home Auditorium 8 Steatohepatitis - what is it? Types, causes, symptoms, diagnosis and treatment. Non-alcoholic steatohepatitis

Steatohepatitis - what is it? Types, causes, symptoms, diagnosis and treatment. Non-alcoholic steatohepatitis

Steatohepatitis is an inflammation of the liver that occurs against the background of its fatty degeneration (hepatosis). Most often it happens due to alcohol, certain medications, and poisoning. When steatohepatitis is diagnosed, a person often does not know what it is or how to treat it. Irreversible changes in liver cells can be stopped by relieving inflammation and protecting the organ. And to do this, you need to find out what caused the fatty infiltration of the liver and eliminate the provoking factors.

What is steatohepatitis and how does it differ from hepatosis?

Any dystrophic changes in liver cells caused by metabolic disorders are called hepatosis. Hepatosis is caused by various liver diseases, including viral etiology associated with or without inflammation of the organ.

Steatohepatitis is a form of hepatosis caused by fatty degeneration of the liver tissue with its inflammation. Liver degeneration occurs under the influence of two factors:

Exogenous – result chemical exposure on the liver as a result of drug treatments for cancer, tuberculosis and HIV infection. This also includes food poisoning as a result of regular consumption of alcoholic beverages, fatty and unhealthy foods.
The hereditary factor was discovered relatively recently. A genetic marker for metabolic syndrome, which is the main cause of fatty liver degeneration, has been discovered. In the presence of this marker in the blood, elevated lipid levels, high diastolic (lower) pressure and insulin resistance of cells are observed.

Regardless of the factor causing steatohepatitis, diagnosis in the early stages, nutritional correction and adequate therapy in combination with physical activity, they promise good prognoses. It is possible to stop the degeneration of liver tissue.

Classification of steatohepatitis by causes and characteristic symptoms

Alcoholic steatohepatitis, or ASH, accounts for no more than 20-30% of the total number of patients with this disease. Other patients or owners hereditary syndrome, or carriers of diseases whose therapy led to fatty degeneration of the liver. Another risk factor is a violation of lipid and hormonal metabolism in the body.

Regardless of the source of occurrence, steatohepatitis has common symptoms:

tugging Blunt pain right and lower chest;
jaundice - the characteristic color of the skin and whites of the eyes;
a person feels the liver when tilting the body - the organ is enlarged;
pain on palpation of the abdomen.

The person feels general malaise and fatigue.

Alcoholic

It is a consequence of drinking alcohol. A woman needs 20-40 g of ethanol per day, which corresponds to 60-120 g of vodka, to start the process of fatty degeneration, and a man needs 2 times more. Ethanol is found in all alcoholic beverages without exception, including beer, liqueurs and dry wine.

What happens to the liver when ethanol enters:

90% of alcohol consumed with alcohol is metabolized in the liver. Its components are split into acetaldehyde and acetone.
These components slow down the oxidation of fatty acids, and they accumulate in the liver, replacing healthy liver cells (hepatocytes) with fatty ones. Symptoms of steatohepatitis occur.
The liver tissue contains the enzyme alcohol dehydrogenase, which takes part in the breakdown of ethanol. The lack of this enzyme leads to the fact that even small doses of ethanol entering the liver occasionally can lead to fatty degeneration. Against this background, chronic hepatosis, or steatohepatitis of minimal activity, develops.

If this process of fatty degeneration has already started, then even minimal doses of alcohol steadily lead to cirrhosis. Unlike non-alcoholic steatohepatitis, it is enough to avoid drinking alcohol to stop the degeneration process.

Non-alcoholic

It occurs against the background of a violation of fat and carbohydrate metabolism in the human body. Non-alcoholic steatohepatitis, or NASH, is caused by:

Hereditary factor, when a genetic marker for metabolic syndrome is detected. It is also called metabolic steatohepatitis.
Obesity when the body mass index exceeds a factor of 30. It is calculated by the formula: weight in kg divided by height in meters squared.
Type 2 diabetes. Up to 60% of people with diabetes suffer from NASH.
Hyperlipidemia (increased levels of lipids in the blood) promotes the accumulation of fat in liver cells.
Increased cholesterol levels in the blood.

Whatever the reason, once the amount of fat in the liver cells exceeds 5-10% of the total weight of the liver, the level begins to increase. free radicals, attacking liver cells and leading to the destruction of cell membranes. And this is a process of inflammation of hepatocytes, provoking cirrhosis or cancer.

Drug

The dosage form of steatohepatitis can develop during drug treatment strong drugs, disrupting lipid metabolism and causing insulin resistance of cells.

If you are concerned about heaviness in the right hypochondrium, bitterness in the mouth, or unexplained weakness, you need to consult a therapist and undergo the necessary tests. If liver problems are detected, you will be referred to a gastroenterologist or hepatologist.

As a result, symptoms appear:

frequent attacks of pain in the right side;
cholestatic syndrome - an increase in bilirubin in the blood due to impaired production or stagnation of bile, resulting in jaundice;
skin rash and itching.

Medicines that can cause liver steatohepatitis:

Tetracycline antibiotics - Tetracycline, Terramycin, Biomycin, Minocycline, used in the treatment of respiratory tract infections, sore throat, scarlet fever, brucillosis, etc.
Hormonal contraceptives.
Antifungal drugs – Ketoconazole, Fluorocytosine, Amphotericin, etc.
All drugs used to treat HIV infection.
Calcium antagonists - Verapamil, Cinnarizine, Bepridil, Diltiazem, Amlodipine, etc. Medicines in this group are constantly taken by people suffering from hypertension and heart rhythm disorders.

Stages and complications

Non-alcoholic steatohepatitis can be primary or secondary:

Primary steatohepatitis occurs against the background of metabolic disorders in the body.
Secondary – against the background of other diseases (type 2 diabetes, endocrine diseases, HIV infection, tuberculosis, etc.).

Regardless of the etiology, there are three degrees of activity of steatohepatitis:

The first degree is the level of minimal activity, when no more than 33% of the liver tissue is affected. Large-droplet fatty foci are evenly distributed over the entire surface. This usually happens due to excessive and improper nutrition, physical inactivity. It is worth changing your diet and lifestyle to stop the process of obesity.
The second degree of steatohepatitis is characterized by liver damage from 33 to 66% of the total mass. This condition is called moderate hepatosis, but without proper treatment and lifestyle changes, cirrhosis is not far away.
The third degree is severe. More than 66% of hepatocytes are affected. A constant, sluggish inflammatory process leading to the final stage – cirrhosis.

A complication of steatohepatitis can be cirrhosis, a severe form of the disease that invariably leads to fatal outcome. The only way to prolong a patient's life is a donor liver transplant.

How is the disease determined?

To diagnose steatohepatitis, a doctor does not need a visual examination and medical history. Usually the patient comes with the following complaints:

sweating and constant fatigue;
pain in the right hypochondrium;
constant thirst and aversion to food;
yellowness of the skin;
skin rashes and severe itching.

General clinical blood test.
A biochemical blood test will show an increase in the level of liver enzymes AST and ALT. This indicates an inflammatory process.
An ultrasound of the affected organ, MRI or CT is performed.
Liver biopsy.

All these diagnostic measures are carried out as prescribed by a doctor. Sometimes an ultrasound and blood tests are enough to make an accurate diagnosis. A biopsy may be required to clarify.

Treatment options

You need to start fighting steatohepatitis with lifestyle changes. In the first degree of damage, this is enough to stop the process.

Quitting alcohol will help prevent further liver damage.

You need to eat less fatty and fried foods. Dietary table No. 5 on for a long time, or better yet forever, should become the basis of nutrition. More movement, sports, complete failure from alcohol. If the disease has reached the 2nd degree, then along with these recommendations it is necessary drug treatment. The doctor will advise you on how to replace the medications that have caused fatty liver degeneration.

Medicines

To relieve the inflammatory process and restore liver function in steatohepatitis, the following drugs are prescribed:

Lipotropic substances - Citrarginine, Alcosul, Bicyclol. They normalize the metabolism of lipids and cholesterol in the body. Thanks to them, fat is mobilized in the liver and oxidized. The level of fatty infiltration is reduced.
Hepatoprotective drugs - Essentiale N, Silymarin Sandoz, Gepabene, Karsil Forte, Levasil, Leganol, etc. These drugs prevent the destruction of cell membranes and stimulate the regeneration of hepatocytes.
Cytoprotectors are antioxidants and antihypoxants. New generation drugs, there is no solid evidence base for their effectiveness yet, but in complex therapy contribute speedy recovery cells of the liver, stomach, mucosa. Such drugs include Cytoflavin in ampoules, Mafusol, Mexidol, Actovegin, Gliatilin.

All medications can be taken only as prescribed by a doctor, after diagnosis.

Folk recipes

In the early stages of steatohepatitis, treatment with folk remedies is welcomed by hepatologists. Serious damage to the liver tissue cannot be cured using traditional methods, but there will be no harm from them. Therefore, it is worth adopting folk methods as auxiliary ones:

Taking 10 g of pine nuts per day has a hepatoprotective effect.
An excellent remedy is pumpkin with honey. It's very easy to prepare. Cut off the top of the pumpkin, remove all the seeds, and pour honey into the hole. Close the cut top like a lid and cover the cut with dough to prevent air from leaking through. Leave in a dark, cool place for 10 days. Then pour the contents into a clean jar and refrigerate. Take 0.5 hour before meals, 1 tbsp. l.
Infusions of mint, lemon balm, rose hips and milk thistle also have an antioxidant and hepatoprotective effect on liver cells. Drink during the day instead of tea or together with it.

Diet

Diet for steatohepatitis is a fundamental factor in treatment. You will have to give up these products forever:

fatty and fried foods;
full fat milk;
lard, sausages, smoked meats are strictly prohibited;
fatty salted herring, smoked fish, fatty varieties exclude fish even when boiled;
chocolate, confectionery;
mayonnaise, herbs, spices;
rich meat and mushroom broths;
strong tea, coffee, carbonated drinks.

You should always have on your table:

fresh and boiled vegetables and fruits;
honey and jam;
dried bread;
vegetable oil and nuts;
cereal porridge;
dietary varieties of meat, fish and seafood;
eggs (no more than 1 per day);
pasta from durum wheat;
green tea, compotes and jelly.

Other measures

For all forms of obesity, including liver tissue, it is important to consume large quantity oxygen to cells. Thanks to oxygen, fats are oxidized and burned in the body.

The further life prognosis is entirely influenced by the degree of activity of the pathology. The non-alcoholic process, if no active treatment is undertaken, will gradually turn into terrible disease- cirrhosis of the liver.

The following will help increase the flow of oxygen:

Breathing exercises daily for 20 minutes in the morning and evening before bed.
Walk at a good pace for at least 45 minutes a day.
Aerobic exercises increase the number of heart contractions and enrich the blood with oxygen.
Swimming has an aerobic effect and helps burn fat in the body.

Treatment prognosis and prevention

The liver is the only organ that can recover completely in the absence of harmful factors And adequate treatment. Therefore, the prognosis for treatment at the first stage is positive, provided that preventive measures are followed:

maintain intensive motor mode;
adhere to dietary nutrition;
keep body weight under control;
do not self-medicate.

Even these easy actions aimed at strengthening your own health will be enough to keep your liver working smoothly.

Literature

Which doctors should you contact if you have non-alcoholic steatohepatitis?

What is Non-alcoholic steatohepatitis

Non-alcoholic steatohepatitis (NASH)- a disease with histological signs of alcohol-induced liver damage that occurs in individuals who do not abuse alcohol.

In 1980, Ludwig et al. described histological changes in the liver, similar to the picture of alcoholic hepatitis, in patients who do not drink alcohol in quantities that cause liver damage. To designate this condition as an independent nosological form, there are terms “diabetic hepatitis”, “pseudoalcoholic hepatitis”, etc., but the most commonly used expression has become “non-alcoholic steatohepatitis” (NASH).

What causes non-alcoholic steatohepatitis?

Risk factors contributing to the progression of NASH are elderly age, obesity, diabetes mellitus, Ac AT/Al AT activity ratio > 1.

Prevalence. The incidence of NASH in Western countries is 7-9%, in Japan - 1.2% among all patients who underwent liver biopsy.

Pathogenesis (what happens?) during Non-alcoholic steatohepatitis

Regardless of the background target organ damage. Dyslipoproteinemia changes in metabolism are characterized by systemic lesions and are accompanied by impaired bile synthesis in hepatocytes, activation of the LPO system, and inhibition of the activity of the liver RES. Damage to this organ is manifested by dystrophy and steatosis. There are primary and secondary NASH. Female gender plays a role in the development of NASH. Primary steatohepatitis most often occurs in individuals with endogenous disorders of lipid and carbohydrate (in type II diabetes mellitus) metabolism, and with obesity; secondary develops as a result of metabolic disorders, taking a number of medications (amiodarone, glucocorticoids, estrogens, non-steroidal anti-inflammatory drugs, antibiotics, calcium anal antagonists), fasting, parenteral nutrition, jejunoileal anomosis, resection of the small intestine, abetalipoproteinemia, lipodystrophy of the extremities, Westphal disease -Wilson-Konovalov, William-Christian disease in approximately 40% of patients cannot be identified as having risk factors. Among patients with NASH, heterozygotes for C282U are more common. The pathogenetic mechanisms of the disease have not been sufficiently studied. Many theories have been proposed for the development of fatty liver. All of them are based on disruption of the processes of synthesis and secretion of triglycerides in the liver. It is believed that hepatic steatosis precedes the development of steatohepatitis. Accumulation of fat in hepatocytes and stellate cells may be a consequence of an increased supply of free fatty acids (FFA) or an increase in their synthesis in the liver, a decrease in the rate of their (3-oxidation in mitochondria, a decrease in the synthesis or secretion of very low density lipoproteins (VLDL). Being highly reactogenic compounds, FFAs are a substrate of lipid peroxidation, which contributes to the swelling of mitochondria, fragility of lysosomes, disruption of the integrity of cell membranes, the formation of Mallory bodies, and stimulates collagen formation. It has been established that in NASH there is an increase in the activity of cytochrome P-450 2E1. According to E Giannim et al. In the development of steatohepatitis, an important role is given to a specific protein, leptin, the content of which in this category of people is increased. Letin regulates food intake and energy expenditure, is associated with the regulation of insulin, and plays a role. important role in the deposition of fat in the liver.

Patients with primary NASH with excess body weight have pronounced reserves of FFA in the body, decreased sensitivity peripheral insulin receptors, increasing insulin levels in the blood. At the same time, insulin activates the synthesis of FFA and triglycerides, reduces the rate of 3-oxidation of FFA in the liver and the secretion of lipids into the bloodstream. These phenomena contribute to an increase in fat content in the liver.

The mechanism of development of secondary NASH in malabsorption syndrome is a deficiency of intake nutritional factors(methionine, cholil), increased mobilization of FFA from fat depots.

The accumulation of potentially toxic FFAs in the cytoplasm of hepatocytes is associated with a genetic predisposition to the development of HAS1. Birth defects(3-oxidation of FFAs can be caused by a violation of the uptake of carnitine by hepatocytes, the transfer of fatty acids into mitochondria (proceeding with the participation of a number of enzymes and carnitine), dysfunction of the multienzyme complex (3-oxidation). Changes in the structure of the mitochondrial DIC are accompanied by inhibition of the oxidative phosphorylation system and the restoration necessary for p -oxidation of NAD+ and FAD I Ludwig distinguishes three main forms of steatohepatitis.

Microvesicular fatty degeneration without fibrosis with minimal inflammation. In this case, a non-progressive course of the process is observed. At the same time, the presence of centrilobular fibrosis may indicate a transition to a progressive course
Macrovesicular fatty degeneration with moderate mixed centrilobular infiltrates or with finely focal necrosis. In some cases, perivascular and perisinusoidal fibrosis is observed in the 3rd zone. This form is characterized by a slowly progressive course with the potential for transformation of steatohepatitis into cirrhosis
Submassive necrosis against the background of fatty degeneration of the liver, the presence of bridge-like central-central necrosis The variant is rare and can result in death within several years

Pathogenetic parallels with the morphological features of the disease have been proven, including signs of fatty degeneration of hepatocytes, steatonecrosis, lobular inflammation. Fatty degeneration of hepatocytes most often manifests itself in the form of large droplets, mainly in the 3rd zone (centrilobular), characterized by the presence of large single lipid droplets in the cytoplasm of hepatocytes with nuclear displacement to the cell periphery. Non-alcoholic steatosis is characterized by the presence of multiple lipid droplets. The nucleus is located in the center of the cell. In NASH, mixed steatosis is also considered small-droplet, since it has a more unfavorable prognosis. In hepatocytes, manifestations of balloon dystrophy and Mallory hyaline bodies are observed. Focal centrilobular necrosis is more common with fine-droplet steatosis. Inflammatory infiltrates of the portal tracts, parenchyma contain lymphocytes, mononuclear cells, histiocytes. Care is characterized by early pericellular, perisinusoidal and perivenular fibrosis. Cirrhosis is detected in 7-16% of adults. In some cases, NASH is accompanied by excessive accumulation of iron in hepatocytes and Kupffer cells.

Symptoms of Non-alcoholic steatohepatitis

Features of clinical manifestations:

NASH is more common in overweight women. Insulin-dependent diabetes mellitus is found in 25-27% of patients. Most patients do not have symptoms characteristic of the disease. A number of people experience discomfort in abdominal cavity, aching pain in the right Dreberye, asthenic syndrome. With small-droplet steatosis there are hemorrhagic syndrome, fainting, arterial hypotension, hypothyroidism, cholelithiasis. In 80% of patients, hepatomegaly is detected, in 20% - splenomegaly. In patients with cardiovascular pathology, widespread atherosclerosis, dyslipoproteinemia, in the vast majority of cases (up to 90%), fatty liver degeneration with elements of fibrosis is detected, which can be considered as a prestage of NASH.

Diagnosis of non-alcoholic steatohepatitis

Diagnostic features:

Diagnosis is based on clinical manifestations, increased activity of aminotransferases, γ-glutamyl transpeptidase, detection of fatty liver infiltration according to ultrasound, exclusion of other etiological factors, and results of liver biopsy. There is an increase in the activity of ALT, AST, in 45% of patients the concentration of bilirubin is increased, there is hyperlipidemia (hypertriglyceridemia, hypercholesterolemia). Half of the overweight patients have type IV hyperlipidemia, increased alkaline phosphatase activity, and decreased prothrombin index. A number of individuals have hypergammaglobulinemia and antibodies to nuclear antigen. The basis for diagnosing NASH is a morphological examination of the liver. Must be excluded viral infection, Westphal-Wilson-Konovalov disease, congenital oti-antitrypsin deficiency, hemochromatosis, autoimmune hepatitis, alcohol consumption in a hepatotoxic dose (more than 20 mg of ethanol per day). Laboratory methods research significantly complements the data morphological research, but are not leading. Depending on the severity of steatosis, balloon dystrophy and inflammation, 3 degrees of activity and 4 stages of fibrosis severity are distinguished. The disease is characterized by a progressive course. In 40% of patients, pronounced fibrotic changes develop; in 15%, a detailed picture of liver cirrhosis is formed, which is often interpreted as cryptogenic.

Treatment of non-alcoholic steatohepatitis

Features of treatment:

In the treatment of NASH, an important place is given to diet, and moderate weight loss is provided in case the disease develops against the background of obesity and diabetes. You need to know that a sharp decrease in body weight can lead to a worsening of the disease. Based on the pathogenesis of NASH, essential phospholipids are used, which are the main elements in the structure of the shell of liver cell organelles and have a normalizing effect on the metabolism of lipids, proteins, and the detoxification function of the liver. For this purpose, the drug Essentiale N is used. Ursodeoxycholic acid (UDCA) drugs, which have a cytoprotective and membrane-stabilizing effect, are indicated in the treatment of the disease. UDCA at a dose of 13-15 mg/kg per day for 10-12 months improves liver tests, reduces lipid deposition in the liver tissue without a significant decrease in body weight. In the presence of an anastomosis with malabsorption syndrome and bacterial overgrowth, the use of metronidazole is indicated. In conditions of progression of liver failure, orthotopic liver transplantation is advisable in some cases.

Forecast:

The course of NASH (large-droplet steatosis) is usually relatively benign; with small-droplet steatosis, the prognosis is more serious. Progression to the stage of liver cirrhosis occurs in 15% of patients. In patients with NASH, the 5- and 10-year survival rates are 67% and 59%, respectively.

According to statistics, liver diseases affecting disorders metabolic processes, for example, non-alcoholic steatohepatitis (NASH), are now being diagnosed with increasing frequency. The disease is especially common among residents of the United States and European countries. You should understand in more detail what steatohepatitis is and why it occurs.

Steatohepatitis is common among residents of the United States and Europe.

Causes of disorders and development of complications

Among the main causes of the disease are:

Impaired metabolism. Provocateurs may be sudden weight loss or weight loss, poor nutrition and lack of protein or carbohydrates.
Overdose of medications. A number of medications and medications capable of provoking the development of the disorder in question.
Previous operations in the gastrointestinal tract.
Hepatocerebral dystrophy.
Relationship with lipid metabolism disorders.

Due to disruption of metabolic processes occurring in the internal organs and relating to fats and insufficiently oxidized foods, changes in the structure of the liver occur in the gastrointestinal tract. Of particular danger is the fact: disorders are difficult to detect using modern diagnostic techniques, and they do not affect the condition of patients.

Liver steatohepatitis requires a thorough examination and timely diagnosis: this will help to take corrective action. effective treatment. If non-alcoholic steatohepatitis and its other forms are not detected and, accordingly, not treated in time, there is a risk of complications, among which cirrhosis is especially prominent.

NAFLD – non-alcoholic fat disease liver - develops as a result of fatty disorders, which provoke a number of possible consequences:

Hypertension.
Obesity.
Chronic hyperglycemia syndrome.
Atherosclerosis, etc.

According to the international medical and medical classification ICD-10 (tenth revision), non-alcoholic steatohepatitis has a unique code K75.8. Turning to this document, it is easy to pay attention to the relationship with the concept of “steatosis”. This term reflects a quantitative indicator of the accumulation of fat droplets and inclusions in hepatocytes - the most important liver cells involved in the processes of synthesis and preservation of the structure and substance of liver tissue.

The disease is also considered in connection with the syndrome of cholestasis - stagnation of bile elements in the liver tissues. The following types of cholestasis are distinguished:

A functional form in which the content of bile acids inside the liver decreases.
A morphological form in which bile accumulates in hepatocytes and ducts.
The clinical form of cholestasis, which in one way or another provokes or is a consequence of varying degrees of activity of steatohepatitis.

Types and symptomatic picture of steatohepatitis

There are several possible forms of occurrence:

Alcoholic steatohepatitis occurs in patients with alcoholism

Alcoholic form. It appears predominantly in patients suffering from alcoholism due to the breakdown of alcohol compounds in the liver cells. This causes a decrease in the functional indicators of the organ. Symptoms of steatohepatitis in this form are reduced to pain in the lower chest, dyspepsia and icteric signs. Most patients experience enlargement and hardening of the liver, and blood vessels esophagus, which is fraught with the formation internal bleeding. Chronic steatohepatitis can be detected only through targeted examination through tests, ultrasound examination, biopsy, etc.
Non-alcoholic steatohepatitis. Often the disease develops as a result of saturation of the liver structures with neutral fats. The result is the development of oxidative and inflammatory processes, structural damage to the integrity of the liver and the occurrence of cirrhosis. Non-alcoholic steatohepatitis is mainly diagnosed in patients with excess weight and pancreatic diseases, with disorders of fat metabolism.

Among other causes of development, malnutrition stands out - deficiency of protein compounds, antitrypsin levels, etc. This form, minimally active steatohepatitis, is characterized by the fact that it occurs unnoticed by the patient. The relationship with other ailments discussed earlier most often forces patients to visit their doctor, as a result of which steatohepatitis is discovered.

Dosage form or moderate steatohepatitis occurs due to taking medications that are unfavorable and harmful to the liver. These include antibiotics, estrogens and immunomodulators, immunostimulants, etc. The prognosis of this form is extremely favorable for the patient - if the first signs are detected, the development of LSH can be stopped with minimal therapy.

Regardless of the stage and form of the course, the general symptomatic picture may include:

Steatohepatitis may be a consequence of obesity
Jaundice.
Continuous feeling of heaviness in the abdomen.
Malaise.
I'm thirsty.
Decreased appetite.
Obesity.
Weight loss.

Development of other ailments - diabetes mellitus, hyperlipidemia, etc.

Important! To exclude the development of complications and timely detect steatohepatitis and accompanying disorders, it is recommended to seek qualified help at the first suspicion.

Stages of diagnosis of steatohepatitis. Forecasts

Steatohepatitis with minimal activity and its other forms, regardless of the difficulty of diagnosis, can be detected through a number of measures: Ultrasound examination of the liver to detect enlargement, thickening or other external changes. The ultrasound method is the most productive, because it allows you to detect visual criteria for the development of steatohepatitis and take action. necessary measures
Submission of laboratory tests. They are designed to reflect the content of cholesterol, bile pigment and other compounds, which will allow the doctor to make a conclusion about the presence of a disorder, if any.
Biopsy and other methods. A biopsy involves the intravital collection of cellular material from an organ from the patient’s body for the purpose of a detailed study of the tendency to disorders or their presence.

Important! The prognosis for any category of patients in the event of detection of any form of the disease will consist of individual characteristics and the degree of development of steatohepatitis. Thus, with moderate steatohepatitis in patients aged 30 to 45 years, the prognosis is extremely positive.

In patients older - 45-60 years and above when detected alcoholic form If accompanied by other diseases, prediction becomes difficult due to the likelihood of complications and difficulties in prescribing appropriate therapy.

Treatment: folk remedies, medications and diet

Taking into account the detected form and degree of liver damage, the disorder can be treated in several ways:

Medications.
Folk remedies.
Diet.

In the first case, for the treatment of steatohepatitis, predominantly the alcoholic form, the following are prescribed:

Hypoglycemics. They are designed to increase the organ's sensitivity to insulin.
Stimulating bile movements, designed to protect and preserve liver cells.
Hepatoprotectors to eliminate the lack of phospholipids in the patient’s body.

Treatment of non-alcoholic steatohepatitis and other forms in case of contraindications to the use of drugs (for example, with LSG) is carried out by adjusting the diet. Dietary intervention is aimed at selecting an individual diet for the patient, depending on the recommendations given by the doctor.

Diet for steatohepatitis includes:

If you have steatohepatitis, you can eat chicken

Chicken meat prepared by boiling or stewing. In this case, patients are advised to avoid skin and cartilage.
Meat of other birds, rabbits, fish meat is allowed, but you should also be more selective in cooking methods - fried and smoked foods are strictly prohibited.
Dairy products, especially kefir, fermented baked milk, cottage cheese and yogurts will only bring benefits. It is important to take into account the mass fraction of fat and try not to consume excessively fatty fermented milk products.
Fresh vegetables and fruits.

Concerning folk remedies– their use can hardly be called advisable, however, as a first measure to combat the disease, you can use:

Herbal tea containing St. John's wort, calendula and other medicinal herbs;
Infusion of sage, agrimony and horsetail;
Viburnum and cranberries.

Important! It is recommended to consume all of the healing drinks only with the approval of the specialist you are seeing. Otherwise, there are no guarantees for successful impact. It is also worth making sure that there are no individual intolerances or allergies to the components of healing infusions.

Preventive measures

Having understood what steatohepatitis is and what consequences it can lead to, it is advisable to touch upon an important topic - preventive measures.

In order to prevent the development and occurrence of the disease, it is recommended to follow a number of simple recommendations:

Required balanced diet. Obtaining from food all the vitamins, compounds and microelements necessary for the body will help strengthen the immune system, improve well-being, and also saturate all organs and systems required for normal functioning substances.
Regardless of age, gender and health (according to medical statistics, often imaginary), it is advisable to refrain from consuming alcoholic beverages, especially strong cocktails and champagne. Drink once a month or on occasion of a significant event, birthday or New Year- normal, but drinking alcohol in unacceptable quantities provokes the development of various complications and leads to certain consequences, among which liver disease is not the least trouble.
Refrain from excessive consumption of medications or take them strictly according to the instructions or prescriptions of a medical specialist. When being treated for other ailments, be diligent in taking pharmaceutical products, is impractical due to the likelihood of side effects.

Video

Hepatic steatosis as an inducer of inflammation and the formation of liver fibrosis.

Steatohepatitis: symptoms and treatment methods Steatohepatitis is one of the most severe liver diseases and is considered an intermediate stage on the path to cirrhosis. This is an inflammatory process that occurs against the background of fatty degeneration of the liver.

Steatohepatitis is one of the most severe liver diseases and is considered an intermediate stage on the path to. This is an inflammatory process that occurs against the background of fatty degeneration of the liver. Modern medicine identifies several main forms of steatohepatitis based on the causes of the disease:

Alcoholic steatohepatitis
Non-alcoholic steatohepatitis
Drug-induced steatohepatitis

ALCOHOL STEATHOEPATITIS

Chronic alcoholic steatohepatitis occurs in 20-30% of people with chronic alcoholism. Inflammatory liver damage is caused by the toxic effects of ethanol.

It is known that up to 98% of alcohol that enters the body is metabolized in the liver through oxidation. Excessive alcohol consumption leads to increased stress on the organ and, as a result, the development of inflammation. Over time, due to constant intoxication, the inflammatory process becomes chronic and in most cases leads to fatty liver degeneration and steatohepatitis. Studies have shown that aceteldehyde, one of the metabolites of alcohol, plays a decisive role in the development of this disease. It is he who accumulates in the liver and destroys it.

Symptoms of alcoholic steatohepatitis:

Dull pain in the right hypochondrium;
Severe asthenia (increased fatigue);
Yellowness of the skin and sclera of the eyes;
Enlargement and hardening of the liver;
Liver pain on palpation;
Signs of portal hypertension (dilation portal vein with ultrasound);
Dyspeptic symptoms (indigestion).

Treatment of chronic alcoholic hepatitis is usually aimed at protecting hepatocytes from destruction, reducing or eliminating inflammation in the liver tissue, inhibiting the development of liver fibrosis and preventing the formation of cirrhosis. A mandatory and main condition for treatment is complete abstinence from drinking alcohol.

METABOLIC NON-ALCOHOLIC STEATHOEPATITIS

Fatty degeneration of the liver can occur not only against the background of alcoholism, but also metabolic disorders in the body, namely a failure in fat metabolism. That is why metabolic non-alcoholic steatohepatitis is also called fatty.

Reasons for the development of non-alcoholic steatohepatitis:

Obesity;
Eating disorder;
Chronic diseases of the digestive system (in to the greatest extent pancreatitis, colitis, etc.);
Hyperlipidemia.

According to statistics, metabolic steatohepatitis most often develops against the background of obesity, as well as diabetes mellitus. The liver “swims” with fat and becomes unable to perform its functions. On the other hand, steatohepatitis can provoke fast weight loss due to a deficiency of proteins, fats, vitamins and other substances necessary for normal operation all systems of the body.

The course of the disease is usually hidden. In most cases, steatohepatitis is diagnosed incidentally during a medical examination for other health problems.

Symptoms of metabolic steatohepatitis (if they occur):

Feeling of heaviness in the stomach;
Pain in the liver area;
General weakness;
Excessive sweating against the backdrop of constant thirst.

Medical therapy should be primarily aimed at ridding the liver of excess fat, accelerating the movement of hepatic triglycerides released, and preventing the depletion of antioxidant defenses.

DRUG-DRUG STEATHOEPATITIS

At long-term use Some medications may disrupt the oxidation of fatty acids, which provokes the development of steatohepatitis and, in the absence of therapeutic therapy, liver cirrhosis. In the most severe cases, liver tissue necrosis of varying degrees may develop.

The following are considered particularly dangerous for the liver:

Synthetic hormonal drugs(including oral contraceptives);
Tetracycline antibiotics (Tetracycline, Terramycin, Biomycin);
Aminoquinolones (Plaquenil, Delagil);
Calcium antagonists (Verapamil, Diltiazem, Nifedipine);
Almost all drugs used to treat HIV;
Antifungal drugs (Amphotericin, Ketoconazole, Fluorocytosine);
Other drugs (Amiodarone, Aspirin, Halothane, A nicotinic acid and etc.).

Patients with already diagnosed liver disorders should be extremely careful with these medications. Taking such drugs by people at risk is possible only under the supervision of a doctor and with the simultaneous use of individually selected hepatoprotectors.

Symptoms of drug-induced steatohepatitis:

Frequent acute pain in the liver area
Development of cholestatic syndrome
Development of jaundice
Skin itching, irritation

PREVENTION OF STEATHOEPATITIS

Modern treatment of steatohepatitis involves influencing the body in several directions at once:

Organization rational nutrition on a specially selected diet,
Normalization of general metabolism in the body and energy metabolism liver,
Protecting liver cells and stabilizing their condition through drug therapy.

It is fundamentally important to organize nutrition in such a way that the body receives a sufficient amount of proteins, which are directly involved in liver renewal.

Prevention of steatohepatitis involves moderate alcohol consumption, balanced diet, timely treatment of diseases that can provoke the development of steatohepatitis, careful use hepatotoxic drugs, administration (for example, with udha).

For quotation: Podymova S.D. Fatty hepatosis, non-alcoholic steatohepatitis. Clinical and morphological features. Forecast. Treatment // Breast cancer. 2005. No. 2. P. 61

Fatty hepatosis (liver steatosis, fatty liver, fatty liver) is an independent disease or syndrome caused by fatty degeneration of liver cells. As an independent disease, it was isolated in the 60s of the last century thanks to the introduction into clinical practice needle biopsy of the liver. It is characterized by pathological intra- and (or) extracellular deposition of fat droplets. The morphological criterion of fatty hepatosis is the content of triglycerides in the liver over 10% of dry weight.

Some clinical statistics indicate a significant prevalence of fatty hepatosis.
Non-alcoholic steatohepatitis (NASH) is an independent nosological unit, which is characterized by an increase in the activity of liver enzymes in the blood and morphological changes in liver biopsies, similar to changes in alcoholic hepatitis - fatty degeneration and inflammatory reaction; however, people with NASH do not drink alcohol in amounts that can cause liver damage. The term “non-alcoholic” emphasizes the isolation of this nosological unit from alcoholic disease.
The main cause of the development of steatohepatitis is considered to be an increased content of free fatty acids in the liver. Although NASH is most often benign and asymptomatic, in some cases liver cirrhosis develops, portal hypertension and liver failure.
The designation non-alcoholic steatohepatitis was first introduced by H. Ludwig et al. in 1980. Essentially, it is close to hepatic steatosis with mesenchymal reaction, used by H. Thaler, S.D. Podymova, V.B. Zolotarevsky in the 60-70s of the last century.
The incidence of NASH among patients who underwent liver biopsy is 7-9% in Western Europe and 1.2% in Japan. Alcoholic hepatitis is diagnosed 10-15 times more often [V.T. Ivashkin, Yu.O. Shulpekova, 2000]. Up to 10% of the total number of patients diagnosed annually with chronic hepatitis in the United States are classified as NASH, and 30-40% of viral cirrhosis is also associated with NASH.
The etiology of fatty hepatosis and non-alcoholic steatohepatitis is multifactorial. Primary and secondary diseases are distinguished. The causes of primary fatty hepatosis and NASH are considered:
- obesity;
- diabetes mellitus type 2;
- hyperlipidemia.
Type 2 diabetes mellitus as part of the metabolic syndrome with excess body weight, hyperinsulinemia, hyperlipidemia often leads to fatty hepatosis.
Hyperlipidemia is characterized by elevated cholesterol or triglycerides, or a combination of both.
Secondary fatty liver disease and NASH are caused by:
. medications with hepatotoxic potential: amiodarone, glucocorticosteroids, synthetic estrogens, tamoxifen, perhexiline maleate, methotrexate, tetracycline, non-steroidal anti-inflammatory drugs;
. malabsorption syndrome, which develops during the application of ileojejunal anastomosis, biliary-pancreatic stoma, gastroplasty for obesity, extended resection of the small intestine;
. chronic diseases gastrointestinal tract, accompanied by malabsorption, especially chronic pancreatitis, nonspecific ulcerative colitis;
. rapid weight loss;
. long-term (over 2 weeks) parenteral nutrition, unbalanced in the content of carbohydrates and fats;
. syndrome of excessive bacterial colonization of the intestine (against the background of small intestinal diverticulosis);
. abetalipoproteinemia;
. lipodystrophy of the limbs;
. Weber-Christian disease;
. Konovalov-Wilson disease.
The pathogenesis of fatty hepatosis and especially NASH is not well understood. It is generally accepted that fatty liver disease precedes NASH. The development of fatty hepatosis - the actual accumulation of lipids (triglycerides) can be a consequence of:
a) increasing the supply of free fatty acids (FFA) to the liver;
b) reducing the rate of b-oxidation of FFAs in liver mitochondria;
c) increased synthesis of fatty acids in liver mitochondria.
Along with this, it becomes difficult to remove fat from the liver due to a decrease in the synthesis or secretion of very low density lipoproteins and the removal of triglycerides in their composition.
The next stage of the disease is the formation of steatohepatitis. It is accompanied by inflammatory-necrotic changes in the liver. Their development, regardless of the etiology of steatosis, is based on universal mechanisms. FFAs are a highly active substrate of lipid peroxidation (LPO). The basis for considering LPO as a universal pathogenetic mechanism of NASH is the fact that the effects of LPO can explain the bulk of the histological changes observed in steatohepatitis. LPO with membrane damage leads to cell necrosis and the formation of giant mitochondria. Aldehydes - LPO products (4-hydroxynonenal and malondialdehyde) - are able to activate liver stellate cells, which are the main producers of collagen, as well as cause cross-linking of cytokeratins with the formation of Mallory bodies and stimulate neutrophil chemotaxis.
A number of authors believe that the presence of oxidized fat in the liver is sufficient to trigger the LPO cascade. However, in many patients, hepatic steatosis never progresses to the stage of development of necrotic-inflammatory changes and fibrosis. In view of this, there is an assumption that, in addition to steatosis (“the first impulse”), the development of steatohepatitis requires the presence of some other factors (“the second impulse”). The role of the second push can be played by taking certain medications.
According to experimental studies, the “second shock” is a source of free radicals that can cause oxidative stress. Such drugs primarily include cationic amplophilic amines - amiodarone, perhexiline and the coronolytic agent 4,4'-diethylaminoethoxyhexestrol (DEAEG); their use is usually accompanied by the development of steatohepatitis. Amiodarone and perhexiline accumulate in mitochondria and not only inhibit fatty acid oxidation (causing hepatic steatosis, the “first push”), but also disrupt electron transport in the respiratory chain.
The latter apparently promotes the production of superoxide anions, causing reactions GENDER, (“second push”), which leads to liver damage and the development of steatohepotitis.
Other sources of oxidative stress leading to the development of steatohepatitis may include increased production of cytochrome P450 2E1, endotoxins and cytokines [M. Carneiro de Mura, 2001].
Increased expression of cytochrome P450 (CYP) 2E1 has been demonstrated in NASH patients and animal models. Possible mediators of cytochrome induction in patients who do not drink alcohol are ketones and/or fatty acid, the influence of which can explain the increase in CYP 2E1 activity during a high-fat diet.
Endotoxins and endotoxin-induced cytokines, including tumor necrosis factor-a (TNF-a) and some TNF-inducible cytokines (such as interleukins (IL)-6 and -8), have also been implicated in the pathogenesis of nonalcoholic steatohepatitis and subsequent development of cirrhosis. Treatment with metronidazole improves the course of the disease that developed after ileojejunal anastomosis and in other situations (for example, with prolonged total parenteral nutrition), which confirms the importance of endotoxemia and endotoxin-induced cytokines in the pathogenesis of NASH.
Apparently, the earliest sign of the development of fibrosis is the activation of liver lipocytes (also known as Ito cells) in the subendothelial space of Disse, caused by a number of factors, including the influence of lipid peroxidation products. This leads to the proliferation of lipocytes and the launch of a cascade of processes in the formation of fibrous tissue.
Morphological characteristics
Clinical and morphological features of fatty hepatosis and NASH will be analyzed based on data from a study of 74 patients with fatty hepatosis of non-alcoholic etiology. In seven patients the puncture was performed twice, in two patients three times and in two patients four times, thus a total of 91 punctures were studied.
When characterizing histological changes, we proceeded from the intensity of obesity, the size of fat droplets, and the severity of inflammatory and sclerotic changes in the portal tracts. Fatty degeneration: zero degree - small drops of fat are captured separate groups liver cells; I degree - moderately expressed focal medium- and large-scale obesity of liver cells; II degree - moderately expressed diffuse small-, medium-, large-droplet, predominantly intracellular obesity; III degree - pronounced diffuse large-droplet obesity with extracellular obesity and the formation of fatty cysts.
Inflammatory and sclerotic changes in connective tissue classified as follows: zero degree - absence of inflammatory changes inside the lobules, intact portal tracts; I degree - focal lymphoid and histiocytic changes in the sinusoids, focal proliferation of stellate reticuloendotheliocytes; II degree - mildly expressed thickening of the portal tracts due to sclerosis, focal histiolymphoid infiltration; III degree - pronounced thickening of individual portal tracts, individual wide layers of connective tissue with strands of fibroblasts, focal histiocytic, leukocyte infiltrates.
Patients with fatty degeneration of degrees I-II-III and fibrosis of degrees I-II were assigned to the group of fatty hepatosis without inflammatory reaction(group 1, 54 patients), patients with fatty degeneration of the II-III degree and fibrosis of the III degree - into the group of fatty hepatosis with an inflammatory reaction (group 2, 20 patients).
From a modern point of view, patients of group 2 according to morphological criteria correspond to non-alcoholic steatohepatitis.
In the majority of patients (67 out of 74 punctures), diffuse obesity was established, in which the liver cells in all parts of the lobules are filled with drops of fat. Focal obesity of hepatocytes was present only in patients of group 1. Diffuse obesity, depending on the predominance of droplets of one size or another, was fine-grained (pulverized), small-droplet, large-droplet and mixed - with small and large fat vacuoles. In cases of mixed and coarse obesity, fatty cysts also appear in the parenchyma.
Fatty degeneration of hepatocytes is often accompanied by activation of regenerative processes in the parenchyma, expressed in the appearance of hepatocytes with large nuclei and large pyroninophilic nucleoli, as well as an increase in the number of multinucleated cells.
In patients with NASH, focal centrilobular necrosis and Mallory hyaline bodies were detected. Half of the patients had balloon dystrophy hepatocytes.
Cellular infiltration and fibrosis. In patients with fatty hepatosis without an inflammatory reaction, strands of fibroblasts, thin networks of collagen fibers and narrow fibrous layers are sometimes visible inside the lobules. Some of these connective tissue growths are located near areas of intense fatty infiltration. In some places, small proliferations of stellate reticuloendotheliocytes are found. Occasionally, small amounts of lymphoid and histiocytic elements are visible in the sinusoids.
The portal tracts are sclerotic, somewhat thickened, the inflammatory reaction is expressed in the appearance of small focal accumulations of histiocytic and lymphoid elements. In the 2nd group of NASH, sclerosis of the portal fields was observed in all biopsies, and the inflammatory reaction was 2 times more frequent than in the 1st group. The intensity of these changes differed significantly. In case of fatty hepatosis, single portal tracts were sclerosed with slight histiolymphoid infiltration. In patients with NASH, individual portal tracts are noticeably thickened, segmented leukocytes are found among the cells of the infiltrates of the portal fields, and accumulations of leukocytes are found inside the lobules. Inflammatory infiltration inside the lobules prevailed over portal changes. The severity of fibrosis can vary from minimal perivascular lesions to the appearance of dense scar tissue and fibrous septa. NASH initially manifests itself as perivenular damage, but in severe cases the disease can spread to the portal tracts, leading to the formation of bridging necrosis and fibrous septa with subsequent development of cirrhosis.
Clinical picture
The disease occurs much more often in women. Among the patients with fatty hepatosis and NASH we observed, there were 2 times more women than men. The disease is most often diagnosed in middle and old age.
Clinical manifestations of fatty hepatosis and NASH, according to the literature, are limited to slight or moderate enlargement of the liver, which is sometimes sensitive to palpation. Liver function tests in patients with fatty hepatosis are often normal; in NASH, the activity of cytolysis and cholestasis enzymes is usually increased.
When analyzing the frequency of various clinical symptoms in 74 patients with fatty hepatosis and NASH, the following results were obtained.
Pain in the right hypochondrium was constant, dull, aching, and was observed in 63 patients. Dyspeptic disorders (feeling of heaviness in the epigastrium, nausea, vomiting, unstable stool) - in 44 patients, but in a number of patients they can be explained by concomitant diseases.
Asthenovegetative disorders (fatigue, weakness, headache) were observed in 28 patients.
Body mass index was elevated in 45% of patients.
Liver enlargement is the most permanent clinical symptom(in 61 patients). It is of moderate density, with smooth surface, rounded and sharp edge, moderately painful on palpation. Severe pain is observed only in isolated cases. Significantly greater liver enlargement is observed in patients with NASH. Thus, in the group of patients with fatty hepatosis, in 22 people the liver protruded more than 3 cm from under the costal arch, in 19 - from 1 to 3 cm, in the remaining 13 patients it was palpated at the edge of the costal arch. In all patients with NASH, the liver protruded 3-5 cm from under the costal arch, and in 3 patients even more than 5 cm.
An enlarged spleen was detected in 14 cases, mainly in patients with non-alcoholic steatohepatitis.
Spider veins and liver palms were found in 10 patients.
Icterus of the sclera was detected in 18 patients, but no patient had severe jaundice.
Functional liver disorders are minor and often not detected by conventional biochemical tests. Urobilinogenuria, delayed retention of bromsulfalein, and hypertriglyceridemia are characteristic. The activity of ALT is slightly increased in patients with fatty hepatosis and exceeds the norm by 1.5-2.5 times in NASH, more than half have increased AST, as well as g-GTP.
In 1/3 of patients, there is a change in the thymol test, an increase in the level of a2-, b- and g-globulins.
Hyperlipidemia (hypertriglyceridemia, hypercholesterolemia) is found in a fifth of patients.
In patients suffering from obesity, type 2 diabetes mellitus, hyperlipidemia (type II b and IV), lipid metabolism disorders are detected in most cases.
Delayed release of bromsulfalein in many cases of fatty hepatosis was the only indicator of impaired functional activity of the liver; delayed retention was observed in 32 of 53 patients, i.e. more often than any other deviation functional test liver.
Diagnosis
Fatty liver degeneration is clearly diagnosed by ultrasound and computed tomography of the liver. Anamnesis and identification of the causes of metabolic disorders, along with palpable hepatomegaly, in most cases allow one to suspect fatty liver degeneration. Glycemic profile disorders, triglyceridemia, and increased cholesterol levels provide significant assistance in diagnosis.
Non-alcoholic steatohepatitis has no specific clinical and biochemical signs. Assessing the degree of inflammation and fibrosis using liver ultrasound is difficult and unreliable.
In view of this, the basis for diagnosing NASH is the data of a puncture biopsy of the liver.
The diagnosis of NASH is based on a combination of three signs:
1) histological characteristics (the most significant is the presence of fatty liver and changes similar to alcoholic hepatitis);
2) absence of alcohol abuse;
3) data from relevant studies to exclude other chronic liver diseases.
When diagnosing NASH, it is necessary to actively search for other causes of liver dysfunction. A carefully collected medical history often allows one to suspect alcohol or drug-induced liver damage. A series of laboratory research, including serology to detect viral hepatitis, iron metabolism and genetic testing to differentiate from idiopathic (hereditary) hemochromatosis, ceruloplasmin levels, a-antitrypsin levels and phenotype, antimitochondrial and antinuclear antibodies, as these tests can detect other potential causes liver diseases.
A puncture biopsy of the liver is necessary to distinguish fatty hepatosis and NASH from chronic viral hepatitis C, nonspecific reactive hepatitis, and granulomatosis. The feasibility of its implementation is indisputable for determining the prognosis of NASH, which depends on the severity of histological changes, and the development of cirrhosis is accompanied by a high risk of increasing liver failure.
Microvesicular steatosis should be highlighted especially - this is a rare pathology, which is a severe, often life-threatening liver injury.
The histological picture has characteristic features: hepatocytes are increased in size, their cytoplasm is light, and characteristically colored microvesicles are found. Ultrastructural examination reveals significant damage to mitochondria.
The etiology of the disease is different. The most common cause is acute fatty liver of pregnancy, Reye's syndrome. In addition, microvesicular steatosis may result from drug-induced injury, e.g. large doses tetracycline intravenously, especially in pregnant women, in the treatment of epilepsy in children with valproic acid, and also when using pirprofen (and possibly salicylates). Microvesicular steatosis is also observed in various infectious diseases (yellow fever, hepatitis D), lipid metabolism disorders. There are isolated observations of massive microvesicular steatosis in Wilson-Konovalov disease.
The prognosis for uncomplicated fatty degeneration is favorable. A few weeks after the causes are eliminated, the pathological deposition of fat from the liver disappears. The working capacity of these patients is usually preserved. Severe fatty liver degeneration reduces the resistance of patients to infections, surgical interventions, and anesthesia. With continued exposure to hepatotoxic factors (hyperlipidemia, metabolic disorders), inflammatory changes may progress with the development of NASH and micronodular cirrhosis.
The frequency of progression of inflammatory changes and liver fibrosis over 4 years, according to various authors, ranges from 5 to 38%, the development of liver cirrhosis was observed in 0-15%.
The results of five studies covering a 10-year follow-up period of patients with morphologically proven NASH established the progression of liver fibrosis and the development of cirrhosis over this period of time in 20-40% of patients. These data indicate that NASH may be a relatively common cause of cryptogenic cirrhosis.
Significant risk factors for the development of liver fibrosis in NASH:
- elderly age,
- significantly increased body mass index,
- increased levels of ALT, glucose, triglycerides in the blood serum,
- increased levels of oxidative stress (malondialdehyde, glutathione).
As a result of long-term clinical observation of 42 patients with fatty hepatosis and NASH, stabilization of the process was determined in 34 people. Against the backdrop of dietary restrictions and the elimination of various harmful substances, my health remained quite satisfactory and my working capacity remained intact. However, patients periodically complained of increased fatigue, especially during periods of overload (exams, prolonged hard work, etc.).
The development of liver cirrhosis was established in 5 patients. Repeated biopsies of these patients revealed a picture of developing micronodular cirrhosis in the liver against the background of fatty degeneration. In 3 of them, repeated liver punctures were performed after 1.5 years. In one patient the puncture was performed three times with an interval of 4.5 years; initial signs of cirrhosis were detected only at the last biopsy. Another patient underwent 4 punctures over 6 years, hemochromatosis (as iron overload syndrome) and initial signs of cirrhosis were identified after 3 years; over the next 3 years, no morphological signs of progression of cirrhosis were found.
A. Propst et al. (1995) compared the survival of patients with alcoholic hepatitis and NASH using Kaplan-Meier survival curves. The authors found that for alcoholic hepatitis the probability of 5- and 10-year survival was 38 and 15%, respectively, and for NASH it was 67 and 59%. They also showed that life expectancy in patients with NASH is no lower than in healthy individuals of the same age and gender.
Treatment
The regimen for patients with fatty hepatosis does not provide for restrictions physical activity. Light physical exercise increases energy expenditure and leads to a decrease in fatty liver disease. In the presence of obesity, it is advisable to reduce body weight. The performance of patients with uncomplicated fatty degeneration is usually preserved.
It is necessary first of all to exclude factors that cause fatty hepatosis.
Diet has a significant, and in some cases, leading importance in the treatment of patients with fatty hepatosis. Prescribe diet No. 5 with a protein content of up to 100-120 g/day, a limited amount of animal fats, enriched with lipotropic factors (cottage cheese, buckwheat, wheat, oatmeal), vitamins and microelements.
Drug therapy for NASH is being developed. Drugs with membrane-stabilizing and antioxidant effects are indicated: a-lipoic acid, heptral, essentiale.
a-lipoic acid (Berlition), being a coenzyme in the enzyme complex of pyruvate dehydrogenase, is involved in the oxidative decarboxylation of pyruvic acid and a-keto acids and thus affects the regulation of energy production in the cell associated with carbohydrate, lipid metabolism, cholesterol metabolism.
The antioxidant effect of Berlition consists of the direct inactivation of free radicals and the restoration of endogenous defense systems against radicals. The effect of Berlition on lipid peroxidation and its protective effect against peroxidation in mitochondria and microsomes have been revealed.
Numerous studies have proven the positive effect of a-lipoic acid on insulin resistance syndrome, which has pathogenetic significance in reducing the severity of obesity and hyperglycemia in patients with NASH.
On the other hand, there is a complex of antioxidants (vitamin E, C, glutathione) with which dehydrolipoic acid interacts, maintaining both lipid and water antioxidant status at physiological level. Moreover, under conditions of massive oxidation of membranes, dehydrolipoic acid recycles vitamin E when it is depleted. Dehydrolipoate also leads to a decrease in the intracellular concentration of Fe++, indirectly promoting the restoration of oxidized glutathione. It is likely that these reactions underlie the protective effect of a-lipoic acid (Berlition) and provide its therapeutic effect.
Berlition is prescribed in a dose of 300 mg (1 tablet) - 1-2 times a day for 1-2 months. In more severe cases, Berlition is administered intravenously at a dose of 600 mg for 2 weeks. followed by 300-600 mg/day. in tablets.
Ursodeoxycholic acid is used at a dose of 13-15 mg/kg per day from 2 to 12 months. In pilot studies, a decrease in transaminase activity and a decrease in liver steatosis were noted. The effect of the drug on the development of fibrosis and the prognosis of the disease requires further study.
Vitamin E - the ability of the drug to reduce oxidative stress served as the basis for use in patients with non-alcoholic steatohepatitis. In a double-blind randomized study, a statistically significant decrease in ALT activity was obtained in 81.8% of patients with NASH after 6 months. taking vitamin E at a dose of 800 IU/day, and in a control study of liver biopsies, a decrease in the inflammatory response was observed in most patients. Thus, vitamin E can be expected to be a promising drug in the treatment of NASH.
Lipofarm (6 tablets per day), Lipostabil (3 capsules per day) are indicated for patients with fatty hepatosis with severe disorders of fat metabolism (hypercholesterolemia, hypertriglyceridemia, hyperlipoproteinemia).

Literature
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