Hepatosis - This is the accumulation of fat in hepatic cells, which is often a liver response to various intoxication (toxic effects).

The reasons

The main causes of fat hepatosis are:

• alcohol abuse
• sugar diabetes in combination with obesity,
• obesity,
• cushing Syndrome,
• myxedema,
• unbalanced nutrition (protein failure),
• chronic diseases digestive system with impaired suction syndrome,
• impact toxic substances.

Symptoms

Patients with fat hepatosis of complaints usually do not prevent. The course of illness is broken, slowly progressive. Since the time there are constant stupid pains in the right hypochondrium, there may be nausea, vomiting, stool disorders.

Diagnostics

To suspect a fatty dystrophy Doctor -Trapeutor can already have a clinical inspection to increase the liver in the size of the palpation of the abdomen. The increase in liver is confirmed by ultrasound abdominal cavity. IN biochemical analysis Blood is detected by the increase in hepatic enzymes (asat, alt, alkaline phosphatase). In some cases, CT, MRI, liver biopsy is carried out to confirm the diagnosis.

Treatment

Traditional medicine of the whole world, in the treatment of fatty hepatosis, hepatomegaly and liver cirrhosis, offers medicinal, replacement and foreground therapy, which can slightly improve the patient's well-being, but inevitably leads to the progression of diseases, since any presence of human blood chemicals affects the human progress Modified liver.

but proper nutrition, Failure to alcohol, the correction of metabolic disorders, as a rule, lead to an improvement in the condition.

Grease hepatosis in the ICD classification:

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The ICD is a system of classification of various diseases and pathologies.

From the moment of its adoption by the world community at the beginning of the 20th century, it passed 10 revisions, so the current edition is called the ICD 10. For the convenience of automation of disease treatment, it is encrypted with codes, knowing the principle of which it is easy to find any disease. So, all diseases of the digestive organs begin with the letter "k". The following two digits define a specific organ or their group. For example, liver disease begin with K70-K77 combinations. Further, depending on the cause of cirrhosis, a code starting with K70 (alcoholic liver disease) and from K74 (fibrosis and liver cirrhosis).

With the introduction of the ICD 10 to the system of medical institutions, the design of the hospital sheets began to be conducted under the new rules, when instead of the name of the disease, the corresponding code is written. It simplifies statistical accounting and allows you to use computer techniques for processing data arrays both as a whole and various types Diseases. Such statistics are necessary for analyzing incidence across regions and states, when developing new drugs, determining their issues, etc. To understand what a person is sick, it is enough to compare the entry in the hospital sheet with the last editors of the classifier.

Classification of cirrhosis

Cirrhosis is a chronic liver disease, characterized by its insufficiency due to the rebirth of tissues. This disease is inclined to progress and differ from other diseases of the liver. Most often cause cirrhosis alcohol (35-41%) and hepatitis C (19-25%). On ICD 10 cirrhosis is divided into:

• K70.3 - alcoholic;
• K74.3 - Primary biliary;
• K74.4 - secondary biliary;
• K74.5 - biliary uncomputed;
• K74.6 - Other and unspecified.

Alcoholic cirrhosis

Cirrhosis of the liver caused by alcohol in the ICD 10 has code K70.3. It was specially isolated to a group of individual diseases, the main reason for which is ethanol, the affecting effect of which does not depend on the type of beverages and is determined only by its number in them. Therefore, a large amount of beer will bring the same harm as a smaller amount of vodka. The disease is characterized by the death of the liver tissue, which is transformed into a rubric, in the form of small nodes, while its proper structure is disturbed and slices are destroyed. The disease leads to the fact that the body ceases to function normally and the body is poisoned by decay products.

Primary biliary cirrhosis

Primary biliary cirrhosis - This is a liver disease associated with immunity. The ICD 10 has Code K74.3. Causes of occurrence autoimmune disease Not installed. With its occurrence the immune system Begins to fight S. own cells bile liver ducts, damaging them. The bile begins to be stamped, which is carried out to the further destruction of the tissue of the organ. Most often, women suffer from such a disease, mainly 40-60 years. The disease is manifested by the skin itching, which at times amplifies, which leads to bleeding raschers. This cirrhosis, like most other types of disease, reduces performance and causes an depressed mood and no appetite.

Secondary biliary cirrhosis

Secondary biliary cirrhosis arises due to the effects of bile, which accumulated in the organ, can not get out of it. The ICD 10 has code K74.4. The reason for the obstruction of bile ducts can be stones or consequences of the operation. Such a disease requires surgical intervention to eliminate the causes of obstruction. Delegation will continue to continue the destructive effects of bile enzymes on the hepatic tissue and the development of the disease. This kind of disease, men suffer two times more often, usually aged 25-50 years, although it is also found in children. The development of the disease is most often from 3 months to 5 years, depending on the degree of obstruction.

Bilyiaric uncomfortable cirrhosis

The word "biliary" occurred from the Latin "Bilis", which means bile. Therefore, cirrhosis associated with inflammatory processes in bile durses, Staging in them bile and its impact on the liver tissue, is called biliary. If at the same time it does not have the distinctive signs of primary or secondary, it is classified according to the ICD 10 as biliary uncomputed cirrhosis. The cause of such types of disease can serve various infections and microorganisms that cause inflammation of intrahepatic biliary tract. In the 10th edition of the classifier, such a disease has a code K74.5.

Other and unspecified cirrhosis

Diseases that in etiology and clinical features do not coincide with previously listed, on the ICD 10 is assigned a general code K74.6. Adding new digits to it allows them to produce their further classification. So unspecified cirrhosis in the 10th edition of the classifier, the code K74.60 was assigned, and the other - K74.69. The latter, in turn, maybe:

• cryptogenic;
• micronodular;
• macronodular;
• mixed type;
• postnotic;
• portal.

What is a fat hepatosis: Code of ICD 10

The development of fat hepatosis is based on violation exchange processes in the human body. As a result of this liver disease, healthy organic fabric is replaced by fat. At the initial stage of development in hepatocytes, fat accumulates, which over time simply leads to dystrophy of hepatic cells.

If the disease is not diagnosed on early stage And the appropriate therapy is not carried out, then in Parenhem, irreversible inflammatory changes occur, which lead to the development of tissue necrosis. If the fat hepatosis is not treated, it can grow into cirrhosis, which is no longer a treaty. In the article, we will consider for what reason the disease is developing, methods for its treatment and classification on the ICD-10.

The reasons for the occurrence of fat hepatosis and its prevalence

The reasons for the development of the disease are still not proven, but the factors that confidently can provoke the emergence of this ailment. These include:

• fullness;
• diabetes;
• violation of exchange processes (lipid);
• mining exercise stress with a nutritional daily diet with large content Fats.

Most cases of the development of fatty hepatosis doctors register precisely in developed countries with the standard of living above average.

There are still a number of factors associated with hormonal failures, such as insulin resistance and the presence of blood sugar. It is impossible to lower the hereditary factor, he also plays a big role. But still the main reason is the wrong power, a sedentary lifestyle and overweight. All reasons are not related to the admission of alcoholic beverages, so fat hepatosis is often called non-alcohol. But if there is also an alcoholic dependence on the above reasons, the fat hepatosis will develop at times rapidly.

In medicine it is very convenient to use coding of diseases for their systematization. Even indicate the diagnosis in the hospital sheet is easier with the codes. Codes of all diseases are represented in International Classification Diseases, injuries and various health problems. At this time there is an option of the tenth revision.

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

• Symptoms of hepatosis;
• Diagnosis of hepatosis;
• Treatment of fat hepatosis.

Treatment of fat hepatosis

The treatment of non-alcohol hepatosis is to eliminate possible risk factors. If the patient suffers from obesity, then you need to try to optimize it. And start with a decrease in the total mass at least 10%. Doctors recommend to achieve the goal to use the minimum physrotype in parallel with diet food. Restrict the use of fats as much as possible in the diet. It should be remembered that a sharp weight loss will not only benefit, it may vice versa to damage, aggravating the course of the disease.

For this purpose, the attending physician may assign thiazolidinoids in combination with biguenides, but this line of drugs is not yet fully studied, for example, on hepato toxicity. Metformin can help adjust the process of metabolic disorders in carbohydrate exchange.

According to the final one can confidently say that when normalizing a daily diet, a decrease in body fat and abandoning bad habits, the patient will feel improvement. And only in this way you can fight with such a disease like non-alcoholic hepatosis.

Become the first commentator!

In the modern world, people are increasingly faced with liver diseases. Everything happens due to improper nutrition, drinking alcohol and a sedentary lifestyle. One of the frequently dated diseases is the staitohypaatosis of the liver. Steatogepatosis What is it, how to treat it, what kind of symptoms and signs are accompanied, which pills should be used with steatohypaatosis? What is the difference between non-alcoholic and alcoholic steatohypatosis?

What is this disease?

So, what is the disease, if you disassemble the word (steatohepatosis) in parts, hepatosis is any disease or change in the liver associated with its structure. And steatosis, or it is also called steatohepatitis - this is (fat) or its accumulation in the liver, which subsequently leads to diffuse changes In the organ, then to violation of the functioning and destruction of the cells of this organ. All this eventually leads to cirrhosis or liver failure.

There is a single regulatory document - the International Classification of Diseases (ICD-10), where each disease has a unique code. Code of liver disease in ICD 10 from K-70-K-77. According to the international classification of liver disease, steatohepatosis has Code K76.0.

There are two types of steatogepatosis:

1. Alcoholic - as everyone knows, the liver is the main filter in the body. With its help, all harmful substances entered the body are filtered. Alcohol passes certain stages in the digestive tract, and toxic substances are distinguished that accumulate in the liver. Allergy arises, and then healthy cells are replaced by fat cells, subsequently the development of alcohol staitohyparatosis of the liver occurs.
2. Non alcohol - the main difference from the previous one is that steatohepatosis is not developing due to alcohol consumption. Grease hepatosis and chronic hepatitis lead to this disease. They gradually reduce the normal functioning of the liver, and fat, salty, smoked food and antibacterial drugs Accelerate the development of the disease. This disease occurs more often in women with excess body, as well as high sugar and cholesterol in the blood. The nature of non-alcoholic steatohypatosis is not accurately studied, it is assumed that this is due to the accumulation of free fatty acids, which are reborn into toxic substances that in turn lead to the accumulation of fat inclusions. Non alcoholic steatohepatosis is usually favorable, it does not go into cirrhosis and the patients do not develop liver failure.

Causes of the disease

The reasons for the emergence of non-alcoholic steatosis is a huge set:

1. Improper diet: Excessive use of oily, smoked, sharp, salty, sweet, baked food leads to an excessive weight gain, and then to such serious consequences.
2. A sedentary lifestyle: if a person feeds correctly, but completely ignores sports, even hiking, it leads to the calorie reserves, which will subsequently strike your liver.
3. Slowing metabolism and disease Predecessors: obesity, diabetes, pancreatitis and other problems resulting in excess weight.
   Incorrect weight loss or long abstinence: a sharp loss of unnecessary kilograms leads the body into a stressful state, which leads to a violation of the work of many internal organs.
4. Durable drug use: Many drugs, especially with their long-term reception, isolated toxic substances that are destructively affect the filter organ.
5. Scientists have proven that alcoholic is found from representatives of a strong sex, and non-alcohol in weak gender.

Disease manifestation

Unfortunately initial stages Diffuse steatosis does not have any pronounced symptoms or is manifested in familiar symptoms for us:

• weakness;
• dizziness;
• heaviness in the right side;
• changing the chair (more often diarrhea than constipation);
• less often nausea, vomiting;
• lack of appetite;
• weight loss;
• allergic rash on the body;
• not always a marked yellow shade of the face.

All these symptoms are characteristic not only for this disease, but also for many others. In order to make sure that you need to immediately contact the hospital.

Diagnostics

So that it is not too late, it takes to pass the dispensarization every year and follow your body.

If you are watching the hospital, it is unlikely that you can find non-alcoholic or alcoholic steatohypatosis of the last stage. If necessary, the therapist with which you are watching will assign all the necessary analyzes and procedures. Usually this:

• Ultrasound liver or all digestive organs;
• computer and magnetic resonance imaging, which will allow you to view the body in more detail (to determine the stage of the disease);
• biopsy - This diagnostic method will help learn liver cells.

The non-alcoholic type of illness does not appear quickly, such steatohepatosis develops very slowly and subsequently flows into a chronic form.

Healing procedures

Treatment should include a set of procedures aimed at:

• eliminate sources, liver dystrophy;
• fighting alcoholism, if necessary, patient;
• resumption of organ cells;
• restoration of normal functioning;
• elimination or at least slow down destructive processes in the body;
• normalization of all organs of the digestive tract;
• healing the body.

Dietary food and moderate physical activity, as well as drugs (anabolics, B12 group vitamins, antibacterial agents, and others) and other physiotherapy measures (hikes in the barocamera, ozone therapy and ultrasound) are added.

The disease is amenable to treatment at the first two stages. At the last stage, the disease is healing only if the patient transplanses a healthy liver, and it is safely joining. The sooner the treatment begins, the faster the person goes on the amendment.

Proper nutrition at fatty dystrophy

If the disease is earned due to excessive alcohol consumption, therefore, it is necessary to exclude alcoholic beverages completely. If due to the wrong diet, then you should forget about the harmful food.

Diet with diffuse steatosis involves limiting the consumption of products that contain a large amount of fat and increase dairy and dairy products. This will reduce the load on the liver and will help remove toxic substances from the body. The main task is to normalize its functions.

It is necessary to eat with a fractional portion of 4-5 times a day.

Products that are worth forget:

• alcoholic and carbonated drinks;
• legumes;
• mushrooms;
• sharp (garlic, horseradish, pepper);
• coffee;
• acidic vegetables and juices (tomato, apples);
• sweets (ice cream, cakes, waffles cookies, candy);
• animal fats, butter;
• mayonnaise, ketchup and other sauces;
• fried, smoked, salty fish and meat.

Products that need to be consumed daily:

• low-fat meat and fish cooked for a pair;
• milk products;
• vegetables and fruits;
• coarse bread or grain bread.

During such a diet, food needs to be prepared for a couple or bake in the oven. Salt consumption should also be reduced to a minimum.

Alternative medicine

Treatment folk remedies It is very popular, but still it is not necessary to get involved in these methods. Before applying funds, it is worth consulted with a specialist. It is impossible to engage in self-medication, as this can lead to adverse consequences.

Several recipes that will help you rehabilitate after the disease:

1. A decoction of rosehip fruits helps to clean the liver from fat. Two tablespoons of rosehips are poured with two glasses boiled water And they insist 8-12 hours. The resulting tool should be served during the day. Course for 3 days.
2. The decoction of flowers and leaves of the Jeroba is well coped with the liver disease.
3. Three large lemons are crushed through a meat grinder or a blender and pour the floor with a liter of boiled water and insist for 8-10 hours. Drink a fluent decoction during the day. For more than 3 days, the decoction is not worth drinking, as Lemon will adversely affect the mucous membrane of the stomach.

In order to prevent the development of non-alcohol steatohypatosis, it should be followed by its body weight, beyond what you eat and drink, lead healthy image Life, to play sports, do not abuse alcohol and medical preparations, do not forget about visits to doctors. Watch not only for your health, but also for the health of your loved ones.

Video

Fat hepatosis.

What is a fat hepatosis: Code of ICD 10

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

If the disease is not diagnosed at an early stage and the appropriate therapy is not carried out, then irreversible inflammatory changes occur in Parenhem, which lead to the development of tissue necrosis. If the fat hepatosis is not treated, it can grow into cirrhosis, which is no longer a treaty. In the article, we will consider for what reason the disease is developing, methods for its treatment and classification on the ICD-10.

The reasons for the occurrence of fat hepatosis and its prevalence

The reasons for the development of the disease are still not proven, but the factors that confidently can provoke the emergence of this ailment. These include:

• fullness;
• diabetes;
• violation of exchange processes (lipid);
• minimum exercise with a nutrient daily diet with a large fat content.

Most cases of the development of fatty hepatosis doctors register precisely in developed countries with the standard of living above average.

There are still a number of factors associated with hormonal failures, such as insulin resistance and the presence of blood sugar. It is impossible to lower the hereditary factor, he also plays a big role. But still the main reason is the wrong power, a sedentary lifestyle and overweight. All reasons are not related to the admission of alcoholic beverages, so fat hepatosis is often called non-alcohol. But if there is also an alcoholic dependence on the above reasons, the fat hepatosis will develop at times rapidly.

In medicine it is very convenient to use coding of diseases for their systematization. Even indicate the diagnosis in the hospital sheet is easier with the codes. Codes of all diseases are represented in the international classification of diseases, injuries and various health problems. At this time there is an option of the tenth revision.

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

• Symptoms of hepatosis;
• Diagnosis of hepatosis;
• Treatment of fat hepatosis.

Treatment of fat hepatosis

The treatment of non-alcohol hepatosis is to eliminate possible risk factors. If the patient suffers from obesity, then you need to try to optimize it. And start with a decrease in the total mass at least 10%. Doctors recommend to achieve the goal to use the minimum physiotload parallel to diet food. Restrict the use of fats as much as possible in the diet. It should be remembered that a sharp weight loss will not only benefit, it may vice versa to damage, aggravating the course of the disease.

For this purpose, the attending physician may assign thiazolidinoids in combination with biguenides, but this line of drugs is not yet fully studied, for example, on hepato toxicity. Metformin can help adjust the process of metabolic disorders in carbohydrate exchange.

According to the final one can confidently say that when normalizing a daily diet, a decrease in body fat and abandoning bad habits, the patient will feel improvement. And only in this way you can fight with such a disease like non-alcoholic hepatosis.

Cholestatic hepatosis of pregnant women

The cholestatic hepatosis of pregnant women is also known as intrahepatic cholestasis of pregnant women, intrahepatic cholestatic jaundice of pregnant women, to a robberry jaundice of pregnant women, idiopathic yellow jaundice, returning cholestatic intrahepatic jaundice.

Code of ICD 10. - K.83.1.

Epidemiology
Intrahranny pregnant woman cholestasis - the second frequency of the cause of jaundice in pregnant women after viral hepatitis. Etheologically, it is connected only with pregnancy. According to WHO, this disease occurs in 0.1 - 2% of pregnant women.

Etiology and pathogenesis
The pathogenesis of the intrahephene cholestasis of pregnant women is not yet fixed. It is assumed that the excess of endogenous sex hormones, the typical period of pregnancy, has a stimulating effect on the processes of bile and inhibitory - on biliary release.

Reducing the selection of bile contributes to the inverse diffusion of bilirubin into the blood. This assumption is confirmed by the fact that this pathological syndrome develops in 80-90% of women in the second half of pregnancy and the lifting of estrogen content correlates with them with the development of skin itch. A certain relationship is noted between the intrahepatic cholestaste of pregnant and jaundice, caused by hormonal contraceptives, although these diseases are not identical. A certain role in the development of intrahepatic cholestasis of pregnant women is given to genetic defects of metabolism of sex hormones, manifested only during pregnancy.

Clinical picture
The intrahepatic pregnant cholestasis is characterized by painful skin itching and jaundice. Skin itch occurs sometimes a few weeks before the appearance of jaundice. Currently, some researchers itching pregnant women consider the initial stage or an erased form of pregnant women's intraheropic cholestasis. Pregnant women sometimes complain about nausea, vomiting, small pains in the top of the abdomen, more often in the right hypochondrium. The pain syndrome for this pathology is not characteristic, otherwise, the condition of pregnant women almost does not change. The liver and spleen, as a rule, are not enlarged. The disease may occur at any time of pregnancy, but more often is marked in the third trimester.

Laboratory diagnostics
With laboratory and biochemical studies, along with an increase in the level of bilirubin in serum (mainly due to its direct fraction) and severe urobilinogenuria, a significant increase (10-100 times) content of bile acids is detected. The increase in their concentration is more often due to chic acid and less than hanodoxychole. When the cholestasy of pregnant women, in addition to increasing the content of bile acids, the activity of a number of excretory enzymes, testifying to cholestasis (alkaline phosphatase, γ-glutomyltranspendase, 5-nucleotidase) increases. The activity of transaminase (alaninotransferase and aspartaminotransferase) remains within the normal range. Most pregnant women with cholestasis increase the concentration of cholesterol, triglycerides, phospholipids, β-lipoproteins. Very often they reduce blood coagulation indicators - II, VII, IX factors, protuberine. Sedimentary samples and proteinogram almost do not change.

Histological liver studies with a benign cholestasis of pregnant women show the preservation of the structure of fractions and portal fields, signs of inflammation and necrosis are missing. Only pathological sign - Focal cholestasis with bile tombami in extended capillaries and deposition of bile pigment in neighboring hepatic cells. Intrahranny cholestasis at first pregnancy is harder to diagnose, with a reuse, it is much easier, since the disease often recurrences.

Differential diagnosis
Differential diagnosis intrahepsed cholestasis of pregnant women should be done with sharp and chronic hepatitis, cholestasis caused by medicines, choletiasis with obtuctive jaundice and primary biliary cirrhosis of the liver. For the cholestasis of pregnant women pathognomonic, its beginning in the II-III trimesters of pregnancy, a recurrent character in subsequent pregnancies, lack of an increase in liver and spleen, normal indicators Transaminase activity in most patients, the disappearance of all symptoms 1-2 weeks after childbirth. Acute viral hepatitis can develop throughout the entire period of pregnancy. It is characterized by an increase in the liver and very often spleen, a sharp increase in the activity of transaminase. Helicitiasis and obstruction jaundice in pregnant women are recognized on the basis of known clinical signsas well as data ultrasonic research jelly system.

In diagnostically difficult cases, the liver biopsy is shown. This manipulation during pregnancy is not more risky than outside it. However, it should be remembered that pregnant women with intrahepan cholestase often change the coagulating blood system, so there is a great risk of bleeding.

Signs of cholestasis caused by the influence of pregnancy disappear after 1-3 weeks after childbirth. Most authors believe that all manifestations of the disease disappear, as a rule, within 1-3 months after delivery.

The course of pregnancy
The obstetric situation, as well as in all patients with liver pathology, is characterized by an increased frequency of premature genera and a large perinatal mortality - up to 11-13%. The high frequency of heavy postpartum bleeding is also noted.

Treatment
There is still no medicine specifically acting on cholestasis. A symptomtatic treatment is carried out, the main task of which is the suppression of the skin itching. For this purpose, it is recommended to use drugs binding excess bile acids in the blood. First of all, a cholestyramine was prescribed for 1-2 weeks.

Currently, ursodeoxycholic acid (URSOFALK) is widely used. The drug has a direct cytoprotective effect on the hepatocyte membrane and cholangiocytes (membrane-stabilizing effect). As a result of the preparation on the gastrointestinal circulation of bile acids, the content of hydrophobic (potentially toxic) acids is reduced. By reducing the absorption of cholestiramine in the intestine and other biochemical effects, the drug has hypocholesteromemic effect.

Some researchers for the purpose of binding bile acids are prescribed antacids from the Nevance group (Maalox, Almagel, Phosfalugel) in an ordinary therapeutic dose for 2-3 weeks. Blind tubes with xylitol, sorbitol, choleretic from a group of cholecystokinetics are shown. Antihistamines are usually not effective, so it is impractical to assign them. Medicinal metabolism occurs mainly in the liver, therefore, the drug overload is extremely undesirable.

Forecast
Intrahranny cholestatic jaundice of pregnant women in most women proceeds benign, the interruption of pregnancy is not shown. At the same time, with the complication of pregnancy, this disease should be carried out for the patient careful medical control, follow the function of the liver, the state of the fetus. These women are recommended to conduct in medical institutions, where optimal treatment will be ensured by a prematurely born child. In critical situations, with the appearance of danger to the fetus, premature delivery should be caused after 37 weeks of pregnancy.

Hundreds of suppliers are carrying medications from hepatitis with from India to Russia, but only M-Pharma will help you buy Sofosbuvir and Daclatasvir and at the same time professional consultants will answer any of your questions throughout the therapy.

Liver disease (K70-K77)

Included: Drug:

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

If necessary, identify the toxic substance uses an additional external cause code (class XX).

Excluded:

• badda Kiaari syndrome (I82.0)

Included:

• hepatic:
  • coma BDU
  • encephalopathy BDA
• hepatitis:
  • fulminant, not classified in other categories, with hepatic insufficiency
  • malignant, not classified in other categories, with hepatic insufficiency
• liver necrosis (cells) with hepatic insufficiency
• yellow atrophy or liver dystrophy

Excluded:

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

Excelred: hepatitis (chronic):

• alcoholic (K70.1)
• drug (K71.-)
• granulomatous NCDR (K75.3)
• non-specific reactive (K75.2)
• viral (B15-B19)

Excluded:

• alcoholic liver fibrosis (K70.2)
• cardial 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.-)
• amo-shaped liver degeneration (E85.-)
• cystic liver disease (congenital) (Q44.6)
• hepatic Vienna Thrombosis (I82.0)
• hepatomegaly BDU (R16.0)
• vienna thrombosis (i81)
• toxic lesion of the liver (K71.-)

In Russia, the International Classification of Diseases of the 10th Review (ICD-10) adopted as a single regulatory document for accounting for incidence, the reasons for the appeals of the population in medical institutions All departments, causes of death.

The ICD-10 has been introduced into the practice of health throughout the territory of the Russian Federation in 1999 by order of the Ministry of Health of Russia from 27.05.97. №170

A new revision (ICD-11) is planned to be planned in 2017 2018.

With changes and additions to WHO.

Processing and transferring changes © MKB-10.com

Source: http://mkb-10.com/index.php?pid\u003d10331

K70-K77 liver disease. V. 2016.

International Classification of Diseases of the 10th Review (ICD-10)

K70-K77 liver disease

K70-K77 liver disease

ray Syndrome (G93.7)

viral Gepatitis (B15-B19)

K70 liver alcoholic disease

K71 toxic liver damage

syndrome in BD Kiari (i82.0)

"Clean" Holes K71.1 toxic liver damage with hepatic necrosis Pechership insufficiency (acute) (chronic), due to lecturers K71.2 Toxic liver damage flowing by the type of acute hepatitis

hald of Atrophia or liver dystrophy

loading insufficiency complicating:

• inboard, enemy or molar pregnancy (O00-O07, O08.8)
• pregnancy, childbirth and postpartum period (O26.6)

yellowee fruit and newborn (P55-P59)

viral Gepatitis (B15-B19)

in combination with toxic leaping of the liver (K71.1)

K74 fibrosis and cirrhosis

kardial liver sclerosis (K76.1)

cirrhosis of the liver:

• alcoholic (K70.3)
• congenital (p78.3)

with toxic leaping of the liver (K71.7-) K74.0 liver fibrosis

• acute or subacute
  • BDA (B17.9)
  • not viral (K72.0)
• viral Gepatitis (B15-B19)

toxic leaping (K71.1)

halangitis without liver abcesses (K83.0)

pylephlebit without the liver abcesses (K75.1) K75.1 Flebit of Pillampite Pillampite Ruled out: Pylephlegital liver abcesses (K75.0)

aMLIDNA Liver Degeneration (E85.-)

cystrous liver disease (congenital) (Q44.6)

liver veins thrombosis (i82.0)

trom Based Vienna (I81.-)

toxic leaping (K71.-)

Ophanging nodule liver hyperplasia

Gepatoptosis K76.9 Uncomfortable liver disease

Portal Hypertension for Schistosomoz B65.- †)

Peating the liver during syphilis (A52.7 †) K77.8 * Liver damage in other diseases classified in other categories of liver hydrauli with:

• berylliosis (J63.2 †)
• cARCOIDOSE (D86.8 †)

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

2. Translation into Russian, a number of medical terms in this article may differ from the translation of the ICD-10 approved by the Ministry of Health of Russia. All comments and refinements to translate, design, etc. are accepted with gratitude by email.

3. BDU - without additional clarifications.

4. NCDR - not classified in other categories.

5. The main codes of major diseases are marked with a cross †, which must be used.

6. The asterisk is marked with optional additional codes related to the manifestation of the disease in separate organ or body area representing an independent clinical problem.

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

What is a fat hepatosis: Code of ICD 10

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

If the disease is not diagnosed at an early stage and the appropriate therapy is not carried out, then irreversible inflammatory changes occur in Parenhem, which lead to the development of tissue necrosis. If the fat hepatosis is not treated, it can grow into cirrhosis, which is no longer a treaty. In the article, we will consider for what reason the disease is developing, methods for its treatment and classification on the ICD-10.

The reasons for the occurrence of fat hepatosis and its prevalence

The reasons for the development of the disease are still not proven, but the factors that confidently can provoke the emergence of this ailment. These include:

• fullness;
• diabetes;
• violation of exchange processes (lipid);
• minimum exercise with a nutrient daily diet with a large fat content.

Most cases of the development of fatty hepatosis doctors register precisely in developed countries with the standard of living above average.

There are still a number of factors associated with hormonal failures, such as insulin resistance and the presence of blood sugar. It is impossible to lower the hereditary factor, he also plays a big role. But still the main reason is the wrong power, a sedentary lifestyle and overweight. All reasons are not related to the admission of alcoholic beverages, so fat hepatosis is often called non-alcohol. But if there is also an alcoholic dependence on the above reasons, the fat hepatosis will develop at times rapidly.

In medicine it is very convenient to use coding of diseases for their systematization. Even indicate the diagnosis in the hospital sheet is easier with the codes. Codes of all diseases are represented in the international classification of diseases, injuries and various health problems. At this time there is an option of the tenth revision.

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

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

Treatment of fat hepatosis

The treatment of non-alcohol hepatosis is to eliminate possible risk factors. If the patient suffers from obesity, then you need to try to optimize it. And start with a decrease in the total mass at least 10%. Doctors recommend to achieve the goal to use the minimum physiotload parallel to diet food. Restrict the use of fats as much as possible in the diet. It should be remembered that a sharp weight loss will not only benefit, it may vice versa to damage, aggravating the course of the disease.

For this purpose, the attending physician may assign thiazolidinoids in combination with biguenides, but this line of drugs is not yet fully studied, for example, on hepato toxicity. Metformin can help adjust the process of metabolic disorders in carbohydrate exchange.

According to the final one can confidently say that when normalizing a daily diet, a decrease in body fat and abandoning bad habits, the patient will feel improvement. And only in this way you can fight with such a disease like non-alcoholic hepatosis.

Source: http://zapechen.ru/Bolezni-Pecheni/Gepatoz/mkb-10.html

Petatosis of the liver

Code of the ICD-10

Related diseases

Names

Description

Symptoms

The reasons

Violation of metabolism - type 2 diabetes mellitus, obesity, hyperitriglyceridemia;

The effect of toxic factors - alcohol, some toxic substances, medicinal preparations;.

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

Chronic diseases of the digestive system with impaired suction syndrome and;

Fat infiltration of liver, not related to the action of alcohol or other toxic substances is called primary or non-alcoholic steatosis (non-alcoholic liver disease). Thus, not always the lesion of the liver is associated with the action of toxic factors (alcohol, drugs).

Today, the prevalence of non-alcohol liver disease is very significant. Approximately the quarter of the population of developed countries is detected by the staitosis of the liver, and in 3.5-11% - non-alcoholic steatohepatitis, including cirrhosis of the liver. Purchase people are non-alcohol fat disease The liver is diagnosed much more often than those with normal weight.

Risk factors for severe disease:

Source: http://kiberis.ru/?p\u003d30417

Beep fat degeneration (K76.0)

Version: MedElement disease reference

general information

Short description

The fatty degeneration of the liver is a disease that is characterized by the lesion of the liver with changes, similar changes in alcoholic liver disease (hepatocyte hepatocyte fatty dystrophy - the main liver cell: a large cell that performs various metabolic functions, including the synthesis and accumulation of various necessary organisms of substances, neutralization of toxic Hepatocyte (Hepatocyte) substances

) However, with fat degeneration of the liver, patients do not consume alcohol in quantities capable of causeing its damage.

The definitions are most commonly used by NAFF:

1. Non alcoholic liver dystrophy (NAFL). The presence of fatty dystrophy without signs of damage to hepatocyte hepatocytes is the main cell of the liver: a large cell performing various metabolic functions, including the synthesis and accumulation of various necessary organisms of substances, neutralizing toxic substances and the formation of bile (Hepatocyte)

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

2. Non alcoholic steatohepatitis (NAZ). The presence of hepatocyte hepatocyte hepatocyte damage and inflammation - the main liver cell: a large cell that performs various metabolic functions, including the synthesis and accumulation of various necessary organisms of substances, neutralizing toxic substances and the formation of bile (Hepatocyte)

(Balmonious dystrophy) with or without signs of fibrosis. It can progress to liver cirrhosis, liver failure and (rarely) to liver cancer.

3. Non alcoholic liver cirrhosis (Nash Cirrhosis). The presence of signs of cirrhosis with current or previous histological signs of steatosis or steatohypatitis.

4. Cryptogenic cirrhosis (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, with a detailed verification, it turns out to be a disease associated with alcohol.

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

K75.81 - Non alcoholic steatohepatitis (NAZ)

K74.0 - liver fibrosis

By 74.6 - another and unspecified liver cirrhosis. \\

Classification

Types of liver degeneration:

1. Macrolsicular type. The accumulation of fat in hepathicitis is wearing a local character and the kernel of the hepatocyte shifts away from the center. For adhesive infiltration of the liver of the macroesicular (large-scale) type as accumulated lipids, triglycerides are actuated. In this case, the morphological criterion of fat hepatosis is the content of triglycerides in the liver over 10% of the dry mass.

2. Microwiest type. The accumulation of fat occurs evenly and the kernel remains in place. With microsicular (fine-flowered) fat degeneration, other (non-triglycerides) of lipids (for example, free fatty acids) accumulate.

Also the focal and diffuse liver steatosis. Most often occurs diffuse steatosis, which is of zonal character (the second and third zone of slices).

Etiology and pathogenesis

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

Hyperinsulinism leads to 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 secretion of lipids in the bloodstream. As a result, hepatocytes hepatocyte fatty dystrophy is developing - the main cell of the liver: a large cell performing various metabolic functions, including the synthesis and accumulation of various necessary organisms of substances, neutralizing toxic substances and the formation of bile (Hepatocyte)

Appearance inflammatory processes It is predominantly centrolobular and is associated with the enhancement of lipid peroxidation.

A certain value is to enhance the absorption of toxins from the intestine.

Sharp decline in body weight;

Chronic protein-energy failure.

Inflammatory bowel diseases;

Coleciakiya celiac disease is a chronic disease caused by the lack of enzymes involved in Gluten digestion.

Diverticulose thin gut;

Microbial contamination Contamination - hit in a specific environment of any impurity changing the property of this medium.

Operations on the gastrointestinal tract.

Type II diabetes;

Triglyceridemia, etc.

Epidemiology

Sign of prevalence: distributed

Sex ratio (m / g): 0.8

Presumably prevalence ranges from 1% to 25% of the overall population in various countries. In developed countries, the average level is 2-9%. Many findings are accidentally discovered during the liver biopsy performed according to other indications.

Most often, the disease is detected in an eating, although not one age (except for children on breastfeeding) Does not exclude the diagnosis.

The ratio of floors is unknown, but the female prevalence is supposed.

Risk factors and groups

The high risk group includes:

more than 30 in% of cases is associated with the development of liver steatosis, the liver steatosis is the most common hepatosis in which fat is accumulated in liver cells.

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

2. Persons diabetes 2nd type or violation of glucose tolerance. In 60% of patients, these states are found in a complex with fatty dystrophy, in 15% with non-alcohol steatogeatite. The severity of liver damage has a connection with the severity of glucose metabolic disorders.

3. Persons with diagnosed hyperlipidemia, which is detected in 20-80% of patients with non-alcoholic steatogeatite. A characteristic fact is a more frequent combination of non-alcohol steatohypatitis with hyperitriglyceridemia than with hypercholesterolemia.

4. Middle age women.

and uncontrolling blood pressure. There is a higher prevalence of liver dystrophy in patients hypertensive disease Without the risk factors for the development of liver dystrophy. The prevalence of the disease is estimated almost 3 times higher than in control groups corresponding to the age and semi and holding blood pressure at the recommended level.

Malabsorption syndrome Malabsorption syndrome (Malabsorption) - a combination of hypovitaminosis, anemia and hypoproteinemia, due to impaired absorption in the small intestine

(as a consequence of the imposition of ileyuyunyl ileyuyuyunal - relating to the iliac and skinny intestine.

anastomosis, extended resection of a small intestine, gastroplasty about obesity, etc.);

and some others.

Clinical picture

Clinical diagnostic criteria

Cymptoms, flow

Most patients with non-alcoholic fatty health complaints are missing.

Insignificant discomfort in the upper right abdominal quadrant (about 50%);

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

Moderate hepatosplegegal hepatosplegegaly - Simultaneous significant increase in liver and spleen

Arterial hypertension ag ( arterial hypertension, hypertension) - persistent increase arterial pressure from 140/90 mm Hg.st. and higher.

Dyslipidemia Dyslipidemia - Violation of the exchange of cholesterol and other lipids (fats), which consists in changing their relationship in the blood

Violation of glucose tolerance.

The appearance of teleangectasis Teleangectasia is a local excessive expansion of capillaries and small vessels.

Ladon erythema Erythema - Limited hyperemia (enlarged blood flow)

Ascite Ascites - the accumulation of transudate in the abdominal cavity

Jaundice, gynecomasty gynecomastia - an increase in the mammary glands in men

Signs of liver failure and other signs of fibrosis, cirrhosis, noncommunicable hepatitis requires an encoding in the respective subheadings.

The revealed connection with alcohol, drug intake, pregnancy and other etiological causes also requires an encoding in other subheadings.

Diagnostics

Laboratory diagnostics

it is detected in 50-90% of patients, but the absence of these signs does not yet exclude the presence of non-alcohol steatogeatite (NAZ).

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

The value of the AST / Alt ratio with NP:

Less than 1 - observed in the initial stages of the disease (for comparison - with acute alcohol hepatitis, this ratio is usually\u003e 2);

Equal to 1 or more - may be an indicator of a 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 double) and gamma-glutlifitranspendase (can be isolated, not associated with an increase in SFF). The level of GGTP\u003e 96.5 U / L increases the risk of fibrosis.

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

IN clinical practice Insulin resistance is evaluated by the ratio of levels of immunoreactive insulin and blood glucose. It should be remembered that this is the calculated indicator that is calculated by various techniques. The indicator is influenced by the level of triglycerides in the blood and racial affiliation.

7. In 20-80% of patients with Nash, a hyperitriglyceridemy has been observed.

Many patients will have low level HDL within the framework of metabolic syndrome.

When progressing the disease, cholesterol level is often reduced.

It should be borne in mind that the low level of the positive titer of antioxculent antibodies is not uncommon under Nash, as well as less than 5% of patients may have a positive low antibody titer to smooth muscles.

characterized rather for cirrhosis or pronounced fibrosis.

Unfortunately, this indicator is not specific; In the 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 identify a NA in patients with excess body, resistance to insulin, hyperlipidemia, as well as patients with diabetes mellitus).

It is possible to use other tests in suspected non-alcoholic fibrosis or hepatitis - fibro test and act-test.

Differential diagnosis

Complications

Fibrosis fibrosis - the growth of fibrous connective tissuewhich occurs, for example, in the outcome of inflammation.

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

In detail (tyrosinemia in patients with tyrosinemia is particularly rapidly developed in patients with tyrosine in blood. The disease leads to an increase in the release of tyrosine compounds, hepatoslenomegali, assembly cirrhosis of the liver, multiple defects of renal channel reabsorption and vitamin D resistant rickets. Tyrosinemia and tyrosyl excretion occur when A number of inherited (p) fermentopaths: fumarilazetoacetase deficiency (type I), aminotransferase tyrosine (type II), 4-hydroxyphenylpirus hydroxylase (type III)

Almost bypassing the stage of "pure" fibrosis);

Hepatic insufficiency (rarely - in parallel with the rapid formation of the cirrhosis).

Treatment

Forecast

Life expectancy in non-alcoholic liver disease is not lower than in healthy faces.

Half patients develop progressive fibrosis, and in 1/6 - liver cirrhosis.

Hospitalization

Prevention

1. Normalization of body weight.

2. Patients must be examined for hepatitis viruses. In the absence of a virus hepatitis, they must 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 steatogepatitis: from pathogenesis to therapy

Danilevskaya N.N. - Gastroenterologist GKB 50, Moscow

Non alcoholic steatohepatitis (NAZ) is inflammatory infilrusion of parenchyma and stromas of the liver with the presence of focal necrosis. Nash is an intermediate link among consecutive stages of one pathological process (non-alcoholic steatosis and non-alcoholic steatophibrosis) and is included in an independent metabolic disease - non-alcoholic liver disease (NAFD). Since there is no unified code in the list of diseases of the ICD-10, which reflects the completeness of the NAFF diagnosis, is currently the most commonly used: to 76.0 - fat degeneration of the liver, not classified in other categories.

The term Nazh was first formulated in 1980. J. Ludwig et al., Studying the nature of changes in the liver of patients with obesity and diabetes mellitus 2, in which there were no instructions for taking alcohol in hepatotoxic doses, but during morphological examination of the liver tissue were Revealed signs characteristic of alcoholic liver disease. And the term of Non Alcoholic Fatty Liver Disease (Non Alcoholic Fatty Liver Disease) was currently used as the general name of various dysmetabolic liver conditions, which are based on excessive intra and extracellular fat accumulation. At the same time, it is necessary to eliminate chronic alcohol intoxication (When the use of alcohol-containing products in terms of pure ethanol is less than 20 g / day), hereditary hemochromatosis, HCV, HBV and HDV infection, increasing the levels of ceruloplasmin and α1-antitripsein, make sure that there is no autoimmune hepatitis.

It must be remembered that there is a certain number of patients who do not consume alcohol, but having a liver damage similar to histological structure with alcoholic.

Studies conducted in Japan and Italy showed that the prevalence of fat hepatosis in the overall population ranges from 3 to 58% (on average 23%). High variability in this data occurs, probably due to the socio-economic differences of the studied settlements.

In the US, non-alcoholic steatohepatitis is the most conventional disease. The percentage of obese people in the overall population increased from 10 to 25% over the period only from 1961 to 1997. In European countries, NAZ is diagnosed approximately 11% of patients who conduct liver biopsy due to increased level Transaminase serum blood. In obese people, the prevalence of the NAG is higher, is 19% and only in 2.7% of cases of the NOS is diagnosed under normal weight.

In fact, the prevalence of the NAS can be even higher among patients without clinical symptoms that do not drink alcohol in significant quantities, if there are no serological markers viral hepatitis. Thus, many patients with increased activity of hepatic enzymes in the blood and negative results of non-invasive studies may have a NA. There are reports of cases of Nash, detected in an eating.

The basis of pathogenesis of NAZ is peripheral insulin resistance. Through tyrosine kinase, an intracellular signal transmission disorder occurs after the insulin receptor is activated. The exact mechanism of violation of this path of metabolism is not completely clear. The decisive, apparently, becomes the release of adipose tissue, especially the adipose tissue of the flop-α, as well as leptin and a number of other protein mediators. FNF-α reduces the regulation of the signal insulin substrate receptor and thereby reduces translocation on the cell membrane of the GLUT-4 protein glucose membrane. As a result, the amount of glucose was reduced by a utilized cell. Peripheral insulin resistance leads to hyperinsulinism, which causes blocking mitochondrial β-oxidation. The hormone of adipose tissue leptin is also important. The resistance to leptin or its deficiency leads to the enhanced accumulation of fats and violation of the β-oxidation of fatty acids in the liver. Also, the pulse tissue adiponctin hormone hormone is reduced, and therefore, intracellular signals are disrupted, such as activation of MAP kinase and peroxisomal proliferative nuclear receptor, which enhances the accumulation of fat in the liver. Free fatty acids are hepato toxic action. Normally, the SBC is neutralized by the following paths: mitochondrial β-oxidation, products and secretion of LPONP, synthesis of binding fatty acids protein, triglyceride synthesis.

With NAFF, various mechanisms for neutralization of free fatty acids are limited. Fat liver Due to the second pathophysiological mechanism, it can be the basis for the progression of the liver pathology in the NAZ with fibrosis. In this regard, the fact that free fatty acids can be induced by cytochrome re (with subsequent products of oxygen reactive forms, which by amplifying the perikisal oxidation of lipids lead to activation of fibronegenesis. Another mechanism is represented by the increased flow of endotoxins from the intestine to the liver. As well as with alcohol lesion of the liver, cytokines are allocated by star krafe cells. The cytokines, primarily FNF-α, contribute, on the one hand, in the pathogenesis of hepatitis, on the other hand, in the development of peripheral insulin resistance. Among the reasons leading to the NAS, consider congenital and acquired metabolic disorders: Wilson's disease - Konovalov, metabolic syndrome, total parenteral nutrition, pronounced loss of body weight, as well as rare pathologies - abetalipoproteinemia, hyoffethyliproprotenemia, tyrosinemia, PERSOKISIS pathology, mitochondria. Polycystic ovarian, celiac disease, contact with solvents. It is known that such suffered surgical interventions as stomach bandage, extensive fine-turn resection, the imposition of bilipancreatic anastomosis or iliac-sublicasy anastomosis also contribute to the development of the NA. A number of drugs from various pharmacological groups (chlorookhin, diltiazem, nifedipine, amiodaron, glucocorticoids, tamoxifen, estrogens, isoniazide, methotrexate, nucleoside analogues) cause Nat.

Clinic and diagnostics NA

Relevance timely diagnosis And the treatment of the NAZ is connected, on the one hand, so that NAFLD, along with obesity, type 2 diabetes, arterial hypertension and dyslipidemia is a component of metabolic syndrome and is an independent risk factor cardiovascular diseases. At the same time, according to the developed data, Nash is 20% of all cases of NAFPP. On the other hand, it was previously believed that Nazh flows benign and rarely progresses to a decompensated liver cirrhosis, but it is currently shown that the CPU may develop in 40% of the cases of NAG and the progression of the NPC to the CPU is determined by the severity of inflammatory changes in hepatocytes. In addition, the disease affects all age groups, including children.

The true data on the prevalence of NAZ is not a few, which is due to its small and asymptomatic flow. Patients rarely impose complaints or they are not particularly specific to the far stages of the disease. Often the possibility of the development of a NAZ is discussed when the transaminase level is detected, the detection of hepatomegaly during the inspection or according to the data of visualizing methods. Improving the echogenicity of the liver under ultrasound was revealed from 14% of 2574 randomly selected residents of Japan. Since the ultrasound allows you to identify only the deposition of fat, but not inflammation, then not all these cases can be considered a NA. Also, under the overweight of the body, the discrepancy of the ultrasound, conducted by different specialists, is possible due to the increase in the thickness of the subcutaneous fat layer, which entails the technical difficulties in the implementation of the study and makes it difficult to evaluate the liver echogenicity. The final diagnosis of the Nat is possible only according to the results of the liver biopsy. According to autopsy NA, it is found in 18.5% of cases of obesity and in 2.7% of healthy persons. In the US, 20% of clinically healthy liver donors revealed fat infiltration, in 7.5% of the NA. In Japan, fatty infiltration was revealed in 9.2% of the liver donors. Histologically well-fat liver dystrophy is manifested in the form of manezicular fatty deposits in hepatocytes and infiltration of hepatic tissue with neutrophils and mononuclear cells, signs of fibrosis or cirrhosis may be present in some cases.

Among the laboratory indicators, most often changing with NOS, the most commonly occurred by an increase of 2-3 times the activity of ALT and AST. In most cases, the AST / Alt can differentiate NAG (treatment

Treatment of Nazh empirical, generally accepted methods. General Recommendations Compliance with the hypocalorial diet, the fight against hypodynailes. Laboratory and histological disorders, as well as the size of the liver with a gradual decrease in body weight, can decrease. However, the improvement is possible even against the background of persistent obesity. It was also noticed that fast decline Body masses are accompanied by the progression of the NA. In addition, the distant positive effect of the decline in body weight is difficult, since it is necessary to maintain a reduced mass of the body, and it is rarely possible to maintain a sick Nash and obesity. With a decompensated CPU within the framework of the NP, the liver transplantation is effective, but the margin in the transplant may recur, especially against the background of increasing body weight and dyslipidemia. The data of dynamic observation after the liver transplantation under NAG is not a few, but its recurrence is described after 6-10 weeks.

Preparations of various pharmacological groups are used for drug therapy. Considering the role of insulin resistance in the pathogenesis of the Nat, the use of biguenides and thiazolidindionov, the effects of which are due to a decrease in gluconeogenesis and synthesis of lipids in the liver, increasing sensitivity to insulin, thereby contributing to reducing obesity.

Preparations containing essential phospholipids are used, which are elements in the structure of the shell of cell organelle liver and have a normalizing effect on the metabolism of lipids, proteins. . In small and short studies, it was shown that the reception of α-tocopherol (vitamin E); combinations of lecithin, vitamin C and low doses of vitamin E; β-carotene; Selena; The group vitamins in somewhat improves liver function.

Recently, the greatest therapeutic efficacy under the NAG was detected in URSO-Osodoxichetic acid preparations (UDHK). In the pilot studies, the use of UPC (in the dosage / kg / day) for 12 months was accompanied by a significant improvement in the indicators of hepatic tests, lipid metabolism, decreasing liver steatosis phenomena, without a significant reduction in body weight.

UDHK is a stereoisomer of deoxychole bile acid, which is generated under the action of microflora of a large intestine. Numerous experimental and clinical researches Allow the diverse properties and EFC effects. The hepatoprotective effect develops due to the fact that the UPCC is able to integrate into the phospholipid layer of the cell membrane, which contributes to its stability and increase the resistance to damaging factors. The anticholentic effect is determined by the induction of the bicarbonate cholesis, which increases the removal of hydrophobic biliary acids into the intestine; Antiapoptic action - due to the displacement of the pool of toxic hydrophobic bile acids that have a toxic effect on hepatocytes and cholangcitis. Immunomodulatory properties are also described (due to the decrease in the expression of HLA-class molecules at hepatocytes and HLA class II on cholangocytes and reducing the products of pro-inflammatory cytokines), litholitic (due to slowing the crystallization of cholesterol) and hypocholesterometer (reduces the absorption of cholesterol in the intestine, its synthesis in the liver and excretion In bile) effects. The positive effect of UDHK on the biochemical indicators of cytolysis and cholestasis under NAZ is described in many studies, and the diverse effects of UPCC determine the use of the drug when wide spectrum Liver diseases.

Currently on the Russian market appeared new drug Haldeksan (World Medicine, United Kingdom), each capsule of which contains 300 mg of UDHK. The growing interest in the preparations of UDHK, in particular to the holootexan, is not accidental, since its pharmacotherapeutic effect is diverse and, naturally, is not limited to nonalhogolny steatogeapatite. Indications for the purpose of Holdexan, in addition to the Nazh, are: uncomplicated bile disease (biliary sweets; dissolution of cholesterol bile stones in bile bubble If it is impossible to remove them with surgical or endoscopic methods; prevention of recurrence of stone formation after cholecystectomy); chronic active hepatitis; toxic (including medicinal) liver damage; liver alcohol disease (ABP); primary biliary cirrhosis of the liver; primary sclerosing cholangitis; fibergation; Atresia of internal biliary tract, congenital atres of bile duct; Dyskinesia of biliary tract with proven UDHK effectiveness with all these diseases.

It should be noted that, unlike other drugs, the HOLOUKSAN has a more convenient dosage - 300 mg. As I wrote in my article L. Vasilyev, 2008: "Let's truth in the eye: in the production of any medicine it is not to count not on a conscientious, but on a lazy patient, and the smaller number of capsules per day will need to be taken, the greater the chance that he Course will be treated to the end. . It can be added that the advantage of the dosage of 300 mg is both in the convenience of calculating the dose of the drug per kg of the patient's weight, depending on the diagnosis (under NAZ, HOLOUKSAN is used from the calculation / kg / day. From 6 months to several years).

Special value is acquired by the properties of hootowxane among comorbid vascular patients, the number of which is growing from the year. Thus, the effectiveness of the use of UDHK under NAZ in patients with IDAs was noted in several studies. In a study conducted in 2006, in Ukraine studied the functional state of the liver of patients with IHS in combination with NSAG, which received hypolypidemic therapy with statins and UPCC (700 mg) for three months. There was a decrease in total hs by 23-44%, triglycerides by 40-41%, LDL 35-36%, a very low density lipoprotein by 25%, an atherogene index by 13-14%, raising HDL by 42%. A significant decrease in the activity of ALT (by 56%) was observed in patients who received statins and UDHK. The results of the EDHK effectiveness study results (700 mg) and statins under NAG 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 undesirable reactions when combined.

In addition, despite the relatively benign current of the NA, in half of the cases, the progression of the pathological process and occasionally the formation of the liver cirrhosis, the appointment of UDHK in patients with IHD and hyperlipidemia is reasonable. So, UDHK (700 mg 700 mg) in combination with statins is likely to have a potentent hypolypidemic effect, entailing the normalization of the lipid spectrum in patients with IBS and NSAG. At the same time, against the background of the combination of drugs, there is no deterioration in the metabolic function of the liver, causing the abolition of treatment with statins.

In general, Hydhexane is prescribed inwards once a day before bedtime or twice a day. The capsule is swallowed entirely, not chewing, drinking with enough liquid. In treating chronic diseases Liver Dosage Hydhexane Aggsm / kg body weight per day, duration of treatment - from several months to 2 years.

1. Ludwig J., Viggiano T.R. Non-Alcoholic Steatohepatitis: Mayo Clinic Experiences with a hitherto unnamed desease // Mayo Clin Proc. 1980, 55: 434 - 8.

2. L.I. Buttova "Non alcoholic liver disease as a manifestation of metabolic syndrome: epidemiology, pathogenesis, characteristics of clinical

manifestations, principles of diagnosis, modern treatment opportunities. " Moscow 2012.

3. M. Karneiro de Mur. Non alcoholic steatohepatitis // Clinical perspectives in gastroenterology, hepatology. - 2001. - № 2. - P. 12-15.

4. Fadeenko G.D. Fat liver: etiopathogenesis, diagnostics, treatment // Gastroenterologist's shortness .. - 2003. - № 3 (13). - P. 9-17.

5. Northern M. Non alcohol liver disease // Doctor.- 2002. - №10. - C.23-26. 1212.

6. Bellentani S, Tinbelli C. Epidemiology and Risk Factors for Fatty Liver. In: Leuschner U. James Off, DancyGier H (EDS.). SteatoHepatitis (Nash and Ash), Kluwer Academic Publishers, Dordrecht 2001, 3-10.].

7. M. Karneiro de Mur. Non alcoholic steatohepatitis // Clinical perspectives in gastroenterology, hepatology. - 2001. - № 2. - P. 12-15].

8. Sherlock W, Duli J. Liver diseases and biliary tract (translation from English), Moscow, 1999, C ..

9. Yakovenko E.P., Grigoriev P.Ya., Agafonov N.A., Yakovenko A.V. et al. Metabolic liver diseases: problems of therapy // Pharmatek. - 2003. - № 10. - P. 47-52.

10. Bellentani S, Saccoccio G, Masutti F et al. PREVALENCE OF AND RISK FACTORS FOR HEPATIC STEATOSIS IN NORTHERN ITALY. ANN INTERN MED 2000; 132:.

11. Chitturi S., Abeygunaskera S., Farrell G.C et al. Nash and Insulin Resistance: Insulin Hepsecretion and Specific Association With the Insulin Resistance Syndrom // Hepatology / - N 35. - P ..

12. Neuschwander-Tetri B.A., Caldwell S.H. Nonalcoholic SteatoHepatitis: Summary of An AaSld Single Topic Conference // Hepatology / - N 37. - P ..

13. Sanyal A.J., Campbell-Sargent C., Mirshahi F., Rizzo W.B. et al. Nonalcoholic SteatoHepatitis: Association of Insulin Resistance and Mitochondrial Abnor-Malities // Gastroenterology /. - N20. - P ..].

14. ONETA C.M., DUFOUR J.F. Non-Alcoholic Fatty Liver Disease: Treatment Options Based on Pathogenic Considerations // Swiss Med.Wkly. - 2002. - N132. - P ..

15. A.O. Buevover Hepatitis. Rational diagnostics. Gootar Media .. Tilg H., Diehl A.M. Cytokines in Alcoholic and nonalcoholic steatohepatitis //n.engl. J. Med. - 2000. - N 343. - P ..

17. Peter R. Maknelli "Secrets of Gastroenterology, the second edition." Binom 2005

18. M. Karneiro de Mur. Non alcoholic steatohepatitis // Clinical perspectives in gastroenterology, hepatology. - 2001. - № 2. - P. 12-15.

19. Ch. Pavlov, I. Bakulin Non alcoholic steatogeptitis: Clinical features and treatment principles // "Doctor" 2007, No. 10, p. 24-28.

20. Yu.M. Stepanov, A.Yu. Filippova, staitosis of the liver and non-alcoholic steatohepatitis: a modern look at the pathogenesis, diagnosis and treatment // Health of Ukraine.2004

21. CERIANI R, BRUNATI S, MORINI L ET AL. Effect of Ursodeoxycholic Acid Plus Diet in Patients with Nonalcoholic SteatoHepatitis (Abstract). Hepatology 1998; 28: 386A (No. 894)

22. GUMA C, VIOLA L, THOME M ET AL. Ursodeoxycholic Acid In The Treatment of Nonalcoholic Steatohepatitis: Results of A Prospective Clinical Controlled Trial (Abstract). Hepatology 1997; 26: 387A (No. 1036).

23. I.G. Bakulin, Yu.G. Sandler Ability to use hepatoprotectors in the practice of Consilium Medicum, Tom 12 / No. 8 2010,

24. rational pharmacotherapy of diseases of the digestive organs / under the general edition of V.T.Ivashkin. M.: Litterra, 2007.

25. Buovers A.O. Capabilities clinical application Ursodeoxycholic acid. Cons. Med. 2005; 7 (6).

26. Holoman J., Glasa J., Kasar J. et al. SERUM MARKERS OF LIVER FIBROSIS IN PATIENTS WITH NON-ALCOCHOLIC STEATOHEPATITIS (NASH). Correlation to Morphology and Effect Of Therapy. J Hepatol 2000; 32: 210.

27. Nadinskaya M.Yu. Investigation of the use of ursodeoxycholic acid in hepatology from the position of medicine based on scientific evidence. CONSILIUM MEDICUM 2003; 6:

28. Lazaridis K.N., Gores G.J., Lindor K.d. Ursodeoxycholic Acid Mechanisms of Action and Clinical Use in Hepatobiliary Disorders. J Hepatol 2001; 35: 134-46.

29. Fedorov I.G., Baykova I.E., Nikitin I.G., Stugzhekov G.I. Non alcoholic steatohepatitis: clinic, pathogenesis, diagnosis, treatment. Grew honey 2004; 2: 46-49.

30. Dolzhenko M.N. Patient S. ischemic disease Hearts and chronic steatohepatitis: how to carry out a hypolyum correction? Ukr honeyb 2007; 1 (57).

31. Shipulin V.P., Dolzhenko M.N. Chronic steatohepatosis: prospective study functional state of cardio-vascular system. Crimea Honey F 2006; 3: 12-16.

32. Rational pharmacotherapy of diseases of the digestive organs. Ed. V.T.Ivashkin, T.Lpina. M.: Literra, 2006; 552 p.

33. Vasilyev L, healthy like ... Bear. Magazine "Pharmacist", №1, 2008.

Masharyova A.A. - D.M., Professor of the Department of Therapy, clinical pharmacology and SMP MGSU (Moscow), the main gastroenterologist SAO DZ Moscow

Danilevskaya N.N. - Gastroenterologist of the Gastroenterological Branch of GKB No. 50