Determining the severity of steatohepatosis, fibrosis, cirrhosis, when other methods are less informative.
• Surgery for obesity or removal of the gallbladder.
• Absolute contraindications for computed tomography and magnetic resonance imaging.

Contraindications for liver biopsy are:

• patient refusal;
• Availability purulent processes in the liver, intra-abdominal cavity;
• skin infections in the area of ​​the biopsy;
• mental illness;
• increased tendency to bleed;
• focal lesions of the liver tumor);
• tense ascites ( accumulation of large amounts of fluid in the abdominal cavity).

A liver biopsy will determine:

• The degree of steatosis ( 0, 1, 2, 3 ) and type of lesion ( large droplet obesity, small droplet obesity).
• The presence of structural changes in the tissue and their stage ( fibrosis, cirrhosis).
• The presence of other liver diseases that accompany steatosis.
• Inflammatory processes that cannot be detected by most non-invasive methods.

Elastography

Elastography ( elastosonography) - a non-invasive method for examining the liver, which is performed using a special apparatus - "Fibroscan". It allows you to assess the degree of fibrosis ( reversible process of replacing normal organ tissue with scar tissue). It is an alternative to the invasive method - liver biopsy.

The principle of its operation is similar to the principle of operation of ultrasound. The doctor presses on the area of ​​the organ being examined with a special sensor and evaluates the elasticity of the tissues in the image before and after compression. Structurally altered sections of tissue shrink in different ways ( due to uneven elasticity) and are displayed in different colors on the screen. Stretch fabric is shown in red and green, while stiffer fabric is shown in blue. Normally, the liver tissue is elastic, but with structural changes ( fibrosis, cirrhosis) its elasticity decreases significantly, the tissue becomes more dense, rigid. The less elastic the tissue, the more pronounced the fibrosis. The procedure is safe and painless, therefore it has no contraindications. It is not performed in pregnant women and patients with ascites due to lack of information.

Indications for liver elastography are:

• diagnosis of liver fibrosis;
• staging of fibrosis.

Elastography reveals:

• structural changes in the liver in the form of fibrosis or cirrhosis;
• fibrosis severity ( F0, F1, F2, F3, F4 on a special scaleMETAVIR);
• severity of steatosis ( minimal, mild, moderate, severe).

Patients with fatty liver should periodically repeat diagnostic procedures. This will allow you to evaluate the effectiveness of the prescribed treatment, therapeutic diet, physical activity. It will also prevent the progression of the disease with a complication in the form of fibrosis ( reversible replacement of healthy tissue with scar tissue) and cirrhosis ( irreversible replacement of tissue with scar tissue with damage to the structure and function of the organ).

Periodic medical control

Indicators	Periodicity
Monitoring weight loss, the effectiveness of treatment, diet and exercise.	Twice a year.
Biochemical analysis ( ALT, AST, cholesterol) and complete blood count.	Twice a year.
Glycemic level ( blood sugar).	Daily for patients with diabetes and every 6 months for others.
ultrasound ( ultrasonography) liver.	Twice a year.
Liver elastography ( Fibroscan).	Once a year.
Liver biopsy.	Every 3 to 5 years, depending on results.
Hepatologist consultation.	The first year - every six months, then annually.
Consultation of a nutritionist, cardiologist, endocrinologist.	Annually, and in the presence of heart disease, the endocrine system is much more frequent.
Other methods.	According to the doctor's instructions.

Treatment of hepatosis with medicines

There is no specific treatment for fatty liver disease. Basically, the treatment is aimed at eliminating or reducing the negative impact of the causes that contribute to fatty degeneration of the liver, as well as strengthening the body as a whole, protecting and restoring liver cells ( hepatocytes), maintenance of diseases in a compensated state ( a state when the body adapts to the disease, which leads to a minimal negative impact of the pathological process). The dosage and duration of treatment are selected by the doctor individually for each patient, taking into account weight, concomitant diseases, stage and degree of his disease.

Treatment goals and essential drugs

Therapeutic strategy	Medicine group	Name	Mechanism of therapeutic action
Protection of liver cells from the negative effects of many factors, as well as restoration of the structure and function of hepatocytes (liver cells)	Hepatoprotectors (drugs that protect liver cells from damage)	Essential Phospholipids (phospholipids - components of the cell wall): livenciale; essliver forte; phosphogliv; resolution pro; antraliv.	Phospholipids are the structural element of cell walls. The intake of these drugs contributes to the restoration and preservation of hepatocytes, prevents the replacement of normal liver tissue with scar tissue, that is, the appearance of fibrosis and cirrhosis.
		Preparations of natural (vegetable)origin: allochol; carsil; liv-52; hepabene; legalon; silimar; Maksar.	Provide antioxidant ( protection of cells from damaging effects active forms oxygen) action. They have a choleretic effect, preventing stagnation of bile and increased load on the liver. Stimulate the production of proteins, contributing to reparative processes ( cell functions to correct and restore) hepatocytes.
		Ursodeoxycholic acid preparations (the least aggressive, natural component of bile that does not have a toxic effect on cells): ursofalk; urdox; ursodez; Livodex.	Improve the immunological functions of the liver. Enhance the formation and excretion of bile, preventing the formation of stones in the gallbladder. Prevent cell death from toxic bile acids. Delay the spread of fibrosis ( reversible process of replacing healthy tissue with scar tissue). Reduce cholesterol levels component of cell membranes, the excess of which leads to an increased risk of developing cardiovascular diseases).
		Amino acid derivatives (amino acids - the main structural component of proteins): prohepar; heptor; hepa-merz; lecithin.	Contribute to the improvement of local blood circulation in the liver. Restore damaged structures of cells and areas of the liver. Delay the formation of connective ( cicatricial) tissue in the liver. Accelerate protein metabolism in liver diseases with parenteral ( intravenous) nutrition. Reduce ammonia levels toxic metabolic product) in blood.
		dietary supplement (biologically active additives): oats; chepaguard active.	Contains natural ingredients. Contribute to the acceleration of decay ( breaking down fats into simpler substances) fats, which protects the liver from fatty infiltration ( accumulation in the tissues of substances that are not normally present). Remove toxins, eliminate spasms, have an anti-inflammatory effect.
Increasing the sensitivity of cells to insulin (pancreatic hormone that promotes glucose uptake)	Hypoglycemic (reducing the concentration of sugar in the blood)facilities	metformin.	Normalizes, reduces body weight. Reduces the concentration of LDL ( low-density lipoproteins - "bad cholesterol", contributing to the development of diseases of cardiovascular diseases) and fats in the blood. Increases the sensitivity of tissues to insulin, which contributes to better absorption of glucose.
		siofor.	Normalizes lipid metabolism ( fat), reduces the concentration of total cholesterol and LDL ( low density lipoproteins, "bad cholesterol").
Decreased lipid levels (fat)	Hypolipidemic (lowering the concentration of lipids in the blood)facilities	Statins: atorvastatin; rosuvastatin.	Reduce the concentration of cholesterol and lipoproteins ( complexes of proteins and fats) in blood. Enhance the uptake and breakdown of LDL low density lipoproteins - "bad cholesterol").
		Fibrates: hemofibrate; clofibrate.	Reduce the amount of lipids ( fat) in the blood, LDL, cholesterol. At the same time, it increases the content of HDL ( high-density lipoproteins - "good cholesterol" that prevent the development of diseases of the heart and blood vessels). They have serious side effects, so they are less commonly used.
Weight loss	Other lipid-lowering agents	orlistat.	Suppresses the breakdown and absorption of fats from the gastrointestinal tract, which leads to weight loss.
		sibutramine.	Accelerates the onset of satiety and maintains this feeling for a long time, which leads to a decrease in the frequency of eating. Increases energy consumption.
Antioxidant action (protection of cells from destruction during oxidative processes, that is, with excessive exposure of cells to reactive oxygen species)	Antioxidants	Antioxidants include: mexidol; vitamins A, E, C.	Stimulates regeneration processes recovery), cell destruction processes are stopped, microcirculation improves, vascular fragility decreases, cholesterol levels in the blood normalize, oxygen consumption by cells is stimulated, transport and utilization of glucose is regulated.
Antihypoxic action (improving the utilization of oxygen by the body, increasing the resistance of tissues and organs to oxygen starvation)	Antihypoxants	Have an antihypoxic effect: carnitine; trimetazidine; hypoxene; actovegin.

Diet for hepatitis

Fatty hepatosis differs from other liver diseases in a more favorable course. It is treatable with full recovery of the liver. Often, recovery is as simple as changing your diet and lifestyle. Therefore, dieting can be the main treatment for the initial stages of steatohepatosis. With proper nutrition, metabolism in the body normalizes, the amount of fat in the liver decreases, and the functioning of the organs of the gastrointestinal tract improves.

Along with weight loss, the risk of developing diabetes mellitus, hypertension ( high blood pressure) disease, cardiovascular disease.

Diet therapy should be selected by a nutritionist individually for each patient, taking into account age, weight, gender and concomitant diseases. An improperly selected diet can only do harm. For diseases of the liver and gallbladder, a specially designed diet should be followed - table No. 5 according to Pevzner and diet No. 8 for obesity. The purpose of the diet is gentle nutrition for the liver.

When following a diet, it is important to remember that:

• Nutrition should be balanced and contain the necessary daily protein intake ( 110 - 130 g), fat ( 80 g, 30% vegetable) and carbohydrates ( 200 - 300 g).
• Sufficient amount of water should be consumed 1.5 - 2 liters excluding tea, compote, soups).
• It is necessary to limit the amount of salt consumed ( 6 - 8 g) and sugar ( 30 g).
• The number of meals should be up to 6-7 times a day ( fractional nutrition ), dinner 3-4 hours before bedtime.
• Food should not be cold or hot.
• Fried foods are completely excluded, and preference is given only to boiled, steamed, baked and stewed foods.
• Products that irritate the gastric mucosa and increase bile secretion are excluded - acidic foods, pickles, spices and others.
• Avoid overeating and eat small meals.
• The use of alcohol is completely excluded.
• Green tea, coffee, cocoa, chicory, hibiscus are excluded.

It is a mistake to think that with steatosis, fats should be completely excluded from the diet. You just need to reduce the amount of fat you eat. Fats with proteins protect the liver from fatty degeneration and contribute to a speedy recovery. With a lack of fat, the body receives them from carbohydrates, which does not have the best effect on health. A low-fat diet causes the same damage to the body as abuse fatty foods. Fats are part of the structure of cells, necessary for the body to assimilate fat-soluble vitamins ( A, D, K, E), are involved in the production of certain hormones, bile acids. The main sources of fats should be vegetable oils ( olive, sunflower) and more than half - food of animal origin.

Allowed and prohibited sources of fat in fatty liver

Fats
fat-free cottage cheese, up to 500 ml of milk per day, kefir, yogurt; lean beef, rabbit meat, turkey, chicken; steam cutlets; seafood ( oysters, mussels, squid); lean fish ( tuna, walleye).	fatty dairy products; Salo; fatty meat ( duck, goose, pork, beef); caviar, sushi, oily fish ( trout, catfish), salty and smoked fish; offal ( liver, tongue); mayonnaise, ketchup, mustard; sausages; canned food.

A sufficient amount of proteins of plant and animal origin should be supplied with food. Proteins play an important role in the normal functioning of the liver, so their deficiency will only increase the fatty infiltration of the liver.

Allowed and prohibited protein sources for fatty liver

Carbohydrates maintain the balance of metabolism, the normal functioning of the liver, and fiber reduces the concentration of cholesterol ( structural fat-like element of cells) in blood. This results in a reduced risk of disease. of cardio-vascular system, tumors of the intestine and stomach. Carbohydrates are simple easily digestible) and complex ( difficult to digest). simple carbohydrates ( glucose, fructose) are found in sweets, sugar, confectionery. They instantly break down, satisfy hunger for a short time and contribute to the storage of fat in reserve. Complex carbohydrates ( fiber, starch) are digested by the body for a long time, dulling the feeling of hunger for a long time. They remove harmful substances, cleanse the intestines, and contribute to the proper functioning of the digestive organs.

Allowed and prohibited sources of carbohydrates in fatty liver

Carbohydrates

Allowed products include: boiled and baked vegetables; raw vegetables in limited quantities; dried fruits; mashed compotes; prunes; nuts; porridge ( oatmeal, buckwheat, barley, muesli); rye bread, croutons, crispbread, bran; honey, marmalade, marshmallow, lollipops; weak black tea, rosehip decoction.

Prohibited products include: bakery products; ice cream; sugar ( more than 30 g per day); carbonated and sweet drinks ( Sprite, Coca Cola, fruit juices); semolina; flour products of the highest grade; pasta; bean products ( nagut, lentil); adjika, horseradish; pickles; chocolate, cream confectionery, condensed milk, waffles; berries and fruits – apples, raspberries, grapes, cranberries, cherries and others; vegetables – radish, eggplant, garlic, onion, corn and others; freshly squeezed juices.

A sample menu for the day should meet the requirements of the diet and include:

• First breakfast– oatmeal on water with milk, fat-free cottage cheese, black tea.
• Lunch- dried fruits, apple, prunes.
• Dinner- vegetable soup with vegetable oils ( corn, olive), buckwheat porridge, compote.
• afternoon tea- bread, unsweetened cookies, rosehip broth.
• Dinner- mashed potatoes with steamed fish, beetroot salad, low-fat kefir.

You need to follow a diet not only for a certain period until recovery. It should become a lifestyle and you need to stick to it constantly. To achieve the best result and maintain it, the diet must be combined with sports. Heavy physical activity is not recommended. Swimming, yoga, Pilates, cycling are best suited.

Is hepatosis treated with folk remedies?

Folk remedies help in the treatment of fatty hepatosis no worse than expensive medicines. A positive effect can be expected only in the initial stages of the disease. In this period, the focus is not on drug treatment, but on following a properly selected diet, which can be combined with taking decoctions, herbal teas, and tinctures. But we must remember that engaging in self-diagnosis and self-treatment can be even more dangerous for health than a complete lack of treatment. The appearance of symptoms of liver disease indicates the progression of the disease with damage to the structure of the liver and its function. And self-treatment with folk remedies will only lead to an aggravation of the situation and the impossibility of further recovery. Therefore, before using any means, you need to consult a doctor.

The goal of folk remedies is to improve liver function, restore liver cells ( hepatocytes), removing toxins, reducing the amount of fat in the body, weight loss. Many medicines are based on medicinal herbs. Therefore, these natural remedies can be an effective treatment. Herbs can be used separately or in herbal preparations with a complex therapeutic effect on the liver.

Used to treat steatohepatosis :

• Bran. Helps remove excess fat from the body. Bran must be insisted in hot boiled water until it cools completely. After the water has cooled, you should take out the bran and eat two tablespoons. They can also be added to cereals and soups. Should be applied up to three times a day.
• milk thistle seeds. Milk thistle is part of many hepatoprotectors ( hepabene, silimar). Has an antioxidant effect protects the liver from negative effect oxidative processes, that is, damage to hepatocytes by an excessive amount of reactive oxygen species). Increases immunity, which helps the body to cope with many negative factors. To prepare the tincture, milk thistle seeds are poured with boiling water ( 200 ml) for an hour. After that, filter and take 1/3 cup 3 times a day half an hour before meals.
• immortelle flowers. Immortelle has a choleretic effect, normalizes metabolism ( metabolism) liver. Flowers immortelle pour 200 ml of water at room temperature and heat for half an hour in a water bath. After that, insist 10 minutes and add warm boiled water to the original volume. Take 1 - 2 tablespoons 3 - 4 times a day 10 minutes before meals.
• Dog-rose fruit. They help to remove toxins from the body, enrich it with trace elements and vitamins. About 50 g of rose hips are infused in 500 ml of boiling water for 12 hours. Take three times a day, 150 ml.
• St. John's wort. Strengthens the walls of blood vessels antibacterial action. A tablespoon of dried herbs pour 300 ml of boiling water, heat in a water bath for 5 minutes. Strain the resulting composition and add boiled water to the original volume.
• Mint leaves. Mint leaves have a choleretic effect, suitable for the prevention of liver diseases. One tablespoon of dried leaves pour 200 ml of boiling water. Leave for 20 minutes and take morning and evening before meals.
• Calendula flowers. They have anti-inflammatory, disinfectant, choleretic action. Contribute to the acceleration of metabolic processes in the liver. One tablespoon of calendula pour 200 ml of boiling water and insist for 20 minutes. Take 100 ml 3 times a day.
• Chamomile flowers. It has a disinfecting, healing effect. Chamomile flowers should be infused for 20 minutes, then strain and take 30 minutes before meals 2-3 times a day.
• Turmeric. A spice that helps restore damaged liver cells. Can be added in small quantities 1 - 2 pinches) when cooking.
• Pine nuts. Strengthen hepatocytes ( liver cells) to prevent their destruction.

What is dangerous liver steatosis ( complications, consequences)?

Steatosis ( accumulation of fat droplets in liver cells with their destruction) is dangerous by progressing to fibrosis and cirrhosis of the liver. Steatosis is a completely reversible process. To do this, you need to change your diet and lead a healthy lifestyle. But with a prolonged negative effect on the liver of many factors and the absence of treatment, the disease passes into more severe stages of the course. The rate of progression is different for each patient. With fatty degeneration with concomitant diabetes mellitus, obesity, alcohol intake, viral hepatitis, the process is significantly accelerated and passes into fibrosis.

Fibrosis is a reversible growth of dense connective tissue ( cicatricial) in the liver with damage to liver cells - hepatocytes. In this way, the inflammatory process is limited to prevent its further spread. Fibrosis has now been shown to be treatable. But, despite this, fibrosis often turns into cirrhosis of the liver.

Cirrhosis is a progressive, irreversible disease in which liver tissue is replaced by scar tissue. This significantly reduces the number of functioning cells. At the initial stages of the development of cirrhosis, it is possible to suspend and even partially restore damaged structures, but in severe cases, the disease is fatal ( patient death). The only treatment is a liver transplant.

Can pregnancy cause fatty liver?

Periodically, pregnancy is complicated by such a pathological condition as fatty liver hepatosis ( cholestatic hepatosis of pregnancy). Hepatosis appears at the beginning of the third trimester ( from 25 - 26 weeks of pregnancy). It is diagnosed in 0.1% - 2% of pregnant women. There is no definite answer about the cause of hepatosis during pregnancy. However, most doctors agree that the trigger is a high level of sex hormones - pregnancy hormones, which causes the manifestation of genetic defects in the processes of bile formation and bile secretion. Therefore, the pathology often acquires a family character and is inherited through the maternal line. Other reasons besides genetic predisposition may be uncontrolled reception vitamin preparations that the liver cannot fully cope with, unbalanced nutrition with excess fats and carbohydrates, which leads to fatty degeneration of the liver and the development of acute fatty hepatosis. Only a doctor can make a correct diagnosis based on laboratory and instrumental examinations.

Symptoms of the manifestation of fatty hepatosis of pregnant women are:

• skin widespread itching;
• icteric staining of the mucous membranes and skin;
• nausea, heartburn, occasional vomiting, loss of appetite;
• feeling of heaviness and moderate pain in the upper abdomen on the right;
• discoloration of feces;
• general weakness, malaise, fatigue.

Cholestatic hepatosis of pregnant women can be dangerous for the mother and fetus, as the risk of oxygen starvation increases ( hypoxia) baby and premature birth . Very common delivery ) at 38 weeks or even earlier, given the severity of the woman's condition. Fatty hepatosis of pregnant women can lead to severe postpartum bleeding, as the production of blood clotting factors by the liver is disrupted, which leads to inadequate functioning of the hemostasis system ( a complex biosystem that maintains blood in a liquid state under normal conditions, and in case of violation of the integrity of the blood vessel, it contributes to stopping bleeding).

Can children get hepatitis?

Hepatosis also occurs in children. Hepatosis is divided into primary ( hereditary, congenital) and secondary ( acquired), as well as pigment ( violation of the metabolic processes of pigments - substances that give color to tissues) and fatty ( violation of fat metabolism with their accumulation in liver cells).

Hereditary hepatoses - liver damage against the background of genetically determined metabolic disorders, manifested by a violation of the intrahepatic metabolism of bilirubin ( main component of bile). Manifested from birth as chronic or intermittent jaundice ( yellowness of the skin and mucous membranes). These hepatoses usually proceed benignly, with almost no effect on the quality of life of the patient, with the exception of Crigler-Najjar syndrome, accompanied by a high level of bilirubin in the blood with toxic damage to the central nervous system, heart and internal organs.

Secondary hepatosis develops against the background of concomitant diseases and an unhealthy lifestyle. Type I diabetes mellitus ( appears in childhood), obesity, congenital hepatitis, toxic effect drugs, cholestatic disorders ( bile stasis), malnutrition are the main causes of liver disease in children.

Can fatty liver be cured?

Fatty liver disease is a reversible liver disease. This pathology can be successfully treated with early stages. Certain treatment does not exist. It all comes down to a change in lifestyle, a review of nutrition, the exclusion of etiological ( causal) factors. In many cases, it is not possible to exclude the causes contributing to the development of hepatosis. For example, incurable diabetes mellitus, congenital metabolic disorders, many endocrinological diseases. In this case, supportive therapy with hepatoprotectors ( drugs that help protect and restore liver cells), lipid-lowering agents ( reducing the concentration of fats in the blood), antihypoxant ( improving the utilization of oxygen by the body, increasing the resistance of tissues and organs to oxygen starvation) and antioxidant ( protecting cells from destruction during excessive exposure to reactive oxygen species) drugs and others. They also support concomitant diseases in the compensation stage, that is, the body's adaptation to a pathological condition with a decrease in negative consequences.

Basically, fatty liver is asymptomatic. It is diagnosed by chance during preventive examinations or diagnostic procedures for other diseases. Therefore, it is rarely possible to detect hepatosis in the early stages. Over time, the situation only worsens and is complicated by fibrosis ( reversible replacement of normal organ tissue with scar tissue) or cirrhosis ( irreversible chronic tissue replacement with scar tissue). In this case, it is very difficult or impossible to cure the liver.

What is the difference between hepatosis and hepatic steatosis?

Steatosis is a type of hepatosis. Hepatosis is a set of liver diseases, which are based on a violation of metabolic processes with a violation of the structure and function of liver cells ( hepatocytes). Steatosis is a pathological abnormal) accumulation of fat in the cells of the body in case of metabolic disorders. Distinguish pigmentary hepatosis (violation of the metabolism of pigments - substances that color the skin and tissues) and fatty liver ( synonyms - liver steatosis, fatty degeneration of the liver, fatty liver, steatohepatosis, fatty degeneration, "fatty" liver).

The development of fatty hepatosis ( steatosis) patients with type 2 diabetes are more susceptible ( incidence of disease from 70% to 90% of patients), obese ( 30% to 95% of patients), with impaired fat metabolism ( 20% to 92% of cases).

For the diagnosis of steatosis, laboratory and instrumental methods are used. Laboratory methods include general and biochemical blood tests. With steatosis, blood tests reveal an increase in transaminase activity ( enzymes in liver cells that speed up chemical reactions) by 4–5 times, an increase in the concentration of cholesterol ( fat-like structural element of cells), lipoproteins ( complexes of proteins and fats) low density, increased blood sugar, bilirubin ( bile pigment), a decrease in the concentration of proteins, and others. Instrumental analyzes include ultrasound ( ultrasound), Magnetic resonance imaging ( MRI), CT scan ( CT), elastography ( Fibroscan) and liver biopsy. During these examinations, an increase in the size of the liver is found ( hepatomegaly), local or diffuse fatty accumulations in liver cells, cysts ( pathological cavities in tissues), fibrosis ( reversible process of replacing healthy liver tissue with scar tissue).

Violation of metabolic processes affects not only the liver. Therefore, steatosis is characteristic not only for the liver ( as in case of hepatitis), but also for the pancreas. The causes of pancreatic steatosis are the same factors as for the liver - this is excessive alcohol intake, obesity, diabetes, certain medications, and many others. Therefore, when making a diagnosis of "steatosis", it is necessary to clarify the pathology of which organ is in question.

Is it possible to do tubazh with fatty hepatosis?

Fatty hepatosis is not a contraindication for tubage. Tyubazh ( from French - tube placement, intubation) is a medical manipulation to cleanse the gallbladder ( digestive organ located under the liver and connected to it by the bile ducts).

The essence of the method is the irritation of the gallbladder with choleretic ( drugs or substances that stimulate the production of bile) means followed by increased excretion of bile. This procedure is carried out in order to prevent stagnation of bile ( cholestasis) and the formation of gallstones. It is used for diseases of the liver, gallbladder and bile ducts with symptoms of inflammation and impaired bile secretion. Absolute contraindication to tubage is calculous cholecystitis ( inflammation of the gallbladder due to the presence of stones). This can lead to a stone from the gallbladder entering the bile duct, resulting in blockage of the lumen of the duct. In this case, only urgent surgical intervention can help.

Tubage can be carried out using a duodenal probe or by taking cholagogues with simultaneous heating of the liver. In the first case in duodenum insert a probe hollow tube) and parenterally ( intravenously) or choleretic substances are injected through the tube. This leads to an increased excretion of bile into the duodenum, from where it is aspirated ( aspirate with a special device called an aspirator) through the probe. Inside take such choleretic substances as a solution of magnesium sulfate, sodium chloride solution, 40% glucose solution, intravenously - histamine, atropine and others.

The second method is probeless tubage ( blind tubage). For this procedure, the patient lies on his right side, bending his knees, and drinks a cholagogue. A warm heating pad is placed under the right side at the level of the liver. As a choleretic agent, a decoction of wild rose, a solution of magnesium sulfate, heated mineral water other. In this position, the patient is about 1.5 - 2 hours. The procedure should be carried out once a week for 2-3 months.

Which doctor treats hepatic steatosis?

A hepatologist deals with the diagnosis, prevention and treatment of liver diseases. But since the cause of liver steatosis can be various diseases, pathological processes and an unhealthy lifestyle, the treatment and diagnosis of the disease should be dealt with in a complex manner. And the hepatologist can appoint a consultation with doctors of other specializations.

A hepatologist may schedule a consultation with doctors such as:

• Gastroenterologist. This is a doctor who treats the organs of the gastrointestinal tract ( gastrointestinal tract). Chronic diseases of the gastrointestinal tract, as well as surgical interventions on the organs of the gastrointestinal tract and long-term parenteral ( intravenous) nutrition leads to improper processing and absorption of nutrients. This leads to a violation of metabolic processes and liver disease with excessive accumulation of fatty inclusions in it.
• Endocrinologist. A doctor who specializes in diseases of the endocrine glands ( thyroid gland, pancreas). endocrine diseases ( diabetes mellitus, thyroid disease, metabolic syndrome - a combination of metabolic, hormonal and clinical disorders) lead to obesity, disrupt the functions of many organs. All these factors are the cause of steatosis. Therefore, the treatment of this pathology without eliminating or compensating for the original cause has no effect.
• Nutritionist. The nutritionist will help the patient to adjust the diet and lifestyle. Since it is malnutrition that often leads to obesity with all the ensuing consequences ( diseases of the cardiovascular system, endocrinological diseases). He will also determine the lack or excess of vitamins, minerals, proteins, fats and carbohydrates from food, and select a diet individually for each patient.
• Obstetrician-gynecologist. Pregnancy may be complicated by hepatic steatosis. This disease can negatively affect the fetus and mother, even lead to death. In severe cases, they come to an artificial termination of pregnancy. Therefore, the hepatologist and obstetrician-gynecologist select supportive drug treatment or perform delivery ( artificial termination of pregnancy) for severe disease. Taking contraceptives ( contraceptives ) changes hormonal background women, which is also a cause of steatosis. In this situation, the gynecologist should choose another method of contraception that does not adversely affect the liver.
• Cardiologist. Heart and liver diseases are closely related. Impaired liver function can be caused by heart failure, chronic oxygen starvation, circulatory disorders. But also liver diseases can lead to aggravation of already existing heart pathologies. Often this is accompanied by endocrine diseases.
• Expert in narcology. A narcologist deals with the treatment of alcohol dependence, which is the cause of a separate group of steatosis - alcoholic steatohepatosis. In liver diseases, alcohol consumption is absolutely contraindicated, because it can lead to cirrhosis of the liver ( irreversible replacement of normal liver tissue with scar tissue) and subsequently to the death of the patient.

Life expectancy in fatty liver

It is impossible to unequivocally answer the question of life expectancy in fatty hepatosis. Everything is strictly individual and depends on the age, stage of the pathological process, concomitant diseases, complications, the effectiveness of treatment and the patient's desire to change his lifestyle. Steatosis does not have a significant effect on life expectancy. Moreover, this disease is easily treatable in its early stages. The prognosis changes significantly with the transition to fibrosis ( reversible growth of scar tissue) and cirrhosis ( irreversible growth of scar tissue). This negatively affects the structure and function of the liver. With a severely neglected course, the absence of proper treatment and the presence of provoking factors, the disease progresses rapidly and life expectancy is significantly reduced.

Fibrosis proceeds more favorably than cirrhosis. There are five stages of fibrosis. Progression can proceed at different speeds. For example, it may take several years from stage 0 to stage 2, and stage 3 to 4 in a fairly short period of time. The progression of fibrosis is significantly affected by diabetes mellitus, obesity, lipid metabolism disorders, age ( progression accelerates significantly after age 50) other. With diet, a healthy lifestyle, and proper treatment, fibrosis can be cured.

Cirrhosis is a severe irreversible disease. Life expectancy with cirrhosis of the liver directly depends on the severity of the disease. With compensated cirrhosis, the body adapts to pathology with the least negative consequences. Thus, preserved hepatocytes ( hepatic cells) perform the functions of dead cells. At this stage, life expectancy is more than seven years in 50% of cases. In the stage of subcompensation, the remaining hepatocytes are depleted and are unable to perform all the necessary functions. Life expectancy is reduced to five years. With decompensated cirrhosis, the patient's condition is extremely severe. Life expectancy up to three years in 10% - 40% of cases.

Does hirudotherapy help? leech treatment) with hepatitis?

Hirudotherapy ( leech treatment) can help in the complex treatment of hepatosis. This procedure is used in inflammatory processes in the liver ( e.g. chronic hepatitis, toxic hepatitis), cirrhosis ( irreversible replacement of normal organ tissue nor scar tissue).

Contraindications to hirudotherapy are:

• pregnancy;
• hypotension ( low blood pressure);
• anemia ( anemia, manifested by a low concentration of red blood cells and hemoglobin);
• hemophilia ( congenital bleeding disorder);
• individual intolerance.

Hirudotherapy technique is very simple. Before the therapy, the procedure area is treated with alcohol. Then leeches are placed on the skin in the zone of biologically active points. Their bite is almost not felt, as they secrete special painkillers. After about 30 - 45 minutes, satiated leeches themselves fall off. A sterile bandage is applied to the wounds. The course of treatment is 12 sessions with a frequency of 1 - 2 times a week.

Massage gymnastics, yoga help improve liver function. All exercises performed while standing on all fours or lying on the right side, minimally load the liver and contribute to the outflow of bile. Among the exercises for the liver, “scissors” can be distinguished ( in the supine position, leg swings are performed in the style of scissors), "a bike" ( in the supine position, cycling is simulated), squats, jumps. It also has a beneficial effect on the liver breathing exercises.

To achieve a therapeutic effect from physical activity, you should follow a diet, diet, do not neglect proper rest, and completely stop smoking and drinking alcohol.

Fatty degeneration of the liver

Fatty degeneration of the liver is a syndrome that occurs due to the progression of fatty degeneration in the liver cells. The course of this disease is characterized by the occurrence of a process of pathological accumulation in the liver cells of fatty deposits in the form of fat drops. The cause of the development of this disease affecting the liver in many cases is the pathological processes occurring in the biliary and intestinal tracts. Risk factors for the development of fatty degeneration of the liver are also the presence of severe obesity in the patient, the second type of diabetes mellitus, malabsorption and maldigestive syndromes, and regular abuse of alcoholic beverages. The consequences of using a number of drugs, such as corticosteroids, tetracyclines, estrogens, as well as non-steroidal anti-inflammatory drugs, can lead to the development of fatty liver. In addition, fatty degeneration of the liver may accompany the course of various viral hepatitis that occur in a chronic form, in particular hepatitis C.

Toxic dystrophy of the liver

Toxic dystrophy of the liver has as its manifestations massive progressive necrotic processes affecting the liver tissues. The disease, as a rule, is acute, and in some cases it can be present in the body in a chronic form, causing liver failure as the pathology progresses.

The cause of massive liver necrosis is mainly the effect of toxic substances contained in food products, including mushrooms, which cause poisoning with arsenic, phosphorus compounds, etc. These intoxications are exogenous in nature. Can also provoke toxic liver dystrophy endogenous intoxications. These include toxicosis that occurs in women during the period when they are carrying a child, thyrotoxicosis. The cause of toxic liver dystrophy is often the disease of viral hepatitis, in which this disease develops as one of the manifestations of its fulminant form.

Toxic degeneration of the liver causes changes in the body that are characteristic of each specific stage of the pathological progress of this disease. Initially, there is an increase in the size of the liver, this organ acquires either a flabby or dense consistency, it becomes characterized by an icteric tint. With the further course of the disease, the liver shrinks in size, and its capsular membrane becomes wrinkled. The liver tissue changes its color to grayish and takes on the appearance of a clay mass. In the later stages, after the third week of the disease, the process of reducing the size of the liver continues, it acquires a reddish tint. There is exposure of the hepatic reticular stroma, in which sinusoids are enlarged and overflowing with blood. Preserved hepatocytes remain only in the peripheral regions of the lobules. These phenomena indicate the transition of hepatic dystrophy to the stage of red dystrophy.

The presence of toxic dystrophy of the liver, which has passed into chronic stage is an extremely rare clinical case, however, it is associated with the likelihood of a patient's death due to progressive liver failure.

Acute liver dystrophy

Acute liver dystrophy predominantly appears as a complication that develops against the background of an unfavorable course of Botkin's disease. Cases of the appearance of this disease in an autonomous form, as evidenced by medical statistics, are extremely rare.

To date, medical research in the field of studying the mechanisms of development of dystrophic phenomena in the liver has not led to an unequivocal answer to the question of the cause of acute hepatic dystrophy. At present, the mechanisms of the pathological progress of this serious illness affecting the liver, and it remains unclear whether there is a correlation with the strength (virulence) of the virus, or whether there is an effect of some other factors.

The presence of brucellosis, relapsing fever, syphilis in a patient, as well as the state of pregnancy and its artificial termination, can lead to a aggravated course of hepatitis of a parenchymal nature. All this causes a high probability of hepatitis degeneration into a severe form of liver dystrophy.

Acute liver dystrophy at the initial stage recreates a clinical picture similar to the onset of the development of Botkin's disease, which is associated with a significant deterioration in the general condition of the patient. In this case, the nervous system is mainly affected, which is manifested in the appearance of various disorders of brain activity. Patients become delusional, tossing about in bed, convulsions and vomiting occur. In some cases, the appearance of such conditions became the justification for the need to hospitalize the patient in a psychiatric clinic. On the other hand, another, opposite reaction of the central nervous system to the development of the pathological process is possible. There may be apathy and depression, a significant decrease in the vitality of the body, increased drowsiness appears. Up to the onset of unconsciousness and hepatic coma.

Alcoholic degeneration of the liver

Alcoholic dystrophy of the liver is a disease caused by excessive consumption of alcoholic beverages for a long period of time exceeding 10-12 years. Alcohol, in an immoderate amount entering the human body, has an extremely negative, hepatotoxic effect.

The appearance of alcoholic hepatic dystrophy can serve as a sign that there is fatty liver or steatosis, cirrhosis, alcoholic hepatitis. In the vast majority of cases, steatosis develops as the earliest stage in the progress of the pathological process in the liver due to alcohol abuse. After the cessation of the regular intake of alcohol in the patient's body, pathological changes due to steatosis developing in the liver return to normal within 2 to 4 weeks. Often, during the course of the disease, its at least some pronounced symptoms may be absent.

Alcoholic liver dystrophy has the same symptoms as chronic alcohol intoxication. It is diagnosed due to the detection of an enlarged size of the parotid glands, the presence of Dupuytren's contracture, palmar erythema. The presence of this disease in the patient's body is also evidenced by the results of laboratory tests and a liver biopsy.

Therapeutic measures for alcoholic liver dystrophy consist primarily in the absolute cessation of alcohol consumption by the patient. A course of treatment with corticosteroid drugs and essential phospholipids is prescribed. If the disease is in terminal stage liver transplant may be indicated.

Diffuse dystrophy of the liver

Diffuse dystrophy of the liver is a pathological process that develops in the parenchyma, which is the main tissue from which this organ is formed. In specific liver cells, hepatocytes, there are processes aimed at detoxifying toxic substances entering the body. Hepatocytes take part in the processes of digestion, their role in this case is reduced to the secretion of bile, in which there are a number of enzymes that break down fats in the gastrointestinal tract. Liver cells ensure the neutralization of harmful substances by transforming them into those that do not pose a threat to the normal functioning of the body, and which are subsequently excreted along with bile.

Diffuse dystrophy of the liver occurs as a result of the fact that the liver cells are not always able to process the poison that enters the body. It happens that they cannot cope with the scale of intoxication, and as a result, poisoning leads to their death. Over time, the cells destroyed in this way are replaced by fibrous connective tissue. The more significant the degree of such damage to the liver, the more it accordingly negatively affects its ability to perform its functions.

As a rule, the development of diffuse pathological progress in the liver is accompanied by a similar process affecting the pancreas as well, since the functions of these two organs are in close connection with each other.

Focal dystrophy of the liver

Focal liver dystrophy presents certain difficulties in diagnosing this disease due to the fact that although there is a deterioration in the functioning of the liver, it is extremely difficult to fix these pathological changes through laboratory tests.

Based on the reasons that caused focal hepatic dystrophy, in each individual case, the presence of various objective and subjective symptoms and manifestations of this disease in each individual patient is characteristic.

Focal liver dystrophy, which occurs, in particular, as a result of regular intoxication with large doses of alcohol, manifests itself in such phenomena as the appearance of shortness of breath, loss of appetite, etc. in some cases, patients note the occurrence of discomfort and heaviness in the right hypochondrium. Such symptoms are characterized by an increase in their intensity during movement.

Often, the detection of fatty infiltration of the liver becomes possible only when performing magnetic resonance imaging - MRI and computed tomography. These diagnostic techniques represent the most effective way to detect focal liver dystrophy in a patient.

Granular dystrophy of the liver

Granular dystrophy of the liver is the most common type of protein degenerative pathology. With this disease, the colloidal properties of the cellular cytoplasm are violated, in which the appearance of a grain-like protein is observed.

The reasons causing the appearance of this liver disease are: the lack of adequate feeding in infancy, and in later age periods - the consequences of intoxication, the presence of infections, impaired functioning of the circulatory systems and lymph flow, as well as exposure to factors that can provoke tissue hypoxia.

As granular degeneration of the liver develops, changes in protein cellular metabolism occur. With the progress of the pathological process of granular dystrophy, the cytoplasm acquires a swollen and cloudy appearance, as a result of which this liver lesion is also characterized as cloudy swelling. The liver affected by this disease acquires a flabby consistency, blood supply is disturbed in it.

In the process of establishing a differentiated diagnosis, granular dystrophy must be separated from the physiological processes of protein synthesis in cells, in which granularity occurs in the protein.

Granular degeneration of the liver is predominantly a reversible process, however, due to severe course disease, there is a possibility of its degeneration into such forms as hyaline-droplet or gyropic dystrophy, as well as necrosis.

Protein degeneration of the liver

Protein degeneration of the liver occurs as a result of a violation of protein metabolism and can be represented by amyloidosis, hyalinosis and granular degeneration.

A characteristic feature of amyloidosis is that in the presence of this disease, a special protein amyloid substance is deposited in the tissues.

Hyalinosis is a type of protein degeneration, which often occurs as a concomitant disease against the background of atherosclerosis. This pathology is characterized mainly by local localization, in particular, it can appear in the vessel wall during the formation of a blood clot. Hyalinosis tends to form translucent protein structures similar to cartilage hyaline tissue.

Protein dystrophy of the liver also acquires the form of granular dystrophy, which means the appearance of drop-shaped and granular protein formations in the cellular protoplasm. Combining into a single whole, these formations show a tendency to completely fill the entire internal cellular space. With granular dystrophy of the liver, protein cell structures are compacted, and the normal functioning of cells is disrupted. Granular dystrophy is fraught with pathological changes of a necrotic nature and leads to cell death.

Hydropic dystrophy of the liver

Hydropic degeneration of the liver, also known as hydropic degeneration, has such a feature that vacuoles containing cytoplasmic fluid appear in the cell. In the presence of this type of hepatic dystrophy, the parenchyma cells are enlarged, the nucleus in them acquires peripheral localization, in some cases its wrinkling or vacuolization is observed.

With the development of pathological changes, the cell overflows with fluid and its ultrastructures decompose. The cell becomes like a container filled with water, and is essentially one continuous vacuole with a bubble-like nucleus placed in it. Similar phenomenon, which is a sign that characterizes colliquational necrosis, is called balloon dystrophy.

Hydropic dystrophy of the liver can only be detected by examination using a microscope, since visual changes are not characteristic of the appearance of tissues and organs.

The prognosis in the presence of this disease seems unfavorable due to the fact that with hydropic degeneration of the liver, the functioning of this organ is significantly impaired. A negative prognostic factor is also that the outcome of this disease is focal or total cell necrosis.

Yellow dystrophy of the liver

Yellow dystrophy of the liver acute form may occur during pregnancy as one of the complications associated with it. The cause of it is the state of acute intoxication, in which this disease is an aggravating factor in the development of infection processes in the body.

Jaundice in a woman during the period in which she bears a child, as well as in the presence of other hepatic pathologies in addition to liver dystrophy, such as cholecystitis and the presence of stones in the liver, can also be present as an autonomous disease provoked by autointoxication of the body. This condition is known as concomitant pregnancy toxicosis.

Yellow liver dystrophy is one of the most serious toxicosis of pregnancy in terms of severity. The disease is caused by severe intoxication with the products of metabolic processes occurring during pregnancy, which differ in other features than the metabolism that occurs in the normal state of the body. Pathological progress at the beginning of its development is characterized by the appearance of jaundice, which is preceded by a period of severe, often very prolonged vomiting. Over time, the condition is aggravated by the fact that the skin and sclera acquire a pronounced icteric appearance, clouding of consciousness occurs, states of delirium and excessive excitation of the nervous system may occur. There is a possibility of multiple subcutaneous hemorrhages, in the composition of urine, the amount of which tends to be significantly reduced, the presence of cyrosine and lecithin is detected, and in addition there is a decrease in hepatic dullness. Due to the further deterioration of the general condition of the patient, there is a possibility of death after a few days.

Parenchymal dystrophy of the liver

Parenchymal dystrophy of the liver is based on the development of the pathological process associated with it, changes in the chemical-physical and morphological characteristics inherent in cellular proteins. The essence of such violations of the functioning of cells is the process of hydration, which the cytoplasm undergoes as a result of the fact that coagulation, denaturation takes place in the cell, or, on the contrary, the phenomenon of colliquation. In those cases in which there is a violation of protein-lipid bonds, membrane cell structures are characterized by the occurrence of destructive processes in them. The consequences of such changes are the development of necrotic processes of a coagulation - dry, or colliquat - wet nature.

Parenchymal dystrophy of the liver is classified according to its varieties as:

Hyaline-drop hydropic horn dystrophy.

Granular dystrophy, which is characterized by the appearance of protein grains in the cells of the parenchyma, can also be attributed to parenchymal dystrophy of the liver. This type of hepatic dystrophy is characterized by an increase in the volume of the organ affected by this disease, the acquisition of a flabby consistency and a dull appearance on the cut. The last given feature causes the fact that granular liver dystrophy is also called dull or cloudy swelling.

Liver dystrophy is a chronic or acute (depending on the form) liver disease that occurs with phenomena of fatty degeneration of hepatocytes (liver cells) or their massive necrosis. Diseases such as hepatosis and cirrhosis are consequences of the process of liver dystrophy.

It is accepted to allocate fatty and toxic dystrophy of the liver.

Toxic dystrophy of the liver

It is manifested by massive progressive necrosis of the liver tissues, is an acute, less often chronically occurring disease, characterized by progressive massive necrosis of the liver and the development of associated liver failure.

Etiology and pathogenesis of toxic liver dystrophy

Massive liver necrosis usually develops mainly with exogenous (food poisoning, including mushrooms, phosphorus, arsenic compounds, etc.) and endogenous (thyrotoxicosis, toxicosis of pregnant women) intoxications. It can occur with viral hepatitis as a manifestation of its fulminant form.

Pathological anatomy in toxic liver dystrophy

The changes that occur in toxic liver dystrophy are different in different periods of the disease. At the onset of the disease, there is some enlargement in the size of the liver, it becomes dense or flabby, with a yellowish tinge. With a further course, the liver decreases in size, becoming flabby, and its capsule acquires a wrinkled structure. Liver tissue becomes gray, clay-like.

Microscopically, the development of fatty degeneration of hepatocytes in the center of the liver lobules is observed, followed by their further necrosis and processes of autolytic decay with the formation of protein-fatty detritus with crystals of the amino acids leucine and tyrosine. With progression, these necrotic changes capture the remaining sections of the lobules. These changes in the liver characterize the onset of the stage of the so-called yellow dystrophy.

After 3 weeks of illness, the liver further decreases in size and becomes red. The reticular stroma of the liver is exposed with enlarged and sharply overflowing with blood sinusoids. Hepatocytes are preserved only along the periphery of the lobules. These changes characterize the onset of the stage of red dystrophy.

Symptoms of toxic liver dystrophy

With massive necrosis of the liver with toxic dystrophy of the liver, the development of jaundice, processes of hyperplasia of the lymph nodes and spleen located near the portal vein, the appearance of multiple hemorrhages in the skin, mucous membranes and serous membranes, necrosis of epithelial cells in the tubules of the kidneys, dystrophic changes in the tissues of the pancreas and myocardium are noted hearts.

With the progression of this form of the disease, patients often die from the development of hepatorenal syndrome and liver failure.

Toxic chronic liver dystrophy is extremely rare, when the disease recurs, during which the postnecrotic form of liver cirrhosis develops.

Fatty degeneration of the liver

It is a disease or syndrome caused by the development of fatty degeneration in the liver cells in the form of a pathological deposition of fat drops in it. The liver cell accumulates fatty deposits.

Etiology of fatty liver

Fatty degeneration of the liver is a reaction of the liver to intoxication, sometimes associated with a number of diseases and pathological conditions. The most common causes of the fatty form of liver dystrophy are pathologies of the intestinal and biliary tracts, severe obesity, bypass intestinal anastomoses, long-term use parenteral nutrition, diabetes mellitus (type 2), maldigestion and malabsorption syndromes, celiac enteropathy, Wilson-Konovalov's disease and a number of genetically determined diseases, chronic alcohol intoxication, the use of certain drugs (corticosteroids, estrogens, tetracyclines, non-steroidal anti-inflammatory drugs, amiodarone). Almost all chronically occurring viral hepatitis, especially chronic hepatitis C, is accompanied by the development of fatty liver.

The pathogenesis of fatty liver

At the heart of the pathogenesis of the described liver disorder is the process of accumulation of triglycerides and cholesterol in the liver tissues due to excessive absorption and formation of free fatty acids and excessive intake of fatty acids in the liver, a decrease in the rate of oxidation of fatty acids inside the mitochondria of hepatocytes, and difficulties in the processes of utilization of fats from the liver.

Pathological anatomy in fatty liver

The liver with fatty degeneration increases in size, becomes yellow or red-brown, its surface remains smooth. In liver cells, fat is determined from triglycerides. The process of accumulation of fats in hepatocytes can be dusty, large or small droplets. A drop of fat pushes the organelles inside the cells to the periphery. Infiltration with fats can cover both single hepatocytes and groups of hepatocytes and even the entire liver parenchyma. With fatty infiltration, hepatocytes die, and fat drops merge with each other and form fatty cysts with the growth of connective tissue.

Clinic of fatty degeneration of the liver

The course of fatty degeneration of the liver is usually asymptomatic and, mainly, the pathology is detected by chance during instrumental research methods. Pain is not a specific symptom of the disease.

Some patients complain of a feeling of heaviness and discomfort in the right hypochondrium, which are usually aggravated by movement. The liver in this disease is enlarged, but tenderness in the liver is quite rare on palpation. Fatty degeneration of the liver, which develops due to chronic alcohol intoxication, often occurs with anorexia, shortness of breath and a number of other symptoms.

Methods for diagnosing liver dystrophy

The use of traditional laboratory tests to confirm these violations is practically not informative. There is a moderate increase in the activities of the enzymes of serum transaminase and alkaline phosphatase. The level of total bilirubin, albumin and prothrombin are mostly within the normal range. There are no other abnormalities in the blood. When conducting an ultrasound, the doctor notes that the echogenicity of the liver tissues is mostly normal or increased. In some cases, only computed tomography and magnetic resonance imaging can reveal the presence of liver dystrophy. For the final confirmation of the diagnosis, a mandatory biopsy of the liver tissues with a histological examination of the obtained biopsy specimens is required.

Treatment of liver dystrophy

An important measure in the treatment of liver dystrophy is the prevention of the development of necrosis and inflammation (steatohepatitis), the treatment of which is much more complicated. Treatment of liver dystrophy consists primarily in the elimination of the etiological causes that caused it, as well as in the symptomatic treatment of concomitant syndromes of the disease.

Among the drugs that improve the functional states of the liver, one of the leading places is occupied by the complex preparation heptral (ademetionine). Second host medication in the treatment of liver dystrophy is the drug "ursodeoxycholic acid".

The information provided is not a recommendation for the treatment of liver dystrophy, but is a brief description of the disease for the purpose of familiarization. Do not forget that self-medication can harm your health. If signs of illness appear or are suspected, you should immediately consult a doctor. Be healthy.

Any disease can be considered as damage to an organ by various pathogens or a change in metabolic processes at the cellular level. In this case, they speak of dystrophy - such a perversion of metabolism, which is accompanied by a violation of the structure. Often this is an adaptive reaction of the body to adverse environmental influences.

Etiology

The change in metabolism, which develops under the influence of external and internal factors, leads to a violation of the structure of cells. This may be malnutrition, adverse living conditions, trauma, intoxication, poisoning, exposure to infection, endocrine disorders, circulatory pathology, hereditary defects. They affect organs directly or through changes in neurohumoral regulation. The severity of dystrophy is affected by the type of tissues, the strength and duration of exposure to the pathological factor, as well as the body's ability to respond to exposure.

These restructurings are companions of any disease. Sometimes they appear initially and cause a picture of the disease, and sometimes the disease itself disrupts cellular metabolism.

Dystrophic changes in the liver occur under the influence of the following factors:

inflammatory diseases - viral hepatitis, infections; toxic damage - the result of exposure to alcohol, drugs, poisons, industrial harmful substances; malnutrition - the predominance of fatty and carbohydrate foods; violation of the outflow of bile; systemic diseases; endocrine disorders; hereditary diseases.

Pathogenesis

A long study of the processes of dystrophy using the methods of biochemistry, histochemistry, electron microscopy showed that any of them is based on a violation of reactions involving enzymes and a change in the function of cellular structures. In the tissues, metabolites of the altered metabolism accumulate in large quantities, the ability to regenerate and the functions of the damaged organ are impaired. As an outcome - a violation of the vital activity of the body.

Dystrophic changes can proceed according to one of the mechanisms:

Decomposition - at the level of molecules, the structure of tissue systems, protein-fat and mineral compounds are restructured. The reason for this is a change in the ratio of nutrients, the accumulation of metabolic products, hypoxia, exposure to toxins, fever, a shift in the acid-base balance (often towards acidosis), a violation of redox reactions and electrolyte balance. Under the influence of these factors, the components of cell organelles and large molecules can disintegrate or change. Proteins are hydrolyzed by lysosomal enzymes and denatured. More complex formations (amyloid, hyaline) are formed along the same path. Infiltration is the impregnation of organ structures with metabolites of proteins, fats or carbohydrates that are freely found in the blood or lymph (accumulation diseases). Transformation - reactions of the transformation of substances into each other - fats - into carbohydrates, carbohydrates into proteins, synthesis of glycogen from glucose. A large number of new substances are collected inside the cell. Modified synthesis is an increase or decrease in the formation of normal substances in tissues - proteins, fats, glycogen, which leads to their deficiency. Changes in synthesis can occur along the way of creating substances that are not usually inherent in this tissue. For example, glycogen is in the kidneys, keratin is in the lacrimal gland.

These pathological mechanisms may develop sequentially or simultaneously. Morphologically, dystrophies will manifest themselves as a violation of the structure of cells. Usually, after damage to various cellular structures, their regeneration begins. In pathology, it is violated even at the molecular level. Inside the cells, various grains, drops, crystals and other inclusions begin to be identified, which should not be there, or their number in healthy cells is insignificant. The process can also proceed in the opposite direction - inclusions or parts of organelles that are usual for them disappear in the cells.

At the organ level, dystrophy is manifested by a change in appearance. The color, size, shape changes, such processes are said to be “rebirth” or degeneration of the organ. The body changes its functioning - the synthesis of various substances, metabolism. If the etiology of dystrophy is removable and there is no deep damage, then there is the possibility of absolute restoration of the organ. In other cases, the processes are irreversible, necrosis develops.

Types of dystrophy

They are classified according to the level of damage they cause:

parenchymal - affect the parenchyma of the organ; stromal-vascular - rearrangements in microvessels and intercellular space; mixed.

If we consider the pathology of a certain metabolism:

protein; fat; carbohydrate; mineral.

By the extent of the process are:

local; general, or systemic.

There are also acquired and hereditary.

Parenchymal dysproteinoses

A change in the metabolism of cytoplasmic proteins, which are in a bound or free state, is called protein dystrophy. Bound proteins are various lipoprotein complexes, while free proteins are represented by cellular enzymes. Their physical and chemical structure changes, various peptide particles are formed in the cytoplasm. This entails a change in the exchange of water and electrolytes, osmotic pressure, and an increase in fluid saturation.

Morphologically, this is manifested by hyaline-droplet and hydropic dystrophy. The final phase in their existence can be cell necrosis. The final stage of the hyaline-drop metabolic disorder is coagulative necrosis, with hydropic at the end of colliquat cell necrosis. It is possible to consider these changes only with the use of microscopy of damaged areas. With hyaline-drop dysproteinosis, hyaline drops are collected in the cells. Cells affected by hydropic dystrophy increase in volume due to vacuoles with liquid transparent contents.

Granular dystrophy, or cloudy swelling - also parenchymal dystrophy, loss of protein in the form of grains. The causes are a variety of infections, circulatory pathology, malnutrition. Functionally, it does not impair the functioning of the organ and sometimes regresses without a trace.

Hydropic dystrophy, on the contrary, causes depression of liver function. It develops against the background of severe and moderate viral hepatitis, prolonged cholestasis, dystrophic form of cirrhosis. The most pronounced type is balloon dystrophy, which, with a prolonged increase, becomes irreversible and turns into colliquational necrosis. The cells are then melted to a liquid state. Immune cells come to the focus, which remove dead tissue. A scar forms in their place.

Hyaline droplet dystrophy in the liver is manifested by a decrease in cell size, thickening of protein formations. A special type is alcoholic hyaline, or Mallory bodies. This is a special protein, the result of the synthesis of hepatocytes. It is located in the cells around the nucleus and has an acidophilic reaction (stained blue). It has leukotaxis - attracts leukocytes, is able to cause immune reactions, stimulates the formation of collagen. In the blood of patients with alcoholism, circulating immune complexes based on alcoholic hyaline are found, which can affect the kidneys with the formation of glomerulonephritis.

Parenchymal lipidosis

Fatty degeneration is the formation of a large amount of lipids in cells or deposition in areas where it was not previously present, as well as the synthesis of fats of an uncharacteristic structure.

The bulk of the accumulated fats in hepatocytes is neutral fat. It forms droplets that gradually merge into a large vacuole. Fat metabolism is disturbed in three cases:

Massive intake of fats into the body, which eventually leads to a lack of enzymes for their digestion. Toxic substances block the synthesis of fats. Lack of amino acids for the formation of lipoproteins and phospholipids.

The following factors provoke the development of lipidosis:

alcoholism; diabetes mellitus; general obesity; toxic damage; hereditary fermentopathy; diseases of the digestive system.

Fatty liver manifests itself in three forms:

disseminated - lipid droplets are located in separate cells; zonal - fats are collected in special areas of the hepatic lobule; diffuse - the distribution of fat throughout the lobule.

By the size of the inclusions, obesity can be large-drop and small-drop.

Long-term alcohol consumption in almost 50% ends with the formation of fatty hepatosis

Ethyl alcohol and its metabolic products increase the synthesis of fatty acids, but reduce their oxidation and the formation of lipoproteins. Cholesterol accumulates in large quantities, which reduces the permeability of cell membranes. Intracellular fat droplets push the nucleus to the periphery. But the synthetic work of the cell is not broken. With the refusal of alcohol, the reverse development of the process occurs. Functions are restored, accumulated lipids are gradually metabolized and excreted from the liver.

But if the patient prefers to drink alcohol further, then this threatens the transition of fatty degeneration into cirrhosis.

In patients with diabetes, fatty degeneration develops in 70% of cases. This is influenced by such factors:

age - more common in the elderly; type 2 diabetes is associated with obesity or impaired lipid metabolism; the severity of ketoacidosis.

As a result of the lack of insulin and the entry of glucose into the cells, lipolysis is activated - the metabolism of fats, aimed at satisfying energy hunger. The concentration of fatty acids in the blood increases, the liver tries to process them into lipoproteins. The excess goes to the resynthesis of triglycerides. But too much is retained in hepatocytes, causing fatty hepatosis.

Fatty degeneration of the liver is a reversible process. main role here the cessation of the influence of the provoking factor plays - the exclusion of alcohol, the normalization of the composition of food, the reduction in the amount of fat, the controlled course of diabetes.

Fatty degeneration of pregnant women

Separately, it is worth considering the development of acute fatty hepatosis during pregnancy. This is a serious condition that often causes death of the mother or fetus. The causes of occurrence are not fully known. Assume the influence of heredity, a genetically determined defect in the mitochondrial enzyme system. This causes disruption of fatty acid oxidation.

Symptoms of pathology are varied. Some may not develop jaundice. But more often there is a classic course: weakness, lethargy, nausea, heartburn. Jaundice gradually increases, its significant severity is a danger to the mother and fetus. Against the background of heartburn, ulcers of the esophagus are formed, vomiting of “coffee grounds” is possible with esophageal bleeding that has taken place. Liver failure develops with a picture of clouding of consciousness. Often this is accompanied by a syndrome of disseminated intravascular coagulation, which causes death.

Suspicion of the development of acute fatty hepatosis in the 3rd trimester of pregnancy is an indication for emergency delivery to save the life of the mother and child.

carbohydrate degeneration

It is manifested by a violation of the structure or deposition of forms of carbohydrates in atypical places. Often this is the storage form - glycogen. In diabetes and glycogenosis, such processes become possible.

In diabetics, the content of glycogen in the cells is significantly reduced, but it accumulates in the nuclei, which is why they acquire an “empty” appearance, debugging along the vessels and nerves, which damages them and leads to the development of diabetic angiopathy.

If the amount of glycogen in the tissues increases, this condition is called glycogenosis. This is observed in anemia, leukemia, in places of inflammation. It accumulates in the muscles, heart, kidneys, vascular walls. Clinically, it can manifest as cardiac or respiratory failure with a fatal outcome.

Symptoms

The underlying disease that caused the dystrophy will give symptoms. Acute processes are accompanied by weakness, malaise, decreased performance. Stretching of the liver capsule or gallbladder disease will be accompanied by pain syndrome. Often it is a dull aching pain under the ribs on the right. Sometimes it radiates to the back, to the area of ​​the right kidney, to the neck, shoulder blade, shoulder on the right.

Patients are concerned about dyspeptic symptoms - nausea, heartburn, may be vomiting. The chair is broken, there are periods of constipation and diarrhea, often accompanied by bloating, flatulence.

A symptom of jaundice may appear after a few hours or days, as a manifestation of a violation of bilirubin metabolism. The first to react are feces and urine. The faeces become discolored and the urine becomes the color of beer. Parallel worries pruritus- irritation of skin receptors by circulating bile acids.

With advanced dystrophic processes, there are signs of a violation of protein metabolism. Immunity is reduced, infectious diseases occur more often. The lack of synthesis of protein coagulation factors is manifested by bleeding gums, hemorrhages in the skin, hemorrhoidal, gastrointestinal, uterine bleeding.

Protein deficiency leads to insufficient water binding, which is manifested by multiple edema, the development of ascites.

The extreme degree of liver failure is hepatic encephalopathy. This is a syndrome that develops as a result of a metabolic disorder and is manifested by a change in consciousness, behavior, and neuromuscular reactions. It can develop acutely within 7 days, or longer, for 3 months.

The severity of violations depends on the speed of development and the causes that caused this condition. There are personality disorders, memory impairment and decreased intelligence.

Encephalopathy occurs in three stages:

Slight personality changes, complaints of sleep disturbance, decreased attention and memory. Severe personality disorders, often inappropriate behavior, mood swings, drowsiness, monotonous speech. Disorientation in time, stupor, mood swings, aggression, delusional states, pathological reflexes. Hepatic coma - a deep depression of consciousness, a decrease in tendon reflexes, the appearance of pathological ones.

In addition to neurological signs, there are other clinical symptoms - jaundice, liver odor, fever, tachycardia. With extensive necrosis, infection may join. Death often occurs from cerebral edema, renal failure, pulmonary edema, toxic or hypovolemic shock.

Diagnostics

The examination begins with the collection of anamnesis data:

patient complaints; time of onset of signs of the disease; their development over time; connection with various factors - alcohol consumption, nutrition, physical activity; indication of unprotected sexual contacts, injections, visits to the dentist, tattoos, blood transfusions in the last 6 months; the presence of gastrointestinal diseases intestinal tract, liver, diabetes, pregnancy.

General examination reveals excess weight, skin discoloration, scratching, bleeding in the skin, rash, pigmentation, swelling of the extremities, or accumulation of fluid in the abdominal cavity.

Liver dystrophy is a morphological characteristic of processes that are caused by the influence of various pathogenic factors. Therefore, the diagnosis aims to establish the disease that led to the development of organ dystrophy. For this, methods are used laboratory diagnostics. General analysis blood reflects the presence of inflammation in the body. A biochemical blood test makes it possible to judge the state of the synthetic function of the liver, the presence of cytolytic reactions, and cell damage.

A study is underway of markers of viral hepatitis, which also cause liver dystrophy.

The next step is an ultrasound. The method is non-invasive and allows to detect diffuse or focal changes in the tissue. By the nature of the ultrasound image, fatty infiltration of the liver, the development of fibrosis or cirrhosis can be assumed. Well seen on ultrasound volumetric formations, cavities, cysts, calcifications, signs of portal hypertension are distinguishable.

The use of x-ray methods allows you to determine the presence of changes in the liver, an increase in its size. Contrasting biliary tract or vessels shows their condition, tortuosity, the presence of constrictions, obstacles to the outflow of bile. Methods such as CT and MRI are also used. There are no specific signs indicating the development of dystrophy. This can be guessed by detecting changes in the parenchyma characteristic of various diseases.

The morphological picture can be established only with the help of a biopsy. But this is a traumatic method that can lead to serious complications. Therefore, it is used only according to indications:

clarification of the etiology of liver disease; chronic viral hepatitis; storage diseases (hemochromatosis, Wilson's syndrome); biliary cirrhosis to determine the degree of inflammatory response and fibrotic changes; carcinoma; monitoring the effect of the treatment of these diseases.

There are conditions in which this method is absolutely contraindicated:

serious condition of the patient; menstrual bleeding in women; signs of a violation of blood clotting; a decrease in platelet levels; obstructive jaundice.

For the diagnosis of fatty degeneration, it is not advisable to use the method. This form has the ability to regress under the influence of treatment and diet. Therefore, the data obtained from the study will be irrelevant after 2-3 weeks.

Treatment

To effectively cope with the disease, therapy should go through the following steps:

rational nutrition; treatment of concomitant pathology; restoration of the liver; consolidation of results.

Conservative therapy

Treatment of concomitant diseases consists in adequate therapy of diabetes mellitus prescribed by an endocrinologist. Diseases of the gastrointestinal tract are treated by a gastroenterologist or a local internist. For the treatment of alcohol addiction, if a person is not able to cope with cravings for alcohol, a narcologist is involved.

For treatment, drugs of various groups are used:

Hepatoprotectors. Antioxidants. Statins.

Hepatoprotectors can have various effects. They stabilize cell membranes, restore their integrity, and improve the synthetic abilities of cells. Contribute to the improvement of the metabolism of bilirubin, fatty acids, proteins. Representatives of the group are drugs Karsil, Liv-52, Hofitol, Essentiale, ursodeoxycholic acid and drugs based on it.

Choleretic drugs Allohol, Holsas are also used. They improve the synthesis of bile, its secretion, regulate the composition, reduce congestion in the liver.

Statins are used to correct the lipid profile of the blood. They reduce the absorption of fats in the intestines, remove excess cholesterol, preventing it from getting back into the blood.

Treatment of a severe form of dystrophy, accompanied by hepatic encephalopathy, takes place in the intensive care unit. Treatment is symptomatic. The patient is transferred to parenteral nutrition and fluid administration, limit the amount of protein. Drugs are used to correct the acid-base state, often this condition develops acidosis, so the introduction of sodium bicarbonate is necessary. Antibiotics are prescribed to suppress intestinal flora.

Sometimes there is a need for extracorporeal detoxification, especially after the addition of kidney failure. To maintain the overall metabolism in large doses, glucocorticoids are used. This state often ends lethal outcome.

Treatment with folk methods

Herbal medicine and traditional medicine can be used as auxiliary methods of treatment after consultation with a doctor. They offer various recipes to get rid of dystrophy.

You can consume 2 tablespoons of lemon juice daily mixed with the same amount of water.

Within a month, drink 2 glasses a day of an infusion made from milk thistle fruits, dandelion root, nettle, birch leaves. This mixture is poured with a glass of boiling water and infused for 15 minutes.

If you cut off the top from a ripe pumpkin and remove the seeds, you get a container into which you need to pour fresh honey and put it in a dark, cool place for half a month. After that, pour the resulting therapeutic composition into a jar and consume one spoonful before meals.

On an empty stomach for a month, they drink a mixture of freshly squeezed carrot juice and warm milk in equal proportions.

Grind milk thistle seeds to a powder. 3 tablespoons brew 0.5 liters of water, boil by half. Drink a tablespoon an hour before meals for 1 month.

Effectively helps a decoction of dried pears and oatmeal. Take 4 tablespoons of oatmeal for a glass of fruit, boil in a liter of water. Eat the entire serving during the day.

St. John's wort, horsetail, rose hips, motherwort shoots mixed in equal parts. Boil a tablespoon of the mixture in a glass of water. Drink the resulting broth during the day, divided into 4 doses.

Mix a tablespoon of petals from wild rose flowers with half a spoon of honey. Eat this mixture after meals with tea.

Diet

Liver treatment does not imply a strict diet as for weight loss. Hunger will do even more damage. Nutrition should be balanced in lipid-protein composition. The fat content is limited due to animal origin - butter, cheeses, lard, meat of fatty breeds. This will reduce the saturation of food with fats, reduce their absorption, and hence the negative impact on the liver.

The amount of protein, on the contrary, should be increased at the expense of animal products. It is their proteins that have a complete composition of amino acids, contain an indispensable group. Protein is needed for the synthetic processes of the liver - the construction of its own enzymes, the formation of lipoproteins from fats, the production of various proteins of the human body - immune system, blood clotting.

The amount of carbohydrates is the largest, they are the energy substrate. But we must remember that preference is given to vegetable carbohydrates, fiber, dietary fiber. Simple sugars contained in sweets, rich pastries, are quickly processed, significantly raise the level of glucose, which will complicate the patient's situation.

Alcohol is absolutely forbidden, it is one of the reasons for the development of dystrophy, so it must be excluded in the first place.

The diet can be described as a dairy-vegetarian diet with the addition of lean meat and fish. Vegetables and fruits can be consumed in any form. The exceptions are sorrel, legumes, mushrooms.

The amount of salt is reduced to 15 g per day. In order not to be mistaken, food is cooked without salt, salted on your plate.

If the cause of dystrophy is diabetes mellitus, nutrition should be built on the system of bread units. It calculates the amount of carbohydrates needed for a person per day. They are distributed according to meals and then, according to special tables, they determine how much one or another product can be eaten. This system helps control glucose levels in diabetics, reduces weight. It can also be used to feed overweight people. Excess weight will gradually go away.

If liver dystrophy has reached a severe state of hepatic encephalopathy, then nutrition is built differently. The amount of protein is limited to 50 g per day. This is necessary so that the liver can cope with the detoxification of protein metabolism products. If the condition worsens, it is generally canceled, parenteral nutrition is started.

Prevention and prognosis

Prevention is aimed at eliminating risk factors for conditions and diseases that lead to the development of dystrophic processes. Excess weight must be taken under control, try to reduce it to acceptable numbers. To do this, you first need to determine the body mass index. If it is above 25, then it's time to think about weight loss.

Even if the weight is normal, but the diet is dominated by foods rich in fats, you should try to reduce their amount, this will reduce the load on the liver enzyme systems.

Starvation and rigid diets will not bring benefits. Protein deficiency will cause malnutrition and the development of fatty degeneration, because. there will be no substrate for the synthesis of protein-fat molecules.

Alcohol, even with a small but regular use, has a toxic effect on liver cells, damages them and causes pathological mechanisms for the synthesis of a non-typical hyaline protein or fat deposition. A complete refusal to drink alcohol in the early stages of fatty degeneration can lead to an improvement in the patient's condition. With advanced cirrhosis, this will hold back the onset of hepatic encephalopathy and the terminal stage.

Viral damage to the liver can be avoided if one is aware of the routes of transmission. To prevent hepatitis A, you need to observe personal hygiene, wash your hands, fruits, and do not use drinking water from open sources. Viruses of types B and C are transmitted through blood, therefore, when performing invasive procedures, use disposable instruments, use only a personal manicure set, do not have unprotected sex, and after a blood transfusion, be examined for hepatitis after 6 months.

Women during pregnancy planning should minimize the manifestations of existing chronic diseases of the gastrointestinal tract, pathology of the biliary tract. During pregnancy, as a result of hormonal changes, there is a risk of developing gestational diabetes mellitus, which can manifest fatty hepatosis as a latent hereditary disorder of estrogen metabolism. Therefore, following a diet low in fat and simple carbohydrates will prevent liver dysfunction.

Any diseases of the gastrointestinal tract should be diagnosed and treated in a timely manner.

The accumulation of fatty tissues in the liver causes this pathology and leads to dysfunction of the organ. The mechanism of the progression of the disease is such that the initial stage is characterized by the accumulation of excess fat in the hepatocytes (liver cells) themselves, and with an excess content, breaks through cell membrane and leads to the proliferation of connective tissue and fatty degeneration of the liver.

Features of such pathologies, as well as a possible treatment plan, are given in our article.

The concept and code of the disease according to ICD-10

Fatty hepatosis is characterized by a different nature of the occurrence and rate of cell transformation. Depending on the origin, two forms of hepatosis are distinguished: alcoholic and non-alcoholic.

They also classify the primary and secondary forms of the disease. In the International Classifier of Diseases, it is registered under the code K 76.0 - fatty degeneration of the liver.

Causes

The risk factors leading to the development of such a disease are common to all characteristic liver diseases. Under the influence of toxic substances, most often alcohol, the excretory function of the liver is disrupted, and healthy hepatocytes die, which are replaced by connective (fibrous) tissue.

The photo shows fatty hepatosis of the liver

Other chemical compounds also contribute to liver poisoning, such as working in hazardous conditions or living in ecologically unfavorable areas.

The health of the liver is influenced by the lifestyle and eating habits of the patient, as well as hereditary factors. Most often, several causes contribute to the onset of the disease at once, so the risk of hepatosis should be considered in the following cases.

For what reasons can a disease occur:

• hereditary predisposition.
• Metabolic disorders in endocrine diseases.
• (usually over ten years).
• Long-term use of certain medications (most often non-steroidal anti-inflammatory drugs).
• Diseases of viral hepatitis.
• Violations of the normal and functioning of the gallbladder.
• Metabolic disorders, obesity.
• Constant food restriction, strict diets and starvation.

A combination of causes leads to the development of fatty hepatosis. In some cases, the cause may not be clear, so no one is immune from such a disease.

Degrees

Depending on the number of affected cells, there are four stages of the disease, which determine the further prognosis for the patient.

Hepatosis classification:

• Zero stage. Separate groups of cells contain fatty inclusions.
• First degree characterized by damage from 10 to 335 hepatocytes. Fat droplets become larger in size, forming separate lesions.
• Second degree determines cell damage at the level of 33 - 66% of the total. Cellular obesity is formed by various kinds of compounds.
• Third stage. Fat inclusions go beyond the boundaries of hepatocytes, forming fatty cysts. Cell damage reaches more than 66%.

Adequate treatment will help eliminate unpleasant symptoms and completely get rid of the disease. It will take years, and the doctor's recommendations must be followed for the rest of your life, but compared to the prospect of cirrhosis and death, this is the most acceptable option.

Symptoms

For the most part, the manifestations of the disease can be seen only in advanced stages.

Prior to this, hepatosis does not manifest itself in any way and the disease can be detected only during a preventive examination, including ultrasound of the abdominal cavity.

Objective complaints begin to appear when more than 10% of the total number of replaced liver cells becomes. At this stage, more than half of the body ceases to perform its functions.

Common complaints are:

1. Soreness in right side.
2. Enlarged liver size, noticeable with.
3. Digestive disorders: vomiting, or constipation.
4. Deterioration of the skin and hair.
5. predisposition to colds, poor immunity and allergic reactions.
6. Reproductive disorders, impossibility of conception.
7. In women, there are deviations of the menstrual cycle, heavy or irregular bleeding.
8. Deterioration of blood clotting.

Usually anxiety symptoms do not appear at once, but increase over time. First, patients complain of soreness and discomfort, then symptoms of intoxication of the body appear, because the affected organ ceases to perform its function.

Video program about the signs of fatty liver hepatosis:

Acute disease in pregnant women: clinical guidelines

Hepatosis of the liver is one of the most complex pathologies of pregnant women. Symptoms can be confused with food poisoning or infectious disease. The correct diagnosis is difficult and acute clinical picture, because the symptoms are diverse.

What are the patients complaining about?

• Frequent vomiting without relief.
• Pain in the abdomen of unclear localization.
• Jaundice of the skin and sclera.
• General deterioration.

According to statistics, this pathology develops between 30 and 38 weeks of pregnancy.

Cases of acute fatty hepatosis occur approximately once in 13,500 - 14,000 births, so timely diagnosis is extremely difficult.

Usually a woman enters the hospital with a suspected infection or late toxicosis, which is considered a threat to not bearing. Unfortunately, the only possible treatment will be delivery as soon as possible followed by drug therapy.

Previously, mortality from such a pathology was almost 100%, now the threat is less (about 25%), but still, such a complication of pregnancy is considered extremely dangerous for the life of the mother and child, so all possible measures should be taken immediately.

alcohol form

Alcohol is the main enemy of the liver, because it leads to its dysfunction.

Hepatosis that has arisen for such reasons quickly degenerates into, which is an irreversible violation of the structure and functions of the liver.

With this development, the prognosis for the patient is extremely negative, because usually the survival rate of patients is about 40% in the first three years.

Fatty hepatosis of the pancreas: treatment

A specialist hepatologist will help prescribe the optimal therapy. Based on the examinations and analysis data, an individual course of medications is selected.

The dosage and regimen will be somewhat different, because such funds should provide unloading of the affected organ, as well as improve functions due to special enzymes.

Treatment includes the following items:

1. Strict diet. Compliance with food restrictions is a prerequisite for successful treatment. The diet should be varied, but as light and nutritious as possible.
2. Lifelong abstinence from alcohol. Even with the development of non-alcoholic fatty hepatosis, giving up bad habits, including smoking, must be conscious.
Leading Patients sedentary image life, are at risk for the development of such a disease, so the necessary plan physical training can be agreed with the doctor.
3. Medical therapy. The selection of drugs is carried out on an individual basis, and such funds will have to be taken in long courses for the rest of your life. According to laboratory tests, the dosage and type of drug are adjusted, but medical support liver function plays an important role in its treatment of hepatosis.
4. Traditional medicine methods, including the use of herbal decoctions. They have a choleretic, cleansing and diuretic effect, are effective in the complex therapy of hepatosis.

A separate word can be said about special preparations - hepatoprotectors. They contribute to the normalization of liver function, even with significant damage to hepatocytes.

Usually, such drugs are safe for long-term use, you can choose the optimal dosage for each patient, and their effectiveness will allow them to be used even in the treatment of cirrhosis.

Essentiale, Galsten, Phosphogliv, Glutargin and Arginine drugs caused particular popularity and trust of patients. In addition, ursodeoxycholic acid preparations are often used, for example, Ursofalk, Grinterol, Ukrliv, Ursodesk and others. They are used for biliary disorders of the biliary tract.

Why is the disease dangerous?

Fatty hepatosis leads to liver dysfunction, which is deadly for the patient.

Gradual intoxication of the body negatively affects the functioning of the heart, kidneys and even lungs, causing irreversible damage. Most often, hepatosis develops into, but this disease is not at all treatable.

In addition, the following complications are noted:

• (enlargement of the liver).
• Disorders of the cardiovascular system.
• Dysfunction of the abdominal vessels.
• General intoxication of the body.
• Progressive.

The development of cirrhosis with diagnosed hepatosis is a matter of time. The degeneration of cells and the growth of connective tissue in hepatosis of the last degree is irreversible, and therefore leads to the appearance of cirrhosis.

The rate of development of such an ailment differs in each individual case, but the prognosis for the patient is very unfavorable.

Diagnostics

It is impossible to determine the disease at an early stage using laboratory tests. Unfortunately, an increase in normal liver enzymes occurs already with progressive hepatosis.

At the zero and first stages, the disease is diagnosed exclusively by special research methods, for example, or. It is distinguished by good information content and safety, which will show all tissue changes.

How to cleanse the liver with traditional medicine?

An effective method of treating and preventing hepatosis is liver cleansing. It can be carried out independently, but a preliminary consultation with a doctor is necessary. If there are no contraindications, and the specialist has approved the chosen method, you can proceed with the procedure.

Options for independent use:

• Preventive cleansing begins with a preliminary cleansing of the intestines.(fasting and enemas, only drinking water is allowed), after two days you need to take two tablets of allochol and lie on your right side. An hour later, drink 50 grams of warm vegetable oil (olive or linseed is best), then 30 grams of lemon juice. Apply a heating pad to your right side and lie down for at least two hours.
• Cleansing with vegetable oil is also very effective. To do this, three days before the event, you must completely abandon food of animal origin, make a cleansing enema the day before. Before cleaning, it is also worth completely eliminating solid foods, replacing with a small amount of natural vegetable juice. Every day at 19 o'clock (the optimal time for the release of bile), you need to drink 100 - 120 grams of warm vegetable oil. After that, it is worth lying down, using a heating pad on the right side. After about two hours, the process of bowel release will begin. You can repeat this cleaning two to three times a year.
• Cleaning with buckwheat porridge. To do this, it is necessary to cook 50 grams of buckwheat chopped per 200 grams of water. Boil for a long time, about 20 - 35 minutes, without salt, oil and other ingredients. Eat porridge in one go while warm. After that, lie on your right side, placing a heating pad under it. After a while, go to the toilet. The feces will be liquid, dark in color, which indicates the effectiveness of cleaning. You can repeat this cleaning no more than once a month.

When carrying out such procedures, it is very important to follow the recommendations of the doctor, and also not to abuse these methods. If you feel worse, be sure to consult your doctor to avoid possible complications.

Diet: sample menu

Adjusting your diet to take into account liver pathologies is not so difficult. To do this, one should take into account the need for fractional nutrition (portions should be designed for 4-5 single meals), cooking technology (cooking, steaming and baking, rarely stewing).

The amount of salt must be reduced, and fat must be removed from the diet.

In general, the composition of the diet remains complete, only alcoholic beverages, “harmful” foods and fatty foods are removed. The information provided will help to accurately determine all the boundaries of what is permitted.

Allowed foods:

• Lean meat, meat products.
• Low-fat fish stewed and boiled.
• Milk boiled sausages.
• Vegetable and milk soups.
• Chicken egg (1 piece per day).
• Mild cheese, ham.
• Kashi on the water.
• Low fat dairy products.
• Boiled or stewed vegetables (can be baked).
• Vegetable salads.
• Omelet for a couple.
• Fresh fruits (except citrus fruits) and non-acidic berries.
• Compotes, jelly, decoctions, weak tea.

It should be borne in mind that the daily rate of fat is reduced to 70 grams. Sour cream, fermented baked milk, fatty cottage cheese are used with caution. It is also worth limiting the consumption of strong tea, coffee, mineral sparkling water.

Legumes should be consumed in very limited quantities. If you have problems with digestion, this product is completely removed from the diet.

Prohibited Products:

• Any kind of alcohol.
• Sweet sparkling water.
• Purchased snacks (chips, nuts and crackers).
• Spicy, fatty and overly spicy dishes.
• Concentrated meat broths.
• Pickles and smoked meats.
• Fresh onion and garlic.
• Fresh radish and radish.

An important requirement of the diet is fractional nutrition. You should divide the diet into several small portions and sit down at the table four to five times a day. You will need to follow a diet for life, for which you will not be long in improving your well-being.

Is it possible to cure the pathology completely?

Hepatosis diagnosed at an early stage is successfully treated medication adjustment. Special preparations and a radical change in lifestyle and eating habits will help to avoid complications.

At the last stage or with insufficient treatment, hepatosis progresses rapidly and leads to severe complications and. In this case, it is impossible to get rid of the disease, the drugs only eliminate the accompanying manifestations and discomfort.

Prevention

The best way to avoid developing this disease is to follow the rules of a healthy lifestyle. A strict diet, the exclusion of alcohol, harmful and difficult to digest food, as well as fractional nutrition - all these activities should become permanent.

It is very important to undergo examinations on time, to treat the acute phase of diseases, preventing the transition to a chronic form. In addition, if there are associated problems, for example, being overweight, you should work hard on yourself to reduce the risks of such a pathology.

Fatty hepatosis is a serious liver disease that leads to irreversible consequences in the organ.

Under the influence of external and internal adverse factors, liver cells accumulate excess fat, which then fills the entire space in the affected organ. Such a pathology often leads to, which is an irreversible disease and a mortal threat to the patient.