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Non-alcoholic steatohepatitis: from pathogenesis to therapy. Steatohepatosis: what it is, what are the causes and treatment of Steatosis in the International Classification of Diseases

Steatohepatitis is a transitional phase of the disease from steatosis to cirrhosis. This pathology affects the cells of the liver tissue, expressed as an inflammatory process that develops on the basis of fatty degeneration. The only good news is that this process is still reversible (unlike liver cirrhosis).

ICD-10 code

Since the ICD-10 (International Classification of Diseases) code does not have a single designation, today the most common coding is K76.0 - fatty liver degeneration, not classified elsewhere.

ICD-10 code

K76.0 Fatty degeneration of liver, not elsewhere classified

Causes of steatohepatitis

To effectively stop the problem, it is necessary to have an idea of ​​both the disease itself and the sources that give rise to it.

This pathology is an inflammation in the liver tissues that occurs against the background of the degeneration of hepatic fat cells. Doctors are divided into several types, which cause various pathologies. Causes of steatohepatitis.

1. Alcoholic genesis. Almost every third person who abuses alcoholic beverages can observe the development of this deviation.
2. Metabolic genesis - pathology based on disturbances in metabolic processes.
   1. Excessively large body weight.
   2. Protein deficiency.
   3. Deficiency of insulin in the body, which causes diabetes mellitus.
   4. Rapid weight loss.
   5. Hunger strike.
   6. Failure in lipid (fat) metabolism - dyslipidemia.
   7. Complete replacement of the patient's natural nutrition with parenteral administration of food (bypassing the digestive system). This is mainly the intravenous route.
   8. Prolonged and repeated administration of glucose into the vein.
3. Medicinal footprint of the disease. A number of drugs are capable of causing poisoning with chemical compounds (intoxication), as well as fatty infiltration, which is due to an increased accumulation of lipid components in liver cells. Such consequences can be observed after taking certain medications:
   1. Cytostatics that block the cell's ability to divide.
   2. Glucocorticoids, directly affecting the human hormonal background.
   3. A number of antibiotic drugs.
   4. Non-steroidal anti-inflammatory drugs (NSAIDs) used as pain relievers, anti-inflammatory and antipyretic drugs.
4. Surgical intervention performed on the organs of the gastrointestinal tract is also capable of provoking this deviation, especially in the case of partial removal of the small intestine.
5. Diverticulosis, a deviation obtained by the formation of a saccular appearance of the wall of the small intestine, can also become the cause of degeneration. At the same time, there is an increased increase in the colony of pathogenic microorganisms in the intestine.
6. Wilson-Konovalov pathology associated with changes in the normal exchange of copper.
7. And a number of other factors. All sources of modern medicine are not yet known for certain.

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Symptoms of steatohepatitis

Symptoms of alcoholic or non-alcoholic steatohepatitis are almost identical. Developing against the background of prolonged alcohol consumption, which leads to disruptions in metabolic processes (including lipid), the changes under consideration primarily affect the liver. After all, it is the "customs" of the organism and the ethyl alcohol that gets inside undergoes neutralization exactly here. With a regular attack of alcohol, the organ ceases to cope with cleaning the body, and its cells begin to receive damage. They stop working, and fat gradually begins to accumulate on the surface. Little by little, the cummulation process leads to the onset of an inflammatory process, and if it is not treated, then further progression can lead to a more serious disease - cirrhosis. This is already an irreversible process, in which the parenchymal liver tissue degenerates with fibrous connective structures, or stroma.

The development of the non-alcoholic form is similar, with only the catalyst of the problem changing.

The main symptoms of steatohepatitis:

• In the area of ​​the liver (under the right hypochondrium), aching pain begins to be felt.
• General weakness appears.
• Nausea.
• There is a loss of body weight.
• Signs of diarrhea may appear.
• The skin becomes yellowish.
• But one of the main indicators of pathology, both with alcoholic and non-alcoholic traces of the disease, is an increase in the dimensional parameters of the liver, which is easily determined even by palpation. When pressing on a diseased organ, the patient feels an increase in pain symptoms.

Non-alcoholic steatohepatitis

The name of the type of pathology speaks for itself - non-alcoholic steatohepatitis, that is, a source not associated with alcoholic beverages became the catalyst for deviations from the norm. It has another term - metabolic.

This type of disease is most often found in the fair sex, endowed with curvaceous forms. It is the excess pounds (obesity) that provoke its inception and progression. And also a hereditary predisposition is capable of provoking a disease.

The reason may be organic: the patient has a history of hypothyroidism, impaired protein metabolism (it may be the result of improper "sitting" on various diets or outright starvation), diabetes mellitus. The patient's love for fatty foods can also be a source.

The essence of the pathological mechanism is a violation of the metabolic response to endogenous or exogenous insulin (insulin resistance). This disease is fraught with the danger not only of a high risk of developing cirrhosis, but also an increase in the likelihood of disturbances in the work of the cardiovascular system, since a malfunction of lipid metabolism provokes an accelerated progression of atherosclerosis.

Mostly a person with fatty liver disease of non-alcoholic genesis, with its chronic course, may not even guess about his problem. In this case, the clinical picture is poorly expressed and does not cause any particular discomfort to the person. In this situation, it can only be recognized during a routine examination.

The situation is much more complicated when diagnosing inflammation of the hepatic structures with small vesicular lipid inclusions. This pathology can cause low blood pressure, light-headedness and fainting, the appearance of internal bleeding or the development of gallstone disease.

Alcoholic steatohepatitis

This type of pathology is usually diagnosed in every third person with a special addiction to the "green snake". At the same time, he does not fundamentally drink strong drinks or low-alcohol beer.

Ethyl alcohol is broken down almost completely in the liver. But if there is an excess of alcohol, the liver cells are not able to process it qualitatively. A failure occurs, their cellular structure begins to collapse, pain symptoms appear. A person feels weight loss, yellowness of the skin appears, belching, stool liquefaction, heartburn are less often observed.

In laboratory studies, alcoholic steatohepatitis is manifested by an increase in the number of liver tests, a decrease in the level of hemoglobin and the development of leukocytosis is observed.

Initially, the therapy of this type of disease involves the rejection of alcohol, and then the patient is offered both drug treatment and dietary nutrition.

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Fatty steatohepatitis

The pathology under consideration, in addition to the above, has a number of other names: fatty liver or fatty degeneration of the liver, caused by degeneration or degeneration of cellular structures. After the appearance of biopsy in the sixties of the last century, this pathology was isolated as a separate disease.

The main characteristic of the pathology under consideration is the appearance of lipid deposits in the cellular or intercellular zone. The morphological parameter is the presence of triglycerides in the organ under consideration, more than one tenth of the dry mass. Physicians subdivide this pathology into certain stages of progression: 1.

Increased lipid content of hepatic cells. At the same time, the structure of hepatocytes and their work remained intact, the mesenchymal (stromal - vascular) reaction of the cells was not observed. 2.

There is an increased lipid content of hepatocytes, the first signs of cell necrosis appear, and there is a mesenchymal (stromal - vascular) reaction of cells. 3.

Precirrhotic stage of development. An irreversible restructuring of the lobular structure of the organ is observed.

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Chronic steatohepatitis

The chronic nature of steatohepatitis develops on the basis of constant alcohol intoxication of the body and affects from 20 to 30% of people suffering from alcohol dependence.

Almost completely, by oxidation with special enzymes, ethyl alcohol is metabolized in the liver tissues. Excessive alcohol load on the body causes a malfunction of the organ, as a result of which a sluggish inflammatory process begins, which leads to a deviation from the normal functioning of a number of liver functions.

Such a patient begins to complain of pain in the right hypochondrium, yellowing of the skin and dyspeptic disorders.

If timely treatment is not carried out, the chronic stage of the disease, sooner or later, its progression can develop into cirrhotic manifestations, which no longer allow restoring the initial integrity and functionality of the liver.

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Minimal activity steatohepatitis

Against the background of general automation, modern people are increasingly beginning to suffer from hypodynamia, which develops against the background of a sedentary lifestyle: from floor to floor by elevator, commuting to work in transport. Many of our compatriots imagine their vacation only as time lying on the couch in front of the TV. Such an approach to life cannot but affect the state of the whole organism and the work of internal organs, in particular.

Fatty and high-calorie foods and a sedentary lifestyle, all this adds up to the appearance of additional pounds. But fat cells begin to "settle" not only in the subcutaneous region, but also on the organs themselves. It is lipid deposits in the cellular and intercellular zone of the renal tissues that give impetus to the progression of the pathology under consideration.

Moderate steatohepatitis

A mild or moderate degree of development of the disease is observed in 10.6% of cases, the pathology under consideration manifests itself especially against the background of progressive steatosis, affecting hepatocytes of the perivenular zone and undergoing apoptotic changes.

The ongoing research and monitoring of numerous cases of the disease confirms the recent assumptions of physicians about steatohepatitis as a bridge from steatosis to cirrhotic transformations.

With a given degree of the disease, there is practically no pathological symptomatology, which prevents early diagnosis. At this stage, the disease can be detected only by chance during a routine examination, so it should not be ignored.

Steatohepatitis during pregnancy

This pathology in a woman who is carrying her baby may be of a genetic nature (that is, a hereditary predisposition to this disease), or develop against the background of another liver disease, which the girl may have had before the moment of conception.

Taking a number of medications (vitamin and mineral complexes) can also provoke a problem. A number of multivitamins for pregnant women contain such chemical compounds that the female body in a state of increased stress (which is pregnancy) is not able to process.

There are frequent cases when, due to his incompetence, the doctor himself prescribes increased doses of drugs for a pregnant woman.

It should not be forgotten that thanks to many incorrect beliefs, some women and their relatives still believe that a pregnant woman should eat for two during this period, which cannot affect the total weight of the expectant mother. Hence the pathological deposits in the liver tissues and, as a result, the development of the disease considered in this article in a pregnant woman.

Diagnostics of the steatohepatitis

The difficulty in diagnosing the disease in question lies in the fact that, in most cases, it has a rather low rate of development, and for the time being does not have a clear clinical picture, not showing itself in any way.

Mostly, the only sign may be pain on palpation, and for a specialist it is also an increase in the size of the liver, a thickening of its structure. Therefore, it is possible to detect the disease in the early stages only during a visit to the doctor at the next preventive examination, or in the case of a person dealing with another problem.

If the patient already has reasons to worry, then you should not postpone the visit to a specialist.

Diagnosis involves an integrated approach to the problem, since such symptoms are inherent in not one, but several diseases:

1. Elucidation of patient complaints by a specialist:
   • What are the symptoms of discomfort.
   • How long ago the attacks began.
   • What events preceded the next attack.
2. Study of the anamnesis.
3. What infectious diseases did I have?
4. What medications were used.
5. Is there a hereditary predisposition.
6. Other.
7. External (physical) examination.
   • The presence of a yellowed cornea of ​​the eye and skin. The intensity of the shade.
   • The condition of the epidermis is assessed for scratching.
   • Obtaining an index of the patient's weight, which makes it possible to assess the presence of obesity.
8. Probing the pathological zone for an enlarged liver and the manifestation of pain symptoms.
   • Tapping and feeling the abdomen to measure the size of the spleen and liver.
   • The degree of painful touch.
9. Due to the fact that alcohol can cause liver changes, the doctor may prescribe a special study, the result of which should be an answer to the question of the presence or absence of a person's addiction to alcoholic beverages.
10. Ultrasound examination of the liver. Here, the dimensional parameters of the organ, morphological and organic changes affecting its tissues are assessed.
11. Laboratory tests are carried out to assess the quantitative components of immunoglobulin A, cholesterol, triglycerides, alkaline phosphatase, bilirubin and other indicators. Based on the degree of deviation from the norm, we can talk about the presence of inflammation in this area.
    • General blood analysis.
    • Blood chemistry.
    • Urine examination.
12. If necessary, a tissue biopsy is performed, which makes it possible to assess the level of pathological changes, and, consequently, the duration of the inflammatory process.
13. Under certain circumstances, computed tomography may be ordered.
14. There may be a need for additional advice from more narrowly focused specialists. For example, a hepatologist, a therapist, a surgeon, and so on.

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Treatment of steatohepatitis

First, you should determine the source of the changes. If alcohol is the catalyst for the problem, then the first thing to do is to give up the "bad" drinks.

In parallel, it is worth eliminating the toxic effect on the body, raising the susceptibility to insulin, strengthening the immune forces, stabilizing and normalizing lipid and other types of metabolism, and restoring the hepatoprotective capabilities of the body.

With this pathology, it is necessary for the patient to revise his diet. Usually the doctor prescribes "Table number 5" for such a patient. Diet food should now become a lifelong habit. When returning to the "old life" (for example, taking alcohol or illicit food), the disease tends to return and manifest itself with renewed vigor.

Pharmacological therapy is also carried out. To improve insulin sensitivity, biguanides are prescribed: metfogamma, bagomet, siofor, metformin - acri, glucophage, avandamet and others.

The hypoglycemic drug metformin - acri is prescribed purely individually for each patient, but not more than 3 g daily, divided into several doses.

Contraindications of the drug include the presence of a person's history of diabetic ketoacidosis or diabetic ancestor, coma, dysfunction of the heart, liver, respiratory organs and kidneys, acute cerebrovascular accident, as well as in case of hypersensitivity to the components of the drug.

To reduce the activity of aminotransferases and protect against destruction of hepatocytes, the doctor prescribes drugs based on ursocholic acid: ursofalk, ursochol, urdoxa, ursodeoxycholic acid, ursosan. Ursodeoxycholic acid capsules are taken orally in a daily dosage, which is calculated as 10-15 mg per kilogram of the patient's weight. The drug is swallowed at bedtime without chewing, with a sufficient amount of water. Contraindications for the appointment of the drug in question include X-ray-positive gallstones, increased intolerance by the human body to one or more components of the drug, atrophy of the gallbladder function and inflammation in it and in the bile ducts, pancreatitis, as well as severe hepatic and / or renal dysfunction.

Hepatotropic drugs, normalizes the content of phospholipids: cholenzyme, allochol, tivortin, enerliv, atoxil, polysorb, phosphogliv, livolin forte, essential forte, sirin, ribavirin, hepatomax and others.

Essentiale forte is prescribed in a starting dosage for adult patients and adolescents over 12 years of age, two capsules three times a day. In this case, maintenance therapy involves the introduction of one capsule three times a day. The medicine is used directly with food, do not chew, together with a small amount of water. The duration of therapy is at least three months. A drug is not prescribed if the body is hypersensitive to its constituents.

Drugs that control the amount of cholesterol in atherosclerosis are statins. This can be: pravastatin, cerivastatin, fluvastatin, atorvastatin, simvastatin, rosuvastatin, lovastatin and others.

Fluvastatin is prescribed with a starting amount of 20 mg once a day (in the evening). If necessary, or in case of failure to achieve therapeutic efficacy, the doctor can double the dosage.

It is contraindicated to administer the drug in the active phase of liver disease, hypersensitivity to the components of the drug or a persistent increase in the accumulation of serum transaminases of unknown etiology, as well as the period of lactation and pregnancy.

The basis of therapy is diet, but if it does not bring significant results, the doctor can introduce lipotropic drugs into the treatment protocol, which allow to normalize metabolic processes and protect the liver from damage. These are silibinin, carsil, legalon, orgitox, legalon, selgon.

Hepatoprotector Carsil is prescribed before meals together with a sufficient amount of water. The duration of therapy is about three months.

In the case of mild and moderate liver damage, the drug is administered in a dosage of one - two pills three times throughout the day, with more severe damage - four pills, which corresponds to 420 mg of the drug, three times a day.

The prophylactic dose is two to three tablets per day.

Contraindications include increased intolerance to the constituents of the drug and the acute stage of poisoning of various etiologies.

If necessary, antibiotics are also prescribed to stop the reproduction and further development of the pathogenic intestinal microflora.

Cytoprotectors, pharmacological compounds that "put" protection on the cells of the body are often used. These are sucralfate, misoprostol, venter, sucrafil, cytotec, alsukral, sukrama.

Misoprostol is given orally at a dose of 0.2 g four times a day, the last dose just before bedtime. If necessary, the dosage can be changed, but this decision remains with the attending physician.

Contraindications include individual intolerance by the human body to one or more components of the drug, including other prostaglandins and their analogues.

The standard of care for steatohepatitis

What can be said about the measures that should be taken when diagnosing the disease considered in this article. First of all, relatives and friends should support a person both morally and physically.

The first thing that is necessary is to adhere to the diet prescribed by the doctor - "Table number 5". It is not at all superfluous and even welcomed when the whole family will support the sufferer in terms of nutrition.

Most often, this disorder in the liver is benign in nature, proceeding rather slowly. But there are cases of degeneration into cirrhosis and liver failure. This will not be allowed in any case. And the first stage of this path is stopping the inflammatory process progressing in the body.

In this case, it is necessary not only to establish the source of the pathology, but also accompanying diseases that can affect the course of therapy, which consists of three main directions:

• Diet therapy.
• Medical treatment.
• Moderate physical activity - physiotherapy exercises.

If possible, in parallel with this pathology, a disease should be stopped that can slow down the effectiveness of the course of treatment, or become a catalyst for its relapse.

• That is, the standard of medical care:
• Examination of the patient.
• Study of his anamnesis.
• Correct diagnosis and reasons for its occurrence.
• Complex therapy that allows you to stop both the main problem and, if possible, concomitant pathology.
• Strict adherence to dietary recommendations.

Diet with steatohepatitis

It is quite difficult to imagine modern medicine without the use of numerous diets developed by specialists for the relief of a particular disease. Modern diet therapy is a fairly tangible lever of influence on painful areas. With the help of the correct use and combination of various food products, it becomes possible to significantly improve the condition of the patient's body, as well as significantly reduce the duration of treatment and rehabilitation therapy.

In the case of our problem, the doctor prescribes "Diet No. 5", the main feature of which is the exclusion of various smoked meats, fried, spicy and fatty foods from the diet. On the contrary, the amount of foods rich in vitamins, useful minerals and trace elements should increase.

If the patient is overweight, then his daily menu should be calculated in such a way that the body receives a sufficient amount of the necessary substances, while gradually getting rid of extra pounds. It is also necessary to ensure that weight is not lost too quickly - this is also not acceptable.

The diet is selected individually, taking into account the severity of the clinical picture, the burdened history and individual characteristics of the person. Therefore, this appointment is the direct prerogative of a qualified specialist.

The daily diet should be hypocaloric and calculated as 25 mg per kilogram of patient weight.

Products allowed for introduction into the diet:

• Non-rich bakery products: biscuits, bread with rye or wheat flour.
• Not very cool coffee (preferably with the addition of milk) or tea.
• Green tea.
• Sugar.
• It is allowed to take a small amount of butter (no more than 50 g per day).
• Various vegetable and fruit juices, fresh juices, fruit compotes, pryachons, fruit drinks.
• Sour cream, hard cheeses and cottage cheese (low fat).
• Vegetable broths and based on them soups with vegetables, you can add pasta, various cereals.
• Preserves and jams.
• Vegetable oil (no more than 50 g daily).
• Various cereals.
• Reduced fat milk and dairy products.
• Sweet fruits and berries, sour fruits should be avoided.
• Lean meats: rabbit, chicken, turkey, beef, etc. Poultry should be cooked and eaten skinless.
• Herbal teas and tinctures.
• Fresh and cooked vegetables.
• Natural honey.
• Various greens.
• Egg (preferably one protein) - no more than one per day.
• River fish.

Dishes should be cooked on the basis of boiled products, steamed or baked.

Foods prohibited for inclusion in the diet:

• Limit or completely remove products from butter dough. These are pancakes, cakes, pancakes, fried pies and so on.
• Steep broths: meat, mushroom, fish.
• Chocolate, cocoa and coffee.
• Root crops that are heavy for the digestive system: radishes and radishes.
• Fatty fish.
• Pickled vegetables.
• Animal and cooking fats.
• From greens: spinach, sorrel, green onion.
• Lard and fatty meat.
• Hot sauces and condiments.
• Mustard and horseradish.
• Sour varieties of fruits and berries.
• Smoked products.
• Canned meat and fish.
• Creams.
• Strong tea.
• Eggs (especially the yolk), hard-boiled or fried (fried).
• Ice cream, especially based on palm oil.
• Alcohol and carbonated drinks.
• Foods that are too cold or too hot.

Take medications with extreme caution, having previously carefully studied the instructions attached to them.

You should be very careful about those products that are consumed. If the human diet is close, and in the treatment of pathology fully comply with the dietary "Table No. 5", then "provocations" from the nutritional side will not be expected. This restriction especially applies to fatty and improperly processed foods.

It is necessary to timely undergo treatment of such diseases as diabetes mellitus, viral infections, correction of dyslipidemic disorders.

Regular preventive examination is required.

Steatohepatitis prognosis

It is possible to predict the consequences of a particular disease only by knowing its clinic, the severity of the course and the individual characteristics of the victim's body. If we are talking about the alcoholic form of the problem under consideration, then, in the presence of large vesicular deposits in cell tissues, we can talk about an increase in the likelihood of degeneration into cirrhosis. While the non-alcoholic process, characterized by a low rate of development, gives a similar result in 15-18% of cases. Moreover, this rebirth is extended in time and can reach up to ten years.

Therefore, these two diseases quite often go side by side "hand in hand" and if it is proved that a conscript has a history of chronic hepatitis - this is precisely the fact that gives reason not to involve such young people in the army.

You can get acquainted with such a list in more detail in the “Provisions on Viyskovo-Likarska Expertise in the Zbroynykh Forces of Ukraine. Ministry of Defense of Ukraine; Order, Regulations, Perelik [...] dated 14.08.2008 No. 402 ", following the link rada.gov.ua

Life is beautiful and some representatives of human society try to take the maximum from it: abundant fatty food, alcohol, even to the store in the next house - by car. If rest - then a restaurant and lying on the couch or on the trestle bed on the beach. And then they start to wonder - steatohepatitis - what it is and where it came from. There is a well-known proverb: "Take care of honor from your youth." In the light of the problem considered in this article, it should be altered: "Take care of your health from a young age." A correct active lifestyle, a healthy diet, a balanced combination of physical activity and rest will help protect yourself from many health problems. Regular check-ups should not be ignored either. This will allow, if the pathology already exists, to recognize it at an early stage. In this case, it will be much easier to stop the problem and without serious consequences.

Hundreds of suppliers carry hepatitis C medicines from India to Russia, but only M-PHARMA will help you buy sofosbuvir and daclatasvir, and professional consultants will answer any questions you may have throughout the therapy.

LIVER DISEASES (K70-K77)

Included: medicinal:

• idiosyncratic (unpredictable) liver disease
• toxic (predictable) liver disease

If it is necessary to identify a toxic substance, an additional external cause code (class XX) is used.

Excluded:

• Budd-Chiari syndrome (I82.0)

Included:

• hepatic:
  • coma NOS
  • encephalopathy NOS
• hepatitis:
  • fulminant, not elsewhere classified, with hepatic impairment
  • malignant, not elsewhere classified, with liver failure
• liver (cell) necrosis with liver failure
• yellow atrophy or liver dystrophy

Excluded:

• alcoholic hepatic impairment (K70.4)
• liver failure complicating:
  • abortion, ectopic or molar pregnancy (O00-O07, O08.8)
• jaundice of fetus and newborn (P55-P59)
• viral hepatitis (B15-B19)
• in combination with toxic liver damage (K71.1)

Excludes: hepatitis (chronic):

• alcoholic (K70.1)
• medicinal (K71.-)
• granulomatous NEC (K75.3)
• reactive nonspecific (K75.2)
• viral (B15-B19)

Excluded:

• alcoholic liver fibrosis (K70.2)
• cardiac sclerosis of the liver (K76.1)
• cirrhosis of the liver):
  • alcoholic (K70.3)
  • congenital (P78.3)
• with toxic liver damage (K71.7)

Excluded:

• alcoholic liver disease (K70.-)
• amyloid degeneration of the liver (E85.-)
• cystic liver disease (congenital) (Q44.6)
• hepatic vein thrombosis (I82.0)
• hepatomegaly NOS (R16.0)
• portal vein thrombosis (I81)
• liver toxicity (K71.-)

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) has been adopted as a single normative document to take into account the incidence, the reasons for the population's visits to medical institutions of all departments, and the causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Ministry of Health of Russia dated 05/27/97. No. 170

A new revision (ICD-11) is planned by WHO in 2017 2018.

As amended and supplemented by WHO

Processing and translation of changes © mkb-10.com

Source: http://mkb-10.com/index.php?pid=10331

K70-K77 Diseases of the liver. V. 2016

International classification of diseases 10th revision (ICD-10)

K70-K77 Liver diseases

K70-K77 Liver diseases

Reye's syndrome (G93.7)

viral hepatitis (B15-B19)

K70 Alcoholic liver disease

K71 Toxic liver damage

Badda-Chiari syndrome (I82.0)

"Pure" cholestasis K71.1 Toxic liver damage with hepatic necrosis Liver failure (acute) (chronic) due to drugs K71.2 Toxic liver damage proceeding as acute hepatitis

yellow atrophy or liver dystrophy

liver failure complicating:

• abortion, extrauterine or molar pregnancy (O00-O07, O08.8)
• pregnancy, childbirth and the puerperium (O26.6)

jaundice of fetus and newborn (P55-P59)

viral hepatitis (B15-B19)

in combination with toxic liver damage (K71.1)

K74 Fibrosis and cirrhosis of liver

cardiac sclerosis of liver (K76.1)

cirrhosis of the liver:

• alcoholic (K70.3)
• congenital (P78.3)

with toxic liver damage (K71.7-) K74.0 Liver fibrosis

• acute or subacute
  • NOS (B17.9)
  • non-viral (K72.0)
• viral hepatitis (B15-B19)

toxic liver damage (K71.1)

cholangitis without liver abscess (K83.0)

pylephlebitis without liver abscess (K75.1) K75.1 Portal phlebitis Pylephlebitis Excluded: pylephlebitic liver abscess (K75.0)

amyloid liver degeneration (E85.-)

cystic liver disease (congenital) (Q44.6)

hepatic vein thrombosis (I82.0)

portal vein thrombosis (I81.-)

toxic liver damage (K71.-)

Focal nodular hyperplasia of the liver

Hepatoptosis K76.9 Liver disease, unspecified

Portal hypertension in schistosomiasis B65.- †)

Liver injury in syphilis (A52.7 †) K77.8 * Liver injury in other diseases classified elsewhere Liver granulema in:

• beryllium disease (J63.2 †)
• sarcoidosis (D86.8 †)

Notes. 1. This version corresponds to the 2016 version of the WHO (ICD-10 Version: 2016), some positions of which may differ from the version of ICD-10 approved by the Ministry of Health of Russia.

2. The translation into Russian of a number of medical terms in this article may differ from the translation in the ICD-10 approved by the Ministry of Health of Russia. All comments and clarifications on translation, design, etc. are accepted with gratitude by e-mail.

3. NOS - no additional clarifications.

4. NCDR - not elsewhere classified.

5. A cross † marks the main codes of the underlying disease, which must be used without fail.

6. An asterisk marks optional additional codes related to the manifestation of the disease in a separate organ or area of ​​the body, which is an independent clinical problem.

Source: http://www.gastroscan.ru/handbook/382/7735

What is fatty hepatosis: ICD code 10

The development of fatty hepatosis is based on the violation of metabolic processes in the human body. As a result of this liver disease, healthy organ tissue is replaced by fatty tissue. At the initial stage of development, fat accumulates in hepatocytes, which, over time, simply leads to degeneration of the liver cells.

If the disease is not diagnosed at an early stage and appropriate therapy is not carried out, then irreversible inflammatory changes occur in the parenchyma, which lead to the development of tissue necrosis. If fatty liver disease is not treated, then it can develop into cirrhosis, which is no longer treatable. In the article, we will consider the reason for the development of the disease, methods of its treatment and classification according to ICD-10.

Causes of fatty hepatosis and its prevalence

The reasons for the development of the disease have not yet been precisely proven, but factors are known that can confidently provoke the onset of this ailment. These include:

• completeness;
• diabetes;
• violation of metabolic processes (lipid);
• minimal exercise with a nutritious daily diet high in fat.

Most cases of fatty hepatosis are registered by doctors in developed countries with a standard of living above average.

There are a number of other factors associated with hormonal disruption, such as insulin resistance and the presence of sugar in the blood. The hereditary factor cannot be omitted either, it also plays an important role. But still, the main reason is unhealthy diet, a sedentary lifestyle and excess weight. All the reasons have nothing to do with the intake of alcoholic beverages, therefore, fatty hepatosis is often called non-alcoholic. But if you add alcohol dependence to the above reasons, then fatty hepatosis will develop many times faster.

In medicine, it is very convenient to use the coding of diseases for their systematization. It is even easier to indicate the diagnosis on the sick leave with the help of a code. Codes for all diseases are represented in the International Classification of Diseases, Injuries and Various Health Problems. Currently, the tenth revision option is in effect.

All liver diseases according to the International classification of the tenth revision are encrypted under the codes K70-K77. And if we talk about fatty hepatosis, then according to ICD 10, it falls under the code K76.0 (fatty liver degeneration).

You can learn more about the symptoms, diagnosis and treatment of hepatosis from separate materials:

Treatment of fatty hepatosis

The treatment regimen for non-alcoholic hepatosis is to eliminate possible risk factors. If the patient is obese, then you need to try to optimize it. And start by reducing the total mass by at least 10%. Doctors recommend using minimal physical activity in parallel with dietary meals to achieve the goal. Limit the use of fats in the diet as much as possible. At the same time, it is worth remembering that drastic weight loss will not only not be beneficial, it can, on the contrary, damage, aggravating the course of the disease.

For this purpose, the attending physician may prescribe thiazolidinoids in combination with biguanides, but this line of drugs has not yet been fully studied, for example, for hepato toxicity. Metformin can help correct metabolic disturbances in carbohydrate metabolism.

As a result, we can confidently say that with the normalization of the daily diet, reducing body fat and giving up bad habits, the patient will feel an improvement. And only in this way it is possible to fight such a disease as non-alcoholic hepatosis.

Source: http://zapechen.ru/bolezni-pecheni/gepatoz/mkb-10.html

Liver steatosis

ICD-10 code

Associated diseases

Names

Description

Symptoms

Causes

Metabolic disorders - type 2 diabetes mellitus, obesity, hypertriglyceridemia;

The action of toxic factors - alcohol, some toxic substances, drugs;

Unbalanced nutrition (overeating, starvation, lack of protein in food);

Chronic diseases of the digestive system with malabsorption syndrome and;

Fatty infiltration of the liver that is not associated with the effects of alcohol or other toxic substances is called primary or non-alcoholic steatosis (non-alcoholic fatty liver disease). Thus, liver damage is not always associated with the action of toxic factors (alcohol, drugs).

Today, the prevalence of non-alcoholic fatty liver disease is significant. Approximately a quarter of the population of developed countries has liver steatosis, and 3.5-11% have non-alcoholic steatohepatitis, including cirrhosis of the liver. Non-alcoholic fatty liver disease is diagnosed much more often in obese people than in people of normal weight.

Risk factors for a severe course of the disease:

Source: http://kiberis.ru/?p=30417

Fatty liver degeneration (K76.0)

Version: MedElement Disease Handbook

general information

Short description

Fatty liver degeneration is a disease characterized by liver damage with changes similar to those in alcoholic liver disease (fatty degeneration of hepatocytes hepatocyte is the main liver cell: a large cell that performs various metabolic functions, including the synthesis and accumulation of various substances necessary for the body, neutralization of toxic substances and the formation of bile (Hepatocyte)

), however, with fatty liver degeneration, patients do not consume alcohol in quantities that can cause liver damage.

The definitions most commonly used in NAFLD are:

1. Non-alcoholic fatty liver disease (NAFL). The presence of fatty degeneration of the liver without signs of damage to hepatocytes hepatocyte - the main cell of the liver: a large cell that performs various metabolic functions, including the synthesis and accumulation of various substances necessary for the body, neutralization of toxic substances and the formation of bile (Hepatocyte)

in the form of balloon dystrophy or without signs of fibrosis. The risk of developing cirrhosis and liver failure is minimal.

2. Non-alcoholic steatohepatitis (NASH). The presence of hepatic steatosis and inflammation with damage to hepatocytes hepatocyte - the main liver cell: a large cell that performs various metabolic functions, including the synthesis and accumulation of various substances necessary for the body, neutralization of toxic substances and the formation of bile (Hepatocyte)

(balloon dystrophy) with or without signs of fibrosis. May progress to liver cirrhosis, liver failure, and (rarely) liver cancer.

3. Non-alcoholic cirrhosis of the liver (NASH Cirrhosis). Presence of signs of cirrhosis with current or previous histological evidence of steatosis or steatohepatitis.

4. Cryptogenic Cirrhosis - cirrhosis without obvious etiological reasons. Patients with cryptogenic cirrhosis usually have high risk factors associated with metabolic disorders such as obesity and metabolic syndrome. Increasingly, cryptogenic cirrhosis, when examined in detail, turns out to be an alcohol-related disease.

5. Assessment of NAFLD activity (NAS). The aggregate of points, calculated with a comprehensive assessment of the signs of steatosis, inflammation and balloon dystrophy. It is a useful tool for the semi-quantitative measurement of histological changes in liver tissue in patients with NAFLD in clinical trials.

K75.81 - Non-alcoholic steatohepatitis (NASH)

K74.0 - Fibrosis of the liver

K 74.6 - Other and unspecified cirrhosis of the liver. \

Classification

Types of fatty liver degeneration:

1. Macrovesicular type. The accumulation of fat in hepaticitis is local in nature and the nucleus of the hepatocyte is shifted away from the center. In case of fatty liver infiltration of the macrovesicular (coarse droplet) type, triglycerides, as a rule, act as accumulated lipids. In this case, the morphological criterion of fatty hepatosis is the content of triglycerides in the liver over 10% of dry weight.

2. Microvesicular type. The accumulation of fat occurs evenly and the core remains in place. With microvesicular (small-droplet) fatty degeneration, lipids other than triglycerides (for example, free fatty acids) accumulate.

There are also focal and diffuse hepatic steatosis. Most often, diffuse steatosis occurs, which is of a zonal nature (the second and third zones of the lobule).

Etiology and pathogenesis

Primary non-alcoholic fatty disease is considered as one of the manifestations of metabolic syndrome.

Hyperinsulinism leads to the activation of the synthesis of free fatty acids and triglycerides, a decrease in the rate of beta-oxidation of fatty acids in the liver and the secretion of lipids into the bloodstream. As a result, fatty degeneration of hepatocytes develops hepatocyte - the main cell of the liver: a large cell that performs various metabolic functions, including the synthesis and accumulation of various substances necessary for the body, neutralization of toxic substances and the formation of bile (Hepatocyte)

The onset of inflammatory processes is predominantly centrilobular in nature and is associated with increased lipid peroxidation.

Increasing the absorption of toxins from the intestines is of certain importance.

A sharp decrease in body weight;

Chronic protein-energy malnutrition.

Inflammatory bowel disease;

Celiac disease Celiac disease is a chronic disease caused by a deficiency of enzymes involved in the digestion of gluten.

Small bowel diverticulosis;

Microbial contamination Contamination is the entry into a certain environment of any impurity that changes the properties of this environment.

Operations on the gastrointestinal tract.

Type II diabetes mellitus;

Triglyceridemia, etc.

Epidemiology

Sign of prevalence: Widespread

Sex ratio (m / f): 0.8

The estimated prevalence is between 1% and 25% of the general population in various countries. In developed countries, the average level is 2-9%. Many findings are accidentally discovered during liver biopsies performed for other indications.

Most often, the disease is detected in age, although no age (except for breastfed children) excludes the diagnosis.

The sex ratio is unknown, but female predominance is assumed.

Factors and risk groups

The high-risk group includes:

more than 30% of cases are associated with the development of hepatic steatosis Liver steatosis is the most common hepatosis, in which fat accumulates in the liver cells

and in 20-47% with non-alcoholic steatohepatosis.

2. Persons with type 2 diabetes mellitus or impaired glucose tolerance. In 60% of patients, these conditions are found in combination with fatty degeneration, in 15% - with non-alcoholic steatohepatitis. The severity of liver damage is related to the severity of the glucose metabolism disorder.

3. Persons with diagnosed hyperlipidemia, which is detected in 20-80% of patients with non-alcoholic steatohepatitis. A characteristic fact is the more frequent combination of non-alcoholic steatohepatitis with hypertriglyceridemia than with hypercholesterolemia.

4. Middle-aged women.

and non-controlling blood pressure. There is a higher prevalence of fatty degeneration of the liver in patients with essential hypertension without risk factors for the development of fatty degeneration of the liver. The prevalence of the disease is estimated to be almost 3 times higher than in the control groups corresponding in age and sex and keeping blood pressure at the recommended level.

Malabsorption syndrome Malabsorption syndrome (malabsorption) is a combination of hypovitaminosis, anemia and hypoproteinemia due to malabsorption in the small intestine

(as a consequence of the imposition of ileojejunal Ileojejunal - related to the ileum and jejunum.

anastomosis, extended resection of the small intestine, gastroplasty for obesity, etc.);

and some others.

Clinical picture

Clinical diagnostic criteria

Symptoms, course

Most patients with non-alcoholic fatty liver disease have no complaints.

Slight discomfort in the upper right quadrant of the abdomen (about 50%);

Pain in the upper right quadrant of the abdomen (30%);

Moderate hepatosplenomegaly Hepatosplenomegaly - simultaneous significant enlargement of the liver and spleen

Arterial hypertension AH (arterial hypertension, hypertension) is a persistent increase in blood pressure from 140/90 mm Hg. and higher.

Dyslipidemia Dyslipidemia is a violation of the metabolism of cholesterol and other lipids (fats), which consists in a change in their ratio in the blood

Impaired glucose tolerance.

The appearance of telangiectasias Telangiectasia is a local excessive expansion of capillaries and small vessels.

Palmar erythema Erythema - limited hyperemia (increased blood supply) of the skin

Ascites Ascites - accumulation of transudate in the abdominal cavity

Jaundice, gynecomastia Gynecomastia - breast enlargement in men

Signs of liver failure and other signs of fibrosis, cirrhosis, non-infectious hepatitis require coding in the appropriate subheadings.

The identified relationship with alcohol, medication, pregnancy and other etiological reasons also requires coding in other subheadings.

Diagnostics

Laboratory diagnostics

are detected in 50-90% of patients, however, the absence of these signs does not exclude the presence of non-alcoholic steatohepatitis (NASH).

The level of serum transaminases is slightly increased - 2-4 times.

The value of the AST / ALT ratio in NASH:

Less than 1 - observed in the initial stages of the disease (for comparison, in acute alcoholic hepatitis, this ratio is usually> 2);

Equal to 1 or more - may be an indicator of more pronounced liver fibrosis;

More than 2 is considered as an unfavorable prognostic sign.

2. In 30-60% of patients, an increase in the activity of alkaline phosphatase (as a rule, no more than twofold) and gamma-glutamyl transpeptidase (may be isolated, not associated with an increase in alkaline phosphatase) is detected. GGTP levels> 96.5 U / L increase the risk of fibrosis.

3. In 12-17% of cases, hyperbilirubinemia occurs within% of the norm.

In clinical practice, insulin resistance is assessed by the ratio of the levels of immunoreactive insulin and blood glucose. It should be remembered that this is a calculated indicator that is calculated by various methods. The indicator is influenced by the level of triglycerides in the blood and race.

7. Hypertriglyceridemia is observed in 20-80% of patients with NASH.

Many patients will have low HDL cholesterol as part of their metabolic syndrome.

As the disease progresses, cholesterol levels often decrease.

It should be borne in mind that a low positive antinuclear antibody titer is not uncommon in NASH, and less than 5% of patients may have a positive low antinuclear antibody titer.

are more characteristic of cirrhosis or severe fibrosis.

Unfortunately, this indicator is not specific; in case of its increase, it is necessary to exclude a number of oncological diseases (bladder, breast, etc.).

11. Complex biochemical tests (BioPredictive, France):

Steato test - allows you to identify the presence and degree of liver steatosis;

Nash test - allows you to detect NASH in patients with overweight, insulin resistance, hyperlipidemia, as well as patients with diabetes mellitus).

It is possible to use other tests if you suspect non-alcoholic fibrosis or hepatitis - Fibro-test and Acti-test.

Differential diagnosis

Complications

Fibrosis Fibrosis is the proliferation of fibrous connective tissue that occurs, for example, as a result of inflammation.

Liver cirrhosis Liver cirrhosis is a chronic progressive disease characterized by dystrophy and necrosis of the hepatic parenchyma, accompanied by its nodular regeneration, diffuse proliferation of connective tissue and deep restructuring of the liver architectonics.

In detail (it develops especially rapidly in patients with tyrosinemia. Tyrosinemia is an increased concentration of tyrosine in the blood. The disease leads to an increase in urinary excretion of tyrosine compounds, hepatosplenomegaly, nodular cirrhosis of the liver, multiple defects of renal tubular reabsorption and vitamin D in resistant rickets. Tyrosinemia and excretion of resistant rickets occur. a number of inherited (p) fermentopathies: fumarylacetoacetase deficiency (type I), tyrosine aminotransferase (type II), 4-hydroxyphenylpyruvate hydroxylase (type III)

Almost bypassing the stage of "pure" fibrosis);

Liver failure (rarely - in parallel with the rapid formation of cirrhosis).

Treatment

Forecast

Life expectancy in non-alcoholic fatty liver disease is no lower than that of healthy individuals.

Half of the patients develop progressive fibrosis, and 1/6 develop liver cirrhosis.

Hospitalization

Prophylaxis

1. Normalization of body weight.

2. Patients should be screened for hepatitis viruses. In the absence of viral hepatitis, they should be offered vaccination against hepatitis B and A.

Source: http://diseases.medelement.com/disease/%D0%B6%D0%B8%D1%80%D0%BE%D0%B2%D0%B0%D1%8F-%D0%B4%D0% B5% D0% B3% D0% B5% D0% BD% D0% B5% D1% 80% D0% B0% D1% 86% D0% B8% D1% 8F-% D0% BF% D0% B5% D1% 87 % D0% B5% D0% BD% D0% B8-k76-0 / 4827

Non-alcoholic steatohepatitis: from pathogenesis to therapy

Danilevskaya N.N. - Gastroenterologist, GKB 50, Moscow

Non-alcoholic steatohepatitis (NASH) is an inflammatory infiltration of the liver parenchyma and stroma with focal necrosis. NASH is an intermediate link among the successive stages of one pathological process (non-alcoholic steatosis and non-alcoholic steatofibrosis) and is part of an independent metabolic disease - non-alcoholic fatty liver disease (NAFLD). Since the list of ICD-10 diseases does not contain a single code reflecting the completeness of the diagnosis of NAFLD, the following is most often used today: K 76.0 - fatty liver degeneration, not classified elsewhere.

The term NASH was first formulated in 1980 by J. Ludwig et al., Studying the nature of changes in the liver of patients with obesity and type 2 diabetes mellitus, who had no history of alcohol intake in hepatotoxic doses, but during a morphological study of liver tissue were revealed signs characteristic of alcoholic liver disease. And the term non alcoholic fatty liver disease, introduced in 2000, is now used as a general name for various dysmetabolic conditions of the liver, which are based on excessive intra- and extracellular fat accumulation. At the same time, it is necessary to exclude chronic alcohol intoxication (when the consumption of alcohol-containing products in terms of pure ethanol is less than 20 g / day), hereditary hemochromatosis, HCV, HBV and HDV infections, increased levels of ceruloplasmin and α1-antitrypsin, make sure that there is no autoimmune hepatitis.

It must be remembered that there is a certain number of patients who do not drink alcohol, but have liver damage similar in histological structure to alcohol.

Studies in Japan and Italy have shown that the prevalence of fatty hepatosis in the general population ranges from 3 to 58% (average 23%). The high variability in these data is probably due to socio-economic differences in the studied settlements.

In the United States, non-alcoholic steatohepatitis is the most common disease. The percentage of obese people in the general population increased from 10% to 25% between 1961 and 1997 alone. In European countries, NASH is diagnosed in approximately 11% of patients undergoing liver biopsy due to elevated serum transaminase levels. In obese people, the prevalence of NASH is higher, accounting for 19%, and only 2.7% of cases of NASH are diagnosed at normal weight.

In fact, the prevalence of NASH may be even higher among asymptomatic patients who do not consume significant amounts of alcohol if serologic markers of viral hepatitis are absent. Thus, many patients with increased activity of liver enzymes in the blood and negative results of non-invasive studies may have NASH. There are reports of cases of NASH being diagnosed with increasing age.

The pathogenesis of NASH is based on peripheral insulin resistance. Through tyrosine kinase, an intracellular signal transduction disorder occurs after activation of the insulin receptor. The exact mechanism of disruption of this metabolic pathway is not completely clear. The decisive, apparently, becomes the release of adipose tissue, especially adipose tissue of the mesentery of TNF-α, as well as leptin and a number of other protein mediators. TNF-α reduces the regulation of the insulin receptor-substrate signal and thereby reduces the translocation of the glucose transporting protein GLUT-4 on the cell membrane. As a result, the amount of glucose utilized by the cell decreases. Peripheral insulin resistance leads to hyperinsulinism, which blocks mitochondrial β-oxidation. The adipose tissue hormone leptin is also important. Leptin resistance or deficiency leads to increased fat accumulation and impaired β-oxidation of fatty acids in the liver. Also, with NAFLD, the level of adiponectin, a hormone of adipose tissue, decreases, and therefore, intracellular signals are disrupted, such as activation of MAP kinase and peroxisomal proliferative nuclear receptor, which increases the accumulation of fat in the liver. Free fatty acids are hepatotoxic. Normally, FFAs are neutralized in the following ways: mitochondrial β-oxidation, production and secretion of VLDL, synthesis of fatty acid binding protein, and triglyceride synthesis.

In NAFLD, the various mechanisms for neutralizing free fatty acids are limited. The fatty liver, due to the second pathophysiological mechanism, can become the basis for the progression of liver pathology in NASH with fibrosis. In this regard, it is important that free fatty acids can induce cytochrome PE1 with subsequent production of reactive oxygen species, which, by increasing lipid peroxidation, lead to activation of fibroneogenesis. Another mechanism is represented by an increased supply of endotoxins from the intestine to the liver. As with alcoholic liver damage, cytokines are released by Kupffer's stellate cells. Cytokines, primarily TNF-α, contribute, on the one hand, to the pathogenesis of hepatitis, and on the other hand, to the development of peripheral insulin resistance. Among the causes leading to NASH, congenital and acquired metabolic disorders are considered: Wilson-Konovalov disease, metabolic syndrome, total parenteral nutrition, severe weight loss, as well as rare pathologies - abetalipoproteinemia, hypobetaliproproteinemia, tyrosinemia, mitochondriopathy pathology. Polycystic ovary disease, celiac disease, and contact with solvents are important. It is known that such previous surgical interventions as gastric banding, extensive small bowel resection, the imposition of a bilipancreatic anastomosis or ileo-small bowel anastomosis also contribute to the development of NASH. A number of drugs from various pharmacological groups (chloroquine, diltiazem, nifedipine, amiodarone, glucocorticoids, tamoxifen, estrogens, isoniazid, methotrexate, nucleoside analogs) cause NASH.

Clinical presentation and diagnosis of NASH

The relevance of timely diagnosis and treatment of NASH is associated, on the one hand, with the fact that NAFLD, along with obesity, type 2 diabetes mellitus, arterial hypertension and dyslipidemia, is a component of metabolic syndrome and is an independent risk factor for cardiovascular diseases. Moreover, according to the accumulated data, NASH accounts for 20% of all cases of NAFLD. On the other hand, it was previously believed that NASH proceeds benignly and rarely progresses to decompensated liver cirrhosis, but it has now been shown that LC can develop in 40% of NASH cases and the progression of NASH to LC is determined by the severity of inflammatory changes in hepatocytes. In addition, the disease affects all age groups, including children.

True data on the prevalence of NASH are few, due to its low and asymptomatic course. Patients rarely present complaints or they are not specific even at an advanced stage of the disease. Often, the possibility of developing NASH is discussed when an increase in transaminase levels is detected, hepatomegaly is detected during an examination, or according to imaging methods. An increase in liver echogenicity by ultrasound was found in 14% of 2574 randomly selected residents of Japan. Since ultrasound can only detect fat deposition and not inflammation, not all of these cases can be considered NASH. Also, with excess body weight, it is possible that the ultrasound findings carried out by different specialists do not coincide, due to an increase in the thickness of the subcutaneous fat layer, which entails technical difficulties in performing the study and makes it difficult to assess the echogenicity of the liver. A definitive diagnosis of NASH is only possible with a liver biopsy. According to autopsy data, NASH occurs in 18.5% of obesity cases and in 2.7% of healthy individuals. In the United States, 20% of clinically healthy liver donors have fatty infiltration, 7.5% NASH. In Japan, fatty infiltration was found in 9.2% of liver donors. Histologically, fatty degeneration of the liver manifests itself in the form of macrovesicular fatty deposits in hepatocytes and infiltration of the liver tissue by neutrophils and mononuclear cells; in some advanced cases, signs of fibrosis or cirrhosis may be present.

Among the laboratory parameters that most often change in NASH, the most common is an increase in the activity of ALT and AST by a factor of 2-3. In most cases, the AST / ALT ratio can be differentiated between NASH (see Table: Treatment

Treatment for NASH is empirical; there are no generally accepted treatments. The general recommendations are adherence to a hypocaloric diet, the fight against hypodynamia. Laboratory and histological abnormalities, as well as the size of the liver, with a gradual decrease in body weight, may decrease. However, improvement is possible even with persisting obesity. It has also been observed that rapid weight loss is accompanied by progression of NASH. In addition, the long-term positive effect of weight loss is difficult to assess, since this requires maintaining a reduced body weight, and patients with NASH and obesity rarely succeed. In decompensated LC, liver transplantation is effective within NASH, but NASH in the graft may recur, especially in the presence of increased body weight and dyslipidemia. Follow-up data after liver transplantation for NASH are few, but its recurrence has been described as early as 6-10 weeks.

For drug therapy, drugs of various pharmacological groups are used. Considering the role of insulin resistance in the pathogenesis of NASH, the use of biguanides and thiazolidinediones is relevant, the effects of which are due to a decrease in gluconeogenesis and lipid synthesis in the liver, an increase in insulin sensitivity, thereby contributing to a decrease in obesity.

Used preparations containing essential phospholipids, which are elements in the structure of the membrane of the liver cell organelles and have a normalizing effect on the metabolism of lipids and proteins. ... In small and short-term studies, it has been shown that taking α-tocopherol (vitamin E); a combination of lecithin, vitamin C and low doses of vitamin E; β-carotene; Selena; vitamins of group B slightly improves the indicators of liver function.

Recently, ursodeoxycholic acid (UDCA) preparations have been shown to have the greatest therapeutic efficacy in NASH. In pilot studies, the use of UDCA (at a dose of mg / kg / day) for 12 months was accompanied by a significant improvement in liver function tests, lipid metabolism, a decrease in liver steatosis, without a significant decrease in body weight.

UDCA is a stereoisomer of deoxycholic bile acid formed by the microflora of the large intestine. Numerous experimental and clinical studies make it possible to highlight the diverse properties and effects of UDCA. The hepatoprotective effect develops due to the fact that UDCA is able to integrate into the phospholipid layer of the cell membrane, which contributes to its stability and increased resistance to damaging factors. The anticholestatic effect is determined by the induction of bicarbonate choleresis, which enhances the excretion of hydrophobic bile acids into the intestine; anti-apoptotic effect - due to displacement of the pool of toxic hydrophobic bile acids, which have a toxic effect on hepatocytes and cholangcytes. Also described are the immunomodulatory properties of UDCA (due to a decrease in the expression of class I HLA molecules on hepatocytes and class II HLA on cholangiocytes and a decrease in the production of proinflammatory cytokines), litholytic (due to a slowdown in the crystallization of cholesterol) and hypocholesterolemic (reduces the absorption of cholesterol in the intestine, its synthesis in the liver and excretion into bile) effects. The positive effect of UDCA on the biochemical parameters of cytolysis and cholestasis in NASH has been described in many studies, and the diverse effects of UDCA determine the use of the drug in a wide range of liver diseases.

Currently, a new drug Choludexan (World Medicine, Great Britain) has appeared on the Russian market, each capsule of which contains 300 mg of UDCA. The growing interest in UDCA drugs, in particular to Choludexan, is not accidental, since its pharmacotherapeutic effect is diverse and, naturally, is not limited to non-alcoholic steatohepatitis. Indications for the appointment of Choludexan, in addition to NASH, are: uncomplicated cholelithiasis (biliary sludge; dissolution of cholesterol gallstones in the gallbladder if it is impossible to remove them by surgical or endoscopic methods; prevention of recurrence of stone formation after cholecystectomy); chronic active hepatitis; toxic (including medicinal) liver damage; alcoholic liver disease (ABD); primary biliary cirrhosis of the liver; primary sclerosing cholangitis; cystic fibrosis; atresia of the intrahepatic biliary tract, congenital atresia of the bile duct; biliary dyskinesia with proven efficacy of UDCA in all these diseases.

It should be noted that, unlike other drugs, Choludexan has a more convenient dosage of 300 mg. As L. Vasiliev, 2008, wrote in his article: “Let's face it: in the production of any medicine one should rely not on a conscientious, but on a lazy patient, and the fewer the number of capsules per day he needs to take, the more chances that he will take the course of treatment to the end. ... It can be added that the advantage of a dosage of 300 mg lies in the convenience of calculating the dose of the drug per kg of patient weight, depending on the diagnosis (for NASH, Choludexan is used from the calculation of mg / kg / day from 6 months to several years).

Of particular value are the properties of Choludexan in comorbid vascular patients, the number of which is growing from year to year. Thus, the effectiveness of the use of UDCA in NASH in patients with coronary artery disease has been noted in several studies. In a study carried out in 2006 in Ukraine, the functional state of the liver of patients with coronary artery disease in combination with NSAH, who received hypolipidemic therapy with statins and UDCA (Choludexan 300 mg), was studied for three months. There was a decrease in total cholesterol by 23 - 24%, triglycerides by 40–41%, LDL by 35–36%, very low density lipoproteins by 25%, atherogenic index by 13–14%, and an increase in HDL by 42%. A significant decrease in ALT activity (by 56%) was observed in patients receiving statins and UDCA. The results of the study of the effectiveness of UDCA (Choludexane 300 mg) and statins in NASH and IHD indicate the validity of the use of drugs in order to achieve a hypolipidemic and cytoprotective effect, as well as the absence of adverse reactions when combined.

In addition, despite the relatively benign course of NASH, in half of the cases, the progression of the pathological process and occasionally the formation of liver cirrhosis are noted, the appointment of UDCA in patients with coronary artery disease and hyperlipidemia is justified. So, UDCA (Choludexane 300 mg) in combination with statins, probably, has a potentiating lipid-lowering effect, leading to the normalization of the lipid spectrum in patients with coronary artery disease and NSAH. At the same time, against the background of a combination of drugs, there is no deterioration in the metabolic function of the liver, which causes the cancellation of treatment with statins.

In general, Choludexan is administered orally once a day before bedtime or twice a day. The capsule is swallowed whole, without chewing, with a sufficient amount of liquid. In the treatment of chronic liver diseases, the dosage of Choludexan is mg / kg of body weight per day, the duration of treatment is from several months to 2 years.

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29. Fedorov I.G., Baykova I.E., Nikitin I.G., Storozhakov G.I. Non-alcoholic steatohepatitis: clinical picture, pathogenesis, diagnosis, treatment. Ros honey w 2004; 2: 46–49.

30. Dolzhenko M.N. A patient with coronary heart disease and chronic steatohepatitis: how to carry out hypolydemic correction? Ukr Med Zh 2007; 1 (57).

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33. Vasiliev L, Healthy as ... a bear. Aptekar magazine, No. 1, 2008.

A.A. Masharova - Doctor of Medical Sciences, Professor of the Department of Therapy, Clinical Pharmacology and Emergency Medicine of the Moscow State Medical University (Moscow), chief gastroenterologist of the SAO DZ Moscow

Danilevskaya N.N. - doctor-gastroenterologist of the gastroenterology department of the City Clinical Hospital No. 50

But back to the characteristics and symptoms of pathology. Steatosis is a disease caused by a violation of phospholipid metabolism, in which both intracellular and extracellular fatty droplets are deposited in the liver parenchyma.

Normally, the human liver contains 5-7% fat. If this percentage reaches 10 or more (in the most severe cases, this percentage rises to 50 - that is, half of the liver parenchyma is fat), this is a good reason to diagnose fatty infiltration. In this article, we will discuss liver steatosis, symptoms and treatment of this condition.

Symptoms

In order to understand what liver steatosis is, it is necessary to know not only the pathogenesis, but also the symptoms of the disease. Liver and pancreatic steatosis is more common in women. Usually, the disease develops asymptomatically over a fairly long period, therefore it most often manifests itself in people over 40 years old. The symptoms of the disease are very similar to the manifestations of hepatitis:

1. enlargement of the liver - its edges, protruding 3-4 centimeters from under the costal arch, are palpated on palpation;
2. decreased performance, fatigue, irritability, apathy, poor sleep, absent-mindedness;
3. pulling pains in the right hypochondrium, which are explained by an enlargement of the liver, stretching the fibrous capsule;
4. unstable stools, vomiting;
5. slight icterus of the sclera of the eyes (the skin usually retains its normal color);
6. foul skin odor as well as bad breath;
7. rashes, itching of the skin.

Etiology

We have already got a general idea of ​​what diffuse liver steatosis is, and now is the time to move on to the details. The reason for the violation of phospholipid metabolism and the consequent increase in the level of free fatty acids in the liver parenchyma is usually an improper lifestyle and nutrition in particular. The modern lifestyle of most clerks predisposes to spend a lot of time sitting (both in front of the monitor and behind the wheel), to eat improperly (fortunately, in supermarkets there is a large selection of all kinds of harmful delicacies), and also periodically take alcohol.

We can say that steatosis is a disease of lazy people.

Obesity to a fair degree contributes to the accumulation of lipids in the liver tissue. Add bad ecology here, and we get a portrait of a typical patient with an obese liver: not too young, not too slim and prone to alcohol. The list of predisposing factors looks like this:

Particular attention should be paid to malnutrition associated with an insufficient amount of protein in the diet.

At first glance, the issue is not as acute as, for example, alcohol or drug abuse. However, this is why nutritional issues are often not given enough attention, which provokes fatty degeneration of the liver. Vegetarians (and especially vegans - the most radical representatives of the movement) deprive themselves of animal protein, which helps the normal absorption of fat. The lack of animal protein food can still be somehow compensated for with cottage cheese, milk and cheese, but vegans do not even accept such nutrition, so they chronically receive less amino acids. At the same time, as compensation, they are often addicted to sweet dishes, which also has a bad effect on the state of the liver.

Alcohol occupies a special niche among the factors contributing to the development of the disease. Most cases of fatty liver degeneration are precisely the result of the abuse of ethanol derivatives. Alcoholic steatosis of the liver often ends with cirrhosis - irreversible changes in liver tissue.

That is why there was even a special abbreviation for NAFLD - liver steatosis, not caused by the use of alcoholic beverages (literally: Non-alcoholic Fatty Liver Disease).

Pathogenesis

The accumulation of fatty droplets in the liver tissues can occur due to the disruption of the natural oxidation of free fatty acids in the liver mitochondria, as well as due to their increased formation and accelerated supply to hepatocytes. Due to the weakened production of lipoproteins, the excretion of triglycerides from the liver worsens. The accumulation of fats in the liver parenchyma can provoke the development of inflammatory and even necrotic processes. It has not yet been possible to establish a direct relationship between these two processes, but it is generally accepted that the intake of hepatotoxic substances that promote the release of free radicals and the onset of oxidative processes can really lead to the development of inflammation and tissue necrosis. In addition, the production of endotoxins (toxic substances produced inside the body), which usually occurs with pathological growth of bacteria in the intestine or the presence of a focus of infection in other organs and tissues, can also become such an impetus.

The development of fatty infiltration can be both diffuse and focal. Diffuse hepatic steatosis is characterized by a uniform deposition of fat in the liver parenchyma. It is easy to guess that focal fat deposits are characteristic of the focal form.

Steatosis in the International Classification of Diseases

Liver steatosis does not have a single code according to the ICD-10 classification. The numerical values ​​of the code change, since liver steatosis, the symptoms of which vary depending on the forms of the disease, can give a different clinic. The following code variants are accepted:

• K 73.0 - chronic hepatitis;
• K 73.9 - chronic cryptogenic hepatitis (of unknown etiology);
• K 76.0 - fatty degeneration of the liver, not mentioned elsewhere;
• Changes in the liver like cirrhosis.

As can be seen from the list, code 76.0 is closest to steatosis, however, it does not always fully reflect the nature of pathological changes occurring in the liver parenchyma, since fatty infiltration can be combined with both the proliferation of connective tissue and inflammatory and necrotic phenomena.

Diagnostics

Due to the absence of vivid symptoms, often accumulated fat in hepatocytes (liver cells) is detected by chance (for example, during a routine examination of a person or during a diagnosis for another disease). When a patient turns to a specialist with complaints of dyspeptic disorders and chronic fatigue, the doctor first of all studies the anamnestic information, concomitant diseases, as well as the peculiarities of the appearance of clinical signs of steatohepatosis.

He focuses on alcoholism, the presence of metabolic diseases and endocrine pathology. During the physical examination, the skin, mucous membranes and palpation (palpation) of the abdomen are assessed.

For the purpose of further examination, laboratory tests and instrumental methods are prescribed.

To study the functional ability of the liver and other internal organs, the doctor prescribes biochemistry. It includes many indicators, but more attention is paid to transaminases. They are intracellular enzymes that, after the destruction of hepatocytes, come out. The degree of their increase characterizes the severity of the pathological process in the liver.

We are talking about alanine aminotransferase and aspartate aminotransferase. In addition, levels of alkaline phosphatase, bilirubin and protein are examined. Changes in steatosis concern the prothrombin index, which gradually decreases, as well as cholesterol and lipoproteins, which increase their content in the blood.

The listed indicators refer to indirect markers of the disease. As for the more accurate ones, they provide information on the quantitative composition of fibrous fibers.

Several biomarkers have been developed for diagnostic purposes. Fibrotest includes:

• haptoglobin;
• alpha-2 macroglobulin;
• gamma glutamyl transpeptidase;
• total volume of bilirubin;
• apolipoprotein A1.

Unlike the above-described marker, Actitest additionally includes ALT. The accuracy of the technique at the initial stage of fibrosis is about 70%, while with pronounced changes in the liver, it reaches 96%.

The fibrometer provides information on the quantitative composition of platelets, gamma-HT, transaminases, urea, as well as prothrombin and alpha-2 macroglobulin. The accuracy of the technique is approximately 87%.

The complex of laboratory studies can include the determination of the level of the gland, the search for markers for viral hepatitis, as well as antibodies (antinuclear and to smooth muscles).

Instrumental methods

The diagnostic complex also includes instrumental methods necessary for visualization and examination of the liver:

The first degree of the disease is characterized by the accumulation of fat in hepatocytes without changing their structure. Already with the second, dystrophy and the formation of multiple cystic formations are observed, around which the cells are compacted. The third degree is manifested by areas of connective tissue that completely violate the structure of the liver, which leads to its dysfunction.

Treatment of steatosis

It is necessary to treat the disease after the diagnosis and taking into account the concomitant pathology in the patient. To date, there are no specific treatment regimens for steatosis. The treatment process often includes several areas:

1. diet food according to table No. 5;
2. weight correction. Given the presence of obesity in patients with liver steatosis, gradual weight loss is required by following the recommendations of a nutritionist. A complete refusal of food or its independent restriction can lead to a sharp deterioration in the general condition of the patient;
3. correction of hyperglycemia, -lipidemia and -cholesterolemia with the help of diet and drugs;
4. refusal from alcohol;
5. abolition of hepatotoxic medications.

Among the effective drugs, it is worth highlighting:

• Ursosan - based on ursodeoxycholic acid, which is a component of bile. It has a protective effect on hepatocytes, reduces cholesterol production and reduces its absorption in the intestine. Also, the medicine prevents stagnation, normalizing bile outflow. It enhances the activity of pancreatic enzymes and somewhat lowers blood glucose;
• Heptral - has amino acids. It has antidepressant, detoxification and hepatoprotective effects;
• Phosphogliv - a medicine with essential phospholipids, which are embedded in the cell membrane and prevent the destruction of hepatocytes;
• Hepa-merz is a protective and detoxifying agent, which contains amino acids (aspartate, ornithine);
• Metformin is an antidiabetic medication that improves glucose absorption. It belongs to the biguanide group. Taking the drug is accompanied by a decrease in thyroid-stimulating hormone, cholesterol, which is necessary to prevent vascular damage. Its main action is to block the synthesis of glucose in the liver and increase the sensitivity of insulin receptors;
• Atorvastatin is prescribed to lower cholesterol.

Diet and recipes for obese liver

Given the pathogenesis of the development of the disease, namely the deposition of fat in hepatocytes against the background of metabolic disorders, the patient's dietary intake is extremely necessary.

The daily menu should be discussed with a doctor, since excess calorie intake or the abuse of harmful foods can cause the progression of the disease.

The basis of the diet is an increase in the amount of protein food, as well as a decrease in lipids and carbohydrates. Each week should include:

1. low-fat dairy products;
2. vegetable products (currants, fruits);
3. bran;
4. cod, hake;
5. chicken, veal;
6. stale baked goods;
7. vegetables;
8. puree soups;
9. porridge (oatmeal, buckwheat, wheat, rice);
10. vegetable oil;
11. green tea.

The daily drinking volume should be 2 liters (berry compotes, jelly, non-carbonated mineral water).

Diet restrictions apply to spicy cheese, eggs, butter, salt and herring. Exclude from the menu:

1. cocoa;
2. sweets;
3. soda;
4. mushrooms;
5. onion garlic;
6. peppercorns, mustard, moonaise;
7. fatty varieties of meat and fish products;
8. peas, beans;
9. legumes;
10. ice cream.

The goal of the diet is to normalize liver function and glycogen synthesis. Meals should be in small portions up to six times a day. This will regulate the passage of bile and prevent cholestasis. Dishes should be prepared by boiling, stewing or baking. The daily fat limit is 70 g. Dinner should not be later than 19.00. The daily calorie content of food is a maximum of 2400 kcal.

The diet is prescribed for at least three months. When ill, patients often complain of poor appetite, so the diet should not only be healthy, but also tasty. Below are recipes for fatty liver hepatosis, which take into account all the recommendations of nutritionists.

Pilaf

The pilaf recipe that the patient used to use is now banned. To facilitate the work of the liver and the entire gastrointestinal tract, it is necessary to comply with certain requirements for its preparation.

The recipe includes 700 g of rice, half a kilo of chicken, 4 carrots and a small onion. Prepare the meat in advance by boiling, changing the water once. Once it is tender, it needs to be chopped and combined with chopped vegetables. We add water to them and simmer over low heat.

After evaporation of the liquid, it is necessary to fill in the finished rice, add a little salt and continue stewing for 3-5 minutes. The groats should be prepared in advance. It must be rinsed, filled with water, the level of which should be 3 cm higher than the rice mass, and then cook until softened.

The recipe includes 30 g of pearl barley, potatoes, a small onion, carrots and a tomato. For dressing, you can use low-fat sour cream. To prepare minced meat, you need to twist the chicken breast with a meat grinder, then add a little salt and form the meatballs.

Barley and vegetables must be boiled in different containers. Now add the porridge and meat balls to the boiled potatoes and carrots. Salt again and remove from heat after 15 minutes. To reduce the calorie content of a dish, you can do without sour cream.

Casseroles

Sometimes you can treat yourself to a casserole. Here are a couple of recipes:

• for cooking, you need pumpkin, noodles, an egg, half a glass of low-fat milk and a small piece of butter. First, you should grind the pumpkin and select 230 g. Now you need to salt it, add a spoonful of sugar and simmer until softened. Cook noodles (200 g) separately, a little without bringing to readiness. Pour milk, melted butter into it and leave for half an hour. It's time to mix everything, add the beaten egg and send in a baking dish in the oven for a quarter of an hour;
• the recipe includes 80 g of chicken and noodles, protein and a piece of butter. Let's start with the meat. It needs to be boiled and chopped with a blender. The noodles are cooked until half cooked and cooled. Now grind the butter with protein and mix with the minced chicken. Add the whole mass to the noodles and bake until tender;
• rice 230 g, cottage cheese 180 g, three apples and the same amount of eggs, 480 ml of milk and raisins. The technological process begins with boiling rice until cooked. Now we grind the cottage cheese through a sieve, beat the eggs with 25 g of sugar, and cut the apples without the peel into cubes. Mix cold rice with the rest of the ingredients, put it in a mold and bake for a quarter of an hour at a temperature of 200 degrees.

What is the danger of fatty liver hepatosis?

Without treatment, hepatic steatosis threatens the development of severe complications. They are presented:

• fibrosis. As the cells die off, they are gradually replaced by connective fibers, which is accompanied by scarring of the organ. Against this background, the functioning of the liver is rapidly deteriorating;
• a disorder of the production and movement of bile along the excretory ducts, as a result of which cholestasis develops and the digestion process is disrupted;
• steatohepatitis, which is characterized by inflammation of the liver tissue against the background of its fatty degeneration.

Separately, cirrhosis should be highlighted, which is dangerous in its manifestations. Against the background of protein deficiency, there is a deficiency of coagulation factors, which is fraught with massive bleeding. In addition, the esophageal veins undergo varicose changes. They become crimped, and their walls become thinner. The patient begins to worry about severe swelling of the extremities. The fluid accumulates not only in the tissues, but also in the cavities (pleural, abdominal), which is accompanied by symptoms characteristic of pleurisy and ascites.

Provided proper treatment and adherence to all medical recommendations, it is possible to slow down the progression of the disease and significantly improve the general condition of a person.

DISEASES OF THE LIVER AND BILARIAN SYSTEM

Fatty hepatosis.

Pigmented hepatosis.

Hemochromatosis.

Wilson-Konovalov's disease.

Amyloidosis of the liver.

Echinococcosis of the liver.

Cholelithiasis.

Chronic cholecystitis.

Chronic cholangitis.

Dyskinesia of the biliary tract.

Postcholecystectomy syndrome.

FAT HEPATOSIS

Definition.

Fatty hepatosis (FH) - hepatic steatosis, chronic fatty liver disease - an independent chronic disease or syndrome caused by fatty degeneration of hepatocytes with intra- and / or extracellular fat deposition.

ICD10: K76.0 - Fatty liver disease, not elsewhere classified.

Etiology.

FG is a polyetiologic disease. It often occurs as a result of metabolic disorders caused by an unbalanced diet. Especially if there is a bad habit or there are circumstances in which the entire daily need for food is satisfied in almost 1 reception. In such cases, taking into account the limited possibilities of depositing carbohydrates and proteins in the liver and other organs, they turn into easily and infinitely deposited fat.

GH is often a secondary syndrome accompanying obesity, diabetes mellitus, endocrine diseases, primarily Cushing's disease, chronic alcoholism, intoxication, including drugs, chronic circulatory failure, metabolic X-syndrome, and many other diseases of internal organs.

Pathogenesis.

As a result of excessive accumulation of fat in the liver tissue, the function of the organ as a dynamic depot of carbohydrates (glycogen) is primarily disturbed, which leads to destabilization of the mechanisms for maintaining normal blood glucose levels. In addition, metabolic changes associated with prolonged exposure to etiological factors can cause toxic and even inflammatory damage to hepatocytes, the formation of steatohepatitis with a gradual transition to liver fibrosis. In many cases, the etiological factors that caused GH can contribute to the formation of homogeneous cholesterol stones in the gallbladder.

The clinical picture.

FG is characterized by complaints of general weakness, reduced ability to work, dull aching pains in the right hypochondrium, poor alcohol tolerance. Many people develop hypoglycemic states in the form of paroxysmal weakness, sweating, feelings of "emptiness" in the abdomen, which quickly pass after eating food, even one candy. Most patients have a tendency to constipation.

The overwhelming majority of patients with FH have a habit of eating 1–2 times a day. Many have a history of drinking large amounts of beer, long-term drug therapy, work under conditions of toxic influences, various diseases of internal organs: diabetes mellitus, metabolic X-syndrome, chronic circulatory failure, etc.

An objective study usually pays attention to the overweight of the patient. Percussion determined liver sizes are increased. The anterior edge of the liver is rounded, compacted, weakly sensitive.

Symptoms of pathological changes in other organs detected during FG are usually related to diseases that led to the formation of fatty degeneration of the liver.

Diagnostics.

General analysis of blood and urine: no deviations.

Biochemical blood test: increased levels of cholesterol, triglycerides, increased activity of AST and ALT.

Ultrasound examination: enlargement of the liver with a diffuse or focal uneven increase in the echogenicity of the liver parenchyma, depletion of the tissue pattern with small vascular elements. There is no portal hypertension. As a rule, signs of pancreatic steatosis are simultaneously detected: an increase in the volume of the gland, diffusely increased echogenicity of its parenchyma in the absence of pathological expansion of the Wirsung duct. Concrements in the gallbladder, signs of diffuse, reticular or polypous cholesterosis of the gallbladder can be recorded.

Laparoscopic examination: the liver is enlarged, its surface is yellowish-brown.

Liver biopsy: diffuse or localized in different parts of the lobule fatty degeneration of liver cells, extrahepatic location of fatty drops. With a long course of the disease, signs of steatohepatitis are revealed - cellular inflammatory infiltration with predominant localization in the center of the lobules. Sometimes infiltrates capture the entire lobule, spread to the portal tracts and the periportal zone, which indicates the likelihood of the formation of liver fibrosis.

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1. Transaminases. Laboratory signs of cytolysis Cytolysis is a process of destruction of eukaryotic cells, expressed in the form of their complete or partial dissolution under the action of lysosomal enzymes. It can be both part of normal physiological processes and a pathological condition arising from damage to the cell by external factors, for example, when the cell is exposed to antibodies
are detected in 50-90% of patients, however, the absence of these signs does not exclude the presence of non-alcoholic steatohepatitis (NASH).
The level of serum transaminases is slightly increased - 2-4 times.
The value of the AST / ALT ratio in NASH:
- less than 1 - observed in the initial stages of the disease (for comparison - in acute alcoholic hepatitis, this ratio is usually> 2);
- equal to 1 or more - may be an indicator of more pronounced liver fibrosis;
- more than 2 - is considered as an unfavorable prognostic sign.

2. In 30-60% of patients, an increase in the activity of alkaline phosphatase (as a rule, no more than twofold) and gamma-glutamyl transpeptidase (may be isolated, not associated with an increase in alkaline phosphatase) is detected. GGTP levels> 96.5 U / L increase the risk of fibrosis.

3. In 12-17% of cases, hyperbilirubinemia occurs within 150-200% of the norm.

4. Signs of a decrease in the protein-synthetic function of the liver develop only with the formation of liver cirrhosis. The presence of hypoalbuminemia without transition to cirrhosis is possible in patients with diabetic nephropathy Nephropathy is the common name for some types of kidney damage.
.

5. Insignificant hypergammaglobulinemia is revealed in 10-25% of patients.

6. 98% of patients have insulin resistance. Its identification is the most important non-invasive diagnostic method.
In clinical practice, insulin resistance is assessed by the ratio of the levels of immunoreactive insulin and blood glucose. It should be remembered that this is a calculated indicator that is calculated by various methods. The indicator is influenced by the level of triglycerides in the blood and race.
Insulin testing is recommended on an empty stomach.

7. Hypertriglyceridemia is observed in 20-80% of patients with NASH.
Many patients will have low HDL cholesterol as part of their metabolic syndrome.
As the disease progresses, cholesterol levels often decrease.

9. Anemia, thrombocytopenia, increased prothrombin time and INR International normalized ratio (INR) is a laboratory indicator determined to assess the external blood coagulation pathway
are more characteristic of cirrhosis or severe fibrosis.

10. Determination of the level of fragments of cytokeratin 18 (TPS-test) is a promising method for studying the activity of the process. The method allows to distinguish the presence of apoptosis of hepatocytes (hepatitis) from fatty liver infiltration without using a biopsy.
Unfortunately, this indicator is not specific; in case of its increase, it is necessary to exclude a number of oncological diseases (bladder, breast, etc.).

11. Complex biochemical tests (BioPredictive, France):
- Steato test - allows you to identify the presence and degree of liver steatosis;
- Nash test - allows you to detect NASH in patients with overweight, insulin resistance, hyperlipidemia, as well as patients with diabetes).
It is possible to use other tests if you suspect non-alcoholic fibrosis or hepatitis - Fibro-test and Acti-test.

Source: diseases.medelement.com