Non-alcoholic fatty liver disease ICD. What is steatosis? Etiology and pathogenesis

But let's return to the characteristics and symptoms of the pathology. Steatosis is a disease caused by a disorder of phospholipid metabolism, in which both intracellular and extracellular deposition of fat droplets occurs in the liver parenchyma.

Normally, the human liver contains 5-7% fat. If this percentage reaches 10 or higher (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 hepatic steatosis, symptoms and treatment of this disease.

Symptoms

In order to understand what hepatic steatosis is, it is necessary to know not only the pathogenesis, but also the symptoms of the disease. Steatosis of the liver and pancreas is more common in women. Usually the disease develops asymptomatically over a fairly long period, so it most often manifests itself in people over 40 years of age. Symptoms of the disease are in many ways similar to those of hepatitis:

enlarged liver - its edges, protruding 3-4 centimeters from under the costal arch, can be felt during palpation;
decreased performance, fatigue, irritability, apathy, poor sleep, absent-mindedness;
nagging pain in the right hypochondrium, which is explained by an enlarged liver stretching the fibrous capsule;
unstable stool, vomiting;
slight icterus of the sclera of the eyes (the skin usually retains its normal color);
unpleasant skin odor and bad breath;
rashes, itching of the skin.

Etiology

We have already received a general idea of what diffuse hepatic steatosis is, and now it’s time to move on to the details. The cause of disturbances in phospholipid metabolism and the resulting increase in the level of free fatty acids in the liver parenchyma is usually an incorrect lifestyle and diet in particular. The modern lifestyle of most clerks predisposes them to spend a lot of time sitting (both in front of the monitor and behind the wheel), eat poorly (fortunately, supermarkets have a large selection of all sorts of unhealthy goodies), and also periodically drink alcohol.

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

Obesity greatly contributes to the accumulation of lipids in liver tissue. Add to this the bad environment, and we get a portrait of a typical patient with fatty liver: not too young, not too slim and predisposed to alcohol. The list of predisposing factors looks something like this:

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

At first glance, the issue is not as acute as, for example, alcohol or drug abuse. However, this is precisely why nutritional issues are often not given enough attention, which provokes fatty liver degeneration. 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 somehow be compensated for by cottage cheese, milk and cheese, but vegans do not accept even such a diet, so they chronically do not receive enough amino acids. At the same time, as compensation, they often indulge in sweet dishes, which also has a bad effect on the condition 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 abuse of ethanol derivatives. Alcoholic liver steatosis often ends in cirrhosis - irreversible changes in liver tissue.

That is why even a special abbreviation NAFLD arose - liver steatosis not caused by alcohol consumption (literally: Non-alcoholic Fatty Liver Disease).

Pathogenesis

The accumulation of fat droplets in liver tissue can occur due to a violation of the natural oxidation of free fatty acids in liver mitochondria, as well as due to their increased formation and accelerated delivery to hepatocytes. Due to weakened production of lipoproteins, the removal of triglycerides from the liver worsens. The accumulation of fats in the liver parenchyma can provoke the development of inflammatory and even necrotic processes. A direct relationship between these two processes has not yet been accurately established, but it is generally accepted that the development of inflammation and tissue necrosis can be caused by the intake of hepatotoxic substances that promote the release of free radicals and the onset of oxidative processes. In addition, the production of endotoxins (toxic substances produced inside the body), which usually occurs when there is pathological growth of bacteria in the intestines 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 in nature. Diffuse hepatic steatosis is characterized by uniform deposition of fats in the liver parenchyma. It is not difficult to guess that the focal form is characterized by focal deposits of fat.

Steatosis in the International Classification of Diseases

According to the ICD-10 classification, hepatic steatosis does not have a single code. The digital values of the code change, since liver steatosis, the symptoms of which vary depending on the forms of the disease, can give a different clinical picture. The following code options are allowed:

K 73.0 - chronic hepatitis;
K 73.9 - chronic cryptogenic hepatitis (of unclear etiology);
K 76.0 - fatty liver, not mentioned in other sections;
Changes in the liver like cirrhosis.

As can be seen from the list, code 76.0 is closest to steatosis, but it does not always fully reflect the nature of the 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 clear symptoms, often accumulated fat in hepatocytes (liver cells) is detected by chance (for example, during a routine examination of a person or during diagnosis for another disease). When a patient contacts a specialist with complaints of dyspeptic disorders and chronic fatigue, the doctor first examines 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 further examination, laboratory tests and instrumental methods are prescribed.

To study the functional capacity 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, are released. 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, the level of alkaline phosphatase, bilirubin and protein is 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 about the quantitative composition of fibrous fibers.

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

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

Unlike the marker described above, 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-GT, transaminases, urea, as well as prothrombin and alpha-2 macroglobulin. The accuracy of the technique is approximately 87%.

The complex of laboratory tests may include determining the level of the gland, searching for markers for viral hepatitis, as well as antibodies (antinuclear and anti-smooth muscle).

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 in the second case, dystrophy and the formation of multiple cystic formations are observed, around which cell compaction occurs. The third degree is manifested by areas of connective tissue that completely disrupt the structure of the liver, which leads to its dysfunction.

Treatment of steatosis

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

dietary nutrition according to table No. 5;
weight correction. Given the presence of obesity in patients with hepatic steatosis, gradual weight loss is required by following the recommendations of a nutritionist. Complete refusal of food or self-limitation can lead to a sharp deterioration in the patient’s general condition;
correction of hyperglycemia, -lipidemia and -cholesterolemia using diet and medications;
giving up alcohol;
discontinuation of hepatotoxic medications.

Among the effective drugs it is worth highlighting:

Ursosan is 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. The medicine also prevents stagnation, normalizing bile flow. It increases the activity of pancreatic enzymes and slightly reduces blood glucose;
Heptral - has amino acids. It has antidepressant, detoxification and hepatoprotective effects;
Phosphogliv is a medicine with essential phospholipids that are embedded in the cell membrane and prevent the destruction of hepatocytes;
Hepa-Merz is a protective and detoxifying agent that contains amino acids (aspartate, ornithine);
Metformin is an antidiabetic medication that improves glucose absorption. It belongs to the group of biguanides. Taking the medicine is accompanied by a decrease in thyroid-stimulating hormone and cholesterol, which is necessary to prevent vascular damage. Its main effect is to block glucose synthesis in the liver and increase the sensitivity of insulin receptors;
Atorvastatin is prescribed to lower cholesterol.

Diet and recipes for fatty liver

Considering the pathogenesis of the development of the disease, namely the deposition of fat in hepatocytes against the background of metabolic disorders, adherence to dietary nutrition for the patient is extremely necessary.

The daily menu should be discussed with your doctor, since exceeding the caloric content of food 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 foods, as well as a decrease in lipids and carbohydrates. Each week should include:

low-fat dairy products;
plant products (currants, fruits);
bran;
cod, hake;
chicken, veal;
stale baked goods;
vegetables;
puree soups;
porridge (oatmeal, buckwheat, wheat, rice);
vegetable oil;
green tea.

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

Diet restrictions include sharp cheese, eggs, butter, salt and herring. The following should be excluded from the menu:

cocoa;
sweets;
soda;
mushrooms;
onion garlic;
pepper seasonings, mustard, mojo;
fatty varieties of meat and fish products;
peas, beans;
legumes;
ice cream.

The goal of the diet is to normalize liver functionality 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 sick, patients often complain of poor appetite, so the diet should be not only healthy, but also tasty. Below are recipes for dishes 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 prohibited. 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 for the dish includes 700 g of rice, half a kilo of chicken, 4 carrots and a small onion. You should prepare the meat in advance by boiling it, changing the water once. As soon as it becomes soft, it needs to be cut and combined with chopped vegetables. Add water to them and simmer over low heat.

After the liquid has evaporated, add the cooked rice, add a little salt and continue simmering for 3-5 minutes. The cereal should be prepared in advance. It needs to be washed, filled with water, the level of which should be 3 cm above the rice mass, and then cooked until softened.

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

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

Casseroles

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

To prepare you will 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 take 230 g. Now you need to salt it, add a spoonful of sugar and simmer until softened. Cook the noodles (200 g) separately, slightly short of cooking. Pour milk and melted butter into it and leave for half an hour. It's time to mix everything, add the beaten egg and place in a baking dish in the oven for a quarter of an hour;
The recipe includes 80 g of chicken and vermicelli, protein and a piece of butter. Let's take care of the meat first. It needs to be boiled and chopped in a blender. The noodles are cooked until half cooked and cooled. Now grind the oil with the protein and mix with the minced chicken. Add the whole mass to the noodles and bake until done;
rice 230 g, cottage cheese 180 g, three apples and the same number of eggs, 480 ml of milk and raisins. The technological process begins with boiling the rice until cooked. Now grind the cottage cheese through a sieve, beat the eggs with 25 g of sugar, and cut the peeled apples 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 200 degrees.

Why is fatty liver disease dangerous?

Without treatment, liver steatosis threatens to develop severe complications. They are presented:

fibrosis. As the cells die, they are gradually replaced by connective fibers, which is accompanied by scarring of the organ. Against this background, the functioning of the liver rapidly deteriorates;
disruption of the production and movement of bile through 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, we should highlight cirrhosis, which is dangerous due to its manifestations. Against the background of protein deficiency, there is a deficiency of coagulation factors, which is fraught with massive bleeding. In addition, esophageal veins undergo varicose changes. They become crimped and their walls become thinner. The patient begins to experience severe swelling of the extremities. Fluid accumulates not only in tissues, but also in cavities (pleural, abdominal), which is accompanied by symptoms characteristic of pleurisy and ascites.

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

Non-alcoholic fatty liver disease (NAFLD)

Version: MedElement Disease Directory

Fatty liver degeneration, not elsewhere classified (K76.0)

Gastroenterology

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

Toxic liver damage - K71.-;

Non-alcoholic steatohepatitis (NASH) - K75.81;

Liver damage during pregnancy, childbirth and the postpartum period - O26.6.

Note 2

Fatty liver degeneration is a form of non-alcoholic fatty liver disease (NAFLD).

Definitions most often used for NAFLD:

1. Non-alcoholic fatty liver (NAFL). Presence of fatty liver without signs of hepatocyte damage 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, the 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). Presence of liver steatosis and inflammation with 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, the neutralization of toxic substances and the formation of bile (Hepatocyte)
(balloon dystrophy) with or without signs of fibrosis. May progress to 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 signs of steatosis or steatohepatitis.

4. Cryptogenic Cirrhosis - cirrhosis without obvious etiological causes. Patients with cryptogenic cirrhosis usually have high risk factors associated with metabolic disorders such as obesity and metabolic syndrome. Increasingly, cryptogenic cirrhosis, upon detailed examination, turns out to be an alcohol-associated disease.

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

To date, the list of ICD-10 diseases does not have a single code reflecting the completeness of the diagnosis of NAFLD, so it is advisable to use one of the following codes:

K 76.0 - Fatty liver degeneration, not elsewhere classified
- K75.81 - Non-alcoholic steatohepatitis (NASH)
- K74.0 - Liver fibrosis
- K 74.6 - Other and unspecified cirrhosis of the liver.\

Classification

Types of fatty liver degeneration:
1. Macrovesicular type. The accumulation of fat in hepatocytes is local in nature and the hepatocyte nucleus moves away from the center. With fatty infiltration of the liver of the macrovesicular (large-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. Fat accumulation occurs evenly and the core remains in place. In microvesicular fatty degeneration, lipids other than triglycerides (eg, free fatty acids) accumulate.

Also distinguished focal and diffuse liver steatosis. The most common is diffuse steatosis, which is zonal in nature (the second and third zones of the lobule).

Etiology and pathogenesis

Primary non-alcoholic fat 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 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, the neutralization of toxic substances and the formation of bile (Hepatocyte)
.
The occurrence 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 some importance.

Secondary fatty liver disease may be the result of the following factors.

1. Nutritional factors:
- sharp decrease in body weight;
- chronic protein-energy deficiency.

2. Parenteral nutrition (including glucose administration).

3. Gastrointestinal lesions causing nutritional disorders:
- inflammatory bowel diseases;
- celiac disease Celiac disease is a chronic disease caused by a deficiency of enzymes involved in the digestion of gluten.
;
- diverticulosis of the small intestine;
- microbial contamination Contamination is the entry into a certain environment of some impurity that changes the properties of this environment.
small intestine;
- operations on the gastrointestinal tract.

4. Metabolic diseases:
- dyslipidemia;
- diabetes mellitus type II;
- triglyceridemia, etc.

Epidemiology

Age: mostly

Sign of prevalence: Common

Sex ratio(m/f): 0.8

There are no precise data on the prevalence of fatty liver degeneration.
The estimated prevalence ranges from 1% to 25% of the general population in various countries. In developed countries the average level is 2-9%. Many findings are discovered incidentally during liver biopsy performed for other indications.
Most often, the disease is detected at the age of 40-60 years, although no age (except for breastfed children) excludes the diagnosis.
The sex ratio is unknown, but a female predominance is expected.

Risk factors and groups

High risk groups include:

1. Persons with excess body weight, especially so-called “visceral obesity”. BMI Body mass index (BMI) is a value that allows you to assess the degree of correspondence between a person’s weight and his height and, thereby, indirectly assess whether the weight is insufficient, normal or excessive. Body mass index is calculated using the formula: I= m/h², where: m is body weight in kilograms, h is height in meters, and is measured in kg/m²
more than 30 in 95-100% of cases is associated with the development of liver 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 occur in combination with fatty degeneration, in 15% - with non-alcoholic steatohepatitis. The severity of liver damage is related to the severity of glucose metabolism disorders.

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.

5. Persons suffering from arterial hypertension and uncontrolled blood pressure. There is a higher prevalence of fatty liver in patients with hypertension without risk factors for fatty liver. The prevalence of the disease is estimated to be almost 3 times higher than in age- and sex-matched control groups that kept blood pressure at the recommended level.

Low risk factor for the formation of secondary fatty liver disease include:
- malabsorption syndrome Malabsorption syndrome (malabsorption) is a combination of hypovitaminosis, anemia and hypoproteinemia caused by malabsorption in the small intestine
(as a consequence of the imposition of ileojejunal Ileojejunal - relating to the ileum and jejunum.
anastomosis, extended resection of the small intestine, gastroplasty for obesity, etc.);

Fast weight loss;

Long-term parenteral nutrition;

Small intestinal bacterial overload syndrome;
- abetalipoproteinemia;

Lipodystrophy of the limbs;

Weber-Christian disease Weber-Christian disease (syn. Weber-Christian panniculitis) is a rare and little-studied disease that is characterized by repeated inflammation of the subcutaneous tissue (panniculitis), which has a nodular nature. Inflammation leaves behind tissue atrophy, manifested by skin retraction. Inflammation is accompanied by fever and changes in internal organs
;

Konovalov-Wilson disease Konovalov-Wilson disease (syn. hepato-cerebral dystrophy) is a hereditary human disease characterized by a combination of liver cirrhosis and degenerative processes in the brain; caused by impaired protein metabolism (hypoproteinemia) and copper; inherited in an autosomal recessive manner
and some others.

Clinical picture

Clinical diagnostic criteria

Obesity; weakness; hepatomegaly; splenomegaly; discomfort in the right upper abdomen; arterial hypertension

Symptoms, course

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

The following may occur symptoms:
- slight discomfort in the upper right quadrant of the abdomen (about 50%);
- pain in the upper right quadrant of the abdomen (30%);
- weakness (60-70%);
- moderate hepatosplenomegaly Hepatosplenomegaly - simultaneous significant enlargement of the liver and spleen
(50-70%).

Signs of chronic liver disease or portal hypertension Portal hypertension is venous hypertension (increased hydrostatic pressure in the veins) in the portal vein system.
are rarely observed.

Usually detected signs of metabolic syndrome:
- obesity (up to 70%);
- arterial hypertension AH (arterial hypertension, hypertension) - a persistent increase in blood pressure from 140/90 mm Hg. and higher.
;
- dyslipidemia Dyslipidemia is a disorder of the metabolism of cholesterol and other lipids (fats), consisting in a change in their ratio in the blood
;
- diabetes;
- impaired glucose tolerance.

Note
The appearance of telangiectasia Telangiectasia is 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 - enlargement of the mammary glands in men
, signs of liver failure and other signs of fibrosis, cirrhosis, non-infectious hepatitis requires coding in the appropriate subheadings.
The identified connection with alcohol, medication, pregnancy and other etiological reasons also requires coding in other subheadings.

Diagnostics

General provisions. In practice, suspicion of non-alcoholic steatohepatitis arises if the patient has obesity, hypertriglyceridemia and elevated transaminase levels. The diagnosis is confirmed by laboratory tests and biopsy. Imaging methods are of little use for confirmation in the early stages.

Anamnesis: exclusion of alcohol abuse, drug injuries, family history of liver disease.

When diagnosing non-alcoholic fatty liver disease, the following are used: visualization methods:

1. Ultrasound. Steatosis can be confirmed provided that the increase in the amount of fatty inclusions in the tissue is at least 30%. Ultrasound has a sensitivity of 83% and a specificity of 98%. Increased echogenicity of the liver and increased distal sound attenuation are revealed. Hepatomegaly is possible. Signs of portal hypertension and indirect assessment of the degree of steatosis are also identified. Good results have been obtained using the Fibroscan device, which allows additional detection of fibrosis and assessment of its degree.

2. Computed tomography. Main CT signs:
- decrease in radiological density of the liver by 3-5 HU (normal 50-75 HU);
- X-ray density of the liver is less than X-ray density of the spleen;
- higher density of intrahepatic vessels, portal and inferior vena cava compared to the density of liver tissue.

3. Magnetic resonance imaging. Can semi-quantitatively estimate fat content in liver . Surpasses ultrasound and CT in diagnostic abilities. Areas of decreased signal intensity on T1-weighted images may indicate local fat accumulation in the liver.

4. FEGDS - it is possible to detect varicose veins of the esophagus during transformation into cirrhosis.

5. Histological examination of liver punctate(gold standard for diagnosis):
- large droplet fatty degeneration;
- balloon dystrophy or degeneration of hepatocytes (in the presence/absence of inflammation, Mallory hyaline bodies, fibrosis or cirrhosis).
The degree of steatosis is assessed using a scoring system.

Assessment of liver steatosis in patients with NAFLD(D.E. Kleiner CRN system, 2005)

6. ECG due to the increased risk of coronary artery disease, it is standardly indicated for all patients with excess body weight, dyslipidemia and hyperglycerinemia, and arterial hypertension.

Laboratory diagnostics

1. Transaminases. Laboratory signs of cytolysis Cytolysis is the 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 either part of normal physiological processes or a pathological condition that occurs when the cell is damaged by external factors, for example, when the cell is exposed to antibodies
are detected in 50-90% of patients, but the absence of these signs does not exclude the presence of non-alcoholic steatohepatitis (NASH).
The level of serum transaminases increased slightly - 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 severe 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 (usually no more than twofold) and gamma-glutamyl transpeptidase (may be isolated, not associated with an increase in alkaline phosphatase) is detected. A GGTP level > 96.5 U/L increases the risk of fibrosis.

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

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 progression to cirrhosis is possible in patients with diabetic nephropathy Nephropathy is the general name for certain types of kidney damage.
.

5. In 10-25% of patients, slight hypergammaglobulinemia is detected.

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

7. 20-80% of patients with NASH have hypertriglyceridemia.
Many patients will have low HDL levels as part of 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 extrinsic pathway of blood coagulation
are more typical for cirrhosis or severe fibrosis.

10. Determination of the level of cytokeratin 18 fragments (TPS-test) is a promising method for studying the activity of the process. The method allows you to distinguish the presence of hepatocyte apoptosis (hepatitis) from fatty infiltration of the liver without the use of a biopsy.
Unfortunately, this indicator is not specific; if it increases, 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 excess body weight, insulin resistance, hyperlipidemia, as well as patients with diabetes).
It is possible to use other tests if non-alcoholic fibrosis or hepatitis is suspected - Fibro-test and Acti-test.

Differential diagnosis

Non-alcoholic fatty liver disease is differentiated from the following diseases:
- hepatitis of various established etiologies, primarily chronic hepatitis B, C, D, E, autoimmune hepatitis and others;
- alcoholic liver disease;
- secondary fatty liver disease (drug-induced hepatitis, metabolic disorders, for example, Wilson's disease, hemochromatosis or alpha-1-antitrypsin deficiency);
- idiopathic fibrosis, sclerosis, cirrhosis of the liver;
- primary sclerosing cholangitis;
- primary biliary cirrhosis;
- hypothyroidism and hyperthyroidism;
- vitamin A poisoning.

Almost all differential diagnosis is based on laboratory tests specific to the diseases listed above and biopsy studies.

Complications

- fibrosis Fibrosis is the proliferation of fibrous connective tissue, occurring, for example, as a result of inflammation.
;
- cirrhosis of the liver Liver cirrhosis is a chronic progressive disease characterized by degeneration and necrosis of the liver parenchyma, accompanied by its nodular regeneration, diffuse proliferation of connective tissue and deep restructuring of the liver architectonics.
(develops especially rapidly in patients with tyrosinemia Tyrosinemia is an increased concentration of tyrosine in the blood. The disease leads to increased urinary excretion of tyrosine compounds, hepatosplenomegaly, nodular cirrhosis, multiple defects in renal tubular reabsorption and vitamin D-resistant rickets. Tyrosinemia and tyrosyl excretion occur in a number of inherited (p) enzymopathies: deficiency of fumarylacetoacetase (type I), tyrosine aminotransferase (type II), 4-hydroxyphenylpyruvate hydroxylase (type III)
, practically bypassing the stage of “pure” fibrosis);
- liver failure (rarely - in parallel with the rapid formation of cirrhosis).

Treatment abroad

Catad_tema Non-alcoholic fatty liver disease - articles

Non-alcoholic steatohepatitis: from pathogenesis to therapy

Masharova A.A. - Doctor of Medical Sciences, Professor of the Department of Therapy, Clinical Pharmacology and Emergency Medicine MGMSU (Moscow), Chief Gastroenterologist of the Northern Administrative District of the Moscow Healthcare District
Danilevskaya N.N. – gastroenterologist, City Clinical Hospital 50, Moscow

Definition

Non-alcoholic steatohepatitis (NASH) is an inflammatory infiltration of the liver parenchyma and stroma with the presence of 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 have a single code reflecting the completeness of the diagnosis of NAFLD, currently the most often used is: K 76.0 – fatty liver degeneration, not classified in other categories.

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 upon morphological examination of liver tissue there were signs characteristic of alcoholic liver disease were identified. And the term non-alcoholic fatty liver disease, introduced in 2000, is currently used as a general name for various dysmetabolic liver conditions, 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, and ensure the absence of autoimmune hepatitis.

Epidemiology

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 conducted in Japan and Italy have shown that the prevalence of fatty liver disease in the general population ranges from 3 to 58% (mean 23%). The high variability in these data is likely due to the socioeconomic differences of the study communities.

In the United States, nonalcoholic 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 who undergo liver biopsy due to elevated serum transaminases. In obese people, the prevalence of NASH is higher, at 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 drink significant amounts of alcohol if serological 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 detected at the age of 10-20 years.

Pathogenesis

The pathogenesis of NASH is based on peripheral insulin resistance. Through tyrosine kinase, intracellular disruption of signal transmission occurs after activation of the insulin receptor. The exact mechanism of disruption of this metabolic pathway is not completely clear. Decisive, apparently, is the release of TNF-α by adipose tissue, especially the adipose tissue of the mesentery, as well as leptin and a number of other protein mediators. TNF-α downregulates 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 fatty acid β-oxidation in the liver. Also, in NAFLD, the level of the adipose tissue hormone adiponectin decreases, and therefore intracellular signals, such as activation of MAP kinase and peroxisomal proliferator-proliferated nuclear receptor, are disrupted, which increases the accumulation of fat in the liver. Free fatty acids have a hepatotoxic effect. 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, various mechanisms for neutralizing free fatty acids are limited. Fatty liver, through a second pathophysiological mechanism, may become the basis for the progression of liver pathology to NASH with fibrosis. In this regard, it is important that free fatty acids can induce cytochrome P 450 2 E1 with the subsequent production of reactive oxygen species, which, by enhancing lipid peroxidation, lead to the 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 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, peroxisome pathology, mitochondriaopathies. Polycystic ovary syndrome, celiac disease, and contact with solvents are important. It is known that previous surgical interventions such as gastric banding, extensive small intestinal resection, bipancreatic anastomosis or ileo-intestinal 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 analogues) cause NASH.

Clinic 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 the metabolic syndrome and is an independent risk factor for cardiovascular diseases. Moreover, according to accumulated data, NASH accounts for 20% of all cases of NAFLD. On the other hand, it was previously believed that NASH is benign and rarely progresses to decompensated cirrhosis, but it has now been shown that cirrhosis can develop in 40% of NASH cases and the progression of NASH to cirrhosis 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 scarce, which is due to its mild 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 elevated transaminase levels are detected, hepatomegaly is detected during examination, or according to imaging studies. Increased liver echogenicity on ultrasound was detected in 14% of 2574 randomly selected Japanese residents. Since ultrasound can only detect fat deposits and not inflammation, not all of these cases can be considered NASH. Also, with excess body weight, there may be a discrepancy between ultrasound conclusions performed by different specialists 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 based on the results of a liver biopsy. According to autopsy data, NASH occurs in 18.5% of obese cases and in 2.7% of healthy individuals. In the USA, 20% of clinically healthy liver donors have fatty infiltration, and 7.5% have NASH. In Japan, fatty infiltration was detected in 9.2% of liver donors. Histologically, fatty liver disease manifests itself as macrovesicular fat 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 a 2-3-fold increase in the activity of ALT and AST. In most cases, the AST/ALT ratio can differentiate NASH ( Treatment

Treatment of NASH is empirical; there are no generally accepted methods. General recommendations include following a low-calorie diet and combating physical inactivity. Laboratory and histological abnormalities, as well as liver size, may decrease with a gradual decrease in body weight. However, improvement is possible even against the background of persistent obesity. It has also been observed that rapid weight loss is accompanied by progression of NASH. In addition, the long-term beneficial effects of weight loss are difficult to assess, since this requires maintaining a reduced body weight, and this is rarely possible in patients with NASH and obesity. In case of decompensated cirrhosis as part of NASH, liver transplantation is effective, but NASH in the graft can recur, especially against the background of weight gain and dyslipidemia. Follow-up data after liver transplantation for NASH are scarce, but its recurrence has been described after 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, increasing sensitivity to insulin, thereby helping to reduce obesity.

Preparations are used that contain essential phospholipids, which are elements in the structure of the membrane of the cellular organelles of the liver and have a normalizing effect on the metabolism of lipids and proteins. . In small and short-term studies, it was shown that taking α-tocopherol (vitamin E); combinations of lecithin, vitamin C and low doses of vitamin E; β-carotene; Selena; B vitamins slightly improve liver function indicators.

Recently, the greatest therapeutic effectiveness in NASH has been identified with ursodeoxycholic acid (UDCA) preparations. In pilot studies, the use of UDCA (at a dose of 13-15 mg/kg/day) for 12 months was accompanied by a significant improvement in liver tests, lipid metabolism, and a decrease in hepatic steatosis, without a significant decrease in body weight.

UDCA is a stereoisomer of deoxycholic bile acid, formed under the influence of colon microflora. 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 the displacement of a pool of toxic hydrophobic bile acids that have a toxic effect on hepatocytes and cholangocytes. The immunomodulatory properties of UDCA are also described (by reducing the expression of HLA class I molecules on hepatocytes and HLA class II on cholangiocytes and reducing the production of pro-inflammatory cytokines), litholytic (due to slowing down 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, UK) has appeared on the Russian market, each capsule of which contains 300 mg of UDCA. The growing interest in UDCA drugs, in particular Choludexan, is not accidental, since its pharmacotherapeutic effect is diverse and, naturally, is not limited to non-alcoholic steatohepatitis. Indications for the use of Choludexan, in addition to NASH, are: uncomplicated cholelithiasis (biliary sludge; dissolution of cholesterol gallstones in the gallbladder when it is impossible to remove them by surgical or endoscopic methods; prevention of recurrent stone formation after cholecystectomy); chronic active hepatitis; toxic (including medicinal) liver damage; alcoholic liver disease (ALD); 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 effectiveness of UDCA in all these diseases.

It should be noted that, unlike other drugs, Choludexan has a more convenient dosage - 300 mg. As L. Vasiliev, 2008, wrote in his article: “Let's face it: in the production of any medicine you should count not on a conscientious, but on a lazy patient, and the fewer capsules per day he needs to take, the greater the chances that he will will complete the course of treatment. . 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 the patient’s weight, depending on the diagnosis (for NASH, Choludexan is used at a rate of 13-15 mg/kg/day from 6 months to several years).

The properties of Choludexan are of particular value in comorbid vascular patients, the number of which is growing from year to year. Thus, the effectiveness of the use of UDCA for NASH in patients with coronary artery disease has been noted in several studies. A study conducted in 2006 in Ukraine examined the functional state of the liver of patients with coronary artery disease in combination with NASH who received lipid-lowering therapy with statins and UDCA (Choludexan 300 mg) 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 a study of the effectiveness of UDCA (Choludexan 300 mg) and statins in NASH and IHD indicate the validity of the use of drugs in order to achieve a lipid-lowering 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 there is progression of the pathological process and occasionally the formation of liver cirrhosis, the prescription of UDCA in patients with coronary artery disease and hyperlipidemia is justified. So, UDCA (Choludexan 300 mg) in combination with statins probably has a potentiating hypolipidemic effect, leading to normalization of the lipid spectrum in patients with ischemic heart 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, causing the abolition of statin treatment.

In general, Choludexan is prescribed orally once a day at 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 10-15 mg/kg body weight per day, the duration of treatment is from several months to 2 years.

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DISEASES OF THE LIVER AND BILIARY SYSTEM

Fatty hepatosis.

Pigmented hepatosis.

Hemochromatosis.

Wilson-Konovalov disease.

Amyloidosis of the liver.

Liver echinococcosis.

Cholelithiasis.

Chronic cholecystitis.

Chronic cholangitis.

Biliary dyskinesia.

Postcholecystectomy syndrome.

FATTY HEPATOSIS

Definition.

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

ICD10: K76.0 – Fatty liver not classified elsewhere.

Etiology.

GH is a multi-etiological disease. Often occurs as a result of metabolic disorders caused by an unbalanced diet. This is especially true if there is a bad habit or there are circumstances in which the entire daily food requirement is satisfied in almost 1 meal. In such cases, taking into account the limited possibilities for storing carbohydrates and proteins in the liver and other organs, they turn into easily and unlimitedly stored 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 disrupted, which leads to destabilization of the mechanisms for maintaining normal blood glucose levels. In addition, metabolic changes associated with long-term 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 cause gallstones can contribute to the formation of homogeneous cholesterol stones in the gallbladder.

Clinical picture.

ZH is characterized by complaints of general weakness, decreased ability to work, dull aching pain in the right hypochondrium, and poor tolerance to alcohol. Many people experience hypoglycemic conditions in the form of paroxysmal, sudden weakness, sweating, and a feeling of “emptiness” in the stomach that quickly passes after eating food, even one candy. Most patients have a tendency to constipation.

The vast majority of patients with gastrointestinal tract have formed the habit of a diet with 1-2 meals a day. Many people have a history of drinking large amounts of beer, long-term drug therapy, working under toxic influences, various diseases of internal organs: diabetes mellitus, metabolic X-syndrome, chronic circulatory failure, etc.

An objective examination usually draws attention to the patient's excess body weight. The size of the liver determined by percussion is increased. The anterior edge of the liver is rounded, compacted, and slightly sensitive.

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

Diagnostics.

General blood and urine analysis: no abnormalities.

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

Ultrasound examination: liver enlargement with a diffuse or focally 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 pancreas, diffusely increased echogenicity of its parenchyma in the absence of pathological expansion of the Wirsung duct. Stones in the gallbladder and signs of diffuse, reticular or polypous cholesterosis of the gallbladder may be recorded.

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

Liver biopsy: diffuse or localized in various parts of the lobule fatty degeneration of liver cells, extrahepatic location of fat 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 involve the entire lobule, spreading to the portal tracts and periportal zone, which indicates the likelihood of the formation of liver fibrosis.

Excluded:

Budd-Chiari syndrome (I82.0)

Included:

hepatic:
- coma NOS
- encephalopathy NOS
hepatitis:
- fulminant, not elsewhere classified, with liver failure
- malignant, not elsewhere classified, with liver failure
necrosis of the liver (cells) with liver failure
yellow atrophy or liver dystrophy

Excluded:

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

Excluded: 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 liver degeneration (E85.-)
cystic liver disease (congenital) (Q44.6)
hepatic vein thrombosis (I82.0)
hepatomegaly NOS (R16.0)
portal vein thrombosis (I81)
toxic liver damage (K71.-)

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

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

What is fatty hepatosis: ICD 10 code

The development of fatty hepatosis is based on a 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 hepatosis is not treated, it can develop into cirrhosis, which can no longer be treated. In the article we will look at the reasons for which the disease develops, 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 occurrence of this disease. These include:

Doctors register most cases of the development of fatty hepatosis in developed countries with an above-average standard of living.

There are a number of other factors associated with hormonal imbalances, such as insulin resistance and blood sugar. The hereditary factor cannot be ignored; it also plays a big role. But still, the main reason is poor diet, sedentary lifestyle and excess weight. All the causes have nothing to do with the consumption of alcoholic beverages, which is why fatty hepatosis is often called non-alcoholic. But if we add alcohol dependence to the above reasons, then fatty hepatosis will develop much more rapidly.

In medicine, it is very convenient to use coding of diseases to systematize them. It’s even easier to indicate a diagnosis on a sick leave certificate using a code. All diseases are coded in the International Classification of Diseases, Injuries and Related Health Problems. At this time, the tenth revision option is in effect.

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

You can learn more about the symptoms, diagnosis and treatment of hepatosis from the following 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 nutrition to achieve the goal. Limit the use of fats in your diet as much as possible. It is worth remembering that sudden weight loss will not only not bring benefits, it can, on the contrary, cause harm, 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 hepatotoxicity. Metformin can help correct the process of metabolic disorders in carbohydrate metabolism.

As a result, we can confidently say that by normalizing the daily diet, reducing body fat mass and giving up bad habits, the patient will feel an improvement. And only in this way can one fight a disease such as non-alcoholic hepatosis.

K70-K77 Liver diseases. V. 2016

International Classification of Diseases, 10th Revision (ICD-10)

K70-K77 Liver diseases

Reye's syndrome (G93.7)

viral hepatitis (B15-B19)

K70 Alcoholic liver disease

K71 Liver toxicity

Budd-Chiari syndrome (I82.0)

“Pure” cholestasis K71.1 Toxic liver damage with hepatic necrosis Liver failure (acute) (chronic), caused by drugs K71.2 Toxic liver damage, occurring as acute hepatitis

yellow atrophy or liver dystrophy

liver failure complicating:

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

jaundice of the fetus and newborn (P55-P59)

viral hepatitis (B15-B19)

in combination with toxic liver damage (K71.1)

K74 Fibrosis and cirrhosis of the liver

cardiac sclerosis of the 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)
- not 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 vein 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 damage in syphilis (A52.7 †) K77.8* Liver damage in other diseases classified elsewhere Liver granulomas in:

berylliose (J63.2†)
sarcoidosis (D86.8 †)

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

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 gratefully received by e-mail.

3. NOS - without further clarification.

4. NEC - not classified in other categories.

5. The main codes of the underlying disease that must be used are marked with a cross †.

6. Optional additional codes that relate to the manifestation of a disease in a separate organ or area of the body that represents an independent clinical problem are marked with an asterisk.

/ Internal diseases / Chapter 3 DISEASES OF THE LIVER AND BILIARY SYSTEM-r

DISEASES OF THE LIVER AND BILIARY SYSTEM

Biliary dyskinesia.

ICD10: K76.0 – Fatty liver degeneration not classified elsewhere.

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

General blood and urine analysis: no abnormalities.

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

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

It is carried out with alcoholic liver disease, chronic hepatitis.

In contrast to LH, alcoholic liver disease is characterized by anamnestic information about long-term alcohol abuse. In liver biopsies of alcoholics, hepatocytes containing Mallory bodies - condensed smooth endoplasmic reticulum - are detected in large numbers. A marker of long-term alcoholism is detected in their blood - transferrin, which does not contain sialic acids.

Chronic hepatitis differs from gastric hepatitis by abnormalities in general and biochemical blood tests, indicating the presence of a chronic inflammatory process in the liver, disorders of the protein-forming and liposynthetic functions of the organ. Markers of infection with hepatitis B, C, D, G viruses are identified. The results of a puncture biopsy of the liver make it possible to reliably distinguish between gastrointestinal tract and chronic hepatitis.

General blood analysis.

Immunological analysis for the presence of markers of hepatitis B, C, D, G viruses.

Ultrasound of the abdominal organs.

Liver puncture biopsy.

Mandatory transition to a fractional diet - 5-6 meals a day with an even distribution of calories and component composition (carbohydrates-proteins-fats) of food. The consumption of animal fats is limited. Dishes containing cottage cheese and plant fibers are recommended. If you are prone to constipation, you should consume steamed rye or wheat bran 1-3 teaspoons 3-4 times a day with meals.

It is imperative to prescribe a daily intake of balanced multivitamin preparations such as “Troll”, “Jungle”, “Enomdan” and the like.

The most effective treatment for GH is Essentiale Forte, which contains essential phospholipids and vitamin E. Unlike Essentiale Forte, Essentiale does not contain vitamin E, nor does Essentiale for parenteral administration. Essentiale-Forte is taken 2 capsules 3 times a day with meals for 1-2 months.

Other lipotropic drugs can be used to treat gastric hyperplasia:

Legalon - 1-2 tablets 3 times a day.

Lipofarm – 2 tablets 3 times a day.

Lipostabil – 1 capsule 3 times a day.

Lipoic acid – 1 tablet (0.025) 3 times a day.

The effectiveness of the treatment can be monitored using ultrasound, which reveals a tendency towards a decrease in the size of the liver and a decrease in the echogenicity of the organ parenchyma.

Usually favorable. By eliminating harmful effects, effective treatment, and taking prophylactic multivitamin medications, a complete recovery is possible.

SELF-CONTROL TESTS

What are the circumstances? can not lead to the formation of fatty hepatosis?

Eating 1-2 times a day.

Excessive consumption of foods containing animal fats.

Eating cottage cheese and plant products.

Professional and household intoxications.

For what diseases can not fatty hepatosis will form.

Chronic circulatory failure.

What diseases and syndromes can not occur with prolonged exposure to the etiological factor that caused the formation of fatty hepatosis?

All can arise.

What are the clinical manifestations not typical for fatty hepatosis?

Excess body weight.

Increased liver size.

Dense, rounded, sensitive edge of the liver.

What abnormalities in a biochemical blood test are not typical for fatty hepatosis?

Increased cholesterol and triglycerides.

Increased activity of AST and ALT.

High bilirubin level.

Which items of the examination plan for patients with fatty hepatosis can be excluded without compromising the quality of diagnosis.

Biochemical blood test: fasting sugar, total protein and its fractions, bilirubin, cholesterol, uric acid, AST, ALT, gamma-glutamyl transpeptidase, transferrin not containing sialic acids.

Immunological analysis for the presence of markers of hepatitis B, C, D, G viruses.

Ultrasound of the abdominal organs.

Liver puncture biopsy.

What ultrasound findings are not typical for fatty liver disease?

Increased liver volume.

High echogenicity of the liver parenchyma.

Signs of pancreatic lipomatosis.

Signs of gallstone disease.

Signs of portal hypertension.

What are the criteria do not allow to distinguish fatty liver degeneration in algoholic disease from fatty hepatosis?

The presence in the blood of transferrin, which does not contain sialic acids.

In biopsy specimens there are many cells containing Malory bodies.

The presence of fat droplets in intracellular vacuoles and outside hepatocytes.

All criteria allow.

None of the criteria allows this to be done.

Switching to a fractional diet with 5-6 meals a day.

Even distribution of caloric intake throughout the day.

Consumption of lipotropic (cottage cheese) and herbal products.

What drugs do not do it give to patients with fatty hepatosis?

What are the clinical manifestations not typical for fatty hepatosis?

Aching pain in the right hypochondrium.

Increased abdominal volume, ascites.

Tendency to constipation.

Pigmented hepatosis is a hereditary disorder of the metabolism and transport of bilirubin in hepatocytes, manifested by constant or recurrent jaundice in the absence of changes in the morphological structure of the liver.

In adults, the following variants of impaired bilirubin metabolism in the liver occur:

Gilbert's syndrome is a syndrome of unconjugated hyperbilirubinemia.

Rotor syndrome is a syndrome of conjugated hyperbilirubinemia.

Dubin-Jones syndrome is a syndrome of conjugated hyperbilirubinemia with excessive deposition of melanin-like pigment in hepatocytes.

The most common unconjugated hyperbilirubinemia in clinical practice is Gilbert's syndrome.

Gilbert's syndrome (GS) is a genetically determined enzymopathy that causes a violation of the conjugation of bilirubin in the liver, which is manifested by an increase in the content of unconjugated bilirubin in the blood, jaundice, and accumulation of lipofuscin pigment in hepatocytes.

ICD10: E80.4 – Gilbert's syndrome.

The syndrome is associated with an autosomal dominant defect in the UGTA1A1 and GNT1 genes, which causes insufficient formation of the enzyme glucuronyltransferase in hepatocytes, which ensures neutralization in the liver, including the conjugation of bilirubin with glucuronic acid. Men suffer from GS 10 times more often than women. The triggering factor for GS may be acute viral hepatitis (“post-hepatitis” unconjugated hyperbilirubinemia).

The main role in the pathogenesis of the disease is played by:

Disturbances in the transport function of proteins that deliver unconjugated bilirubin to the smooth endoplasmic reticulum - microsomes of hepatocytes.

Inferiority of the microsomal enzyme UDP-glucuronyltransferase, which is involved in the conjugation of bilirubin with glucuronic and other acids.

In GS, as well as in other forms of pigmented hepatosis, the liver retains a histological structure identical to normal. However, accumulation of a golden or brown pigment, lipofuscin, can be detected in hepatocytes. As a rule, there are no signs of dystrophy, necrosis, or fibrosis in the liver with GS, as with other pigmented hepatoses.

In the gallbladder of patients with gallstones, stones consisting of bilirubin can form.

All patients with GS complain of periodically occurring jaundice of the sclera and skin. There are usually no other complaints. Only in isolated cases do fatigue and a feeling of heaviness in the right hypochondrium appear. Jaundice occurs and increases under conditions of emotional and physical stress, during respiratory infections, after surgery, after drinking alcohol, during fasting or a low-calorie (less than 1/3 of the norm) diet low in fat (vegetarianism), after taking certain medications (nicotinic acid , rifampicin). Patients with GS are often neurotic, as they are concerned about their jaundice.

The leading symptom of the disease is icterus of the sclera. Yellowness of the skin occurs only in some patients. A dull-yellow coloration of the skin is characteristic, especially on the face. In some cases, partial staining of the palms, feet, axillary areas, and nasolabial triangle is observed. In some cases, despite the increased level of bilirubin in the blood, the skin has a normal color - cholemia without jaundice. In some patients, facial pigmentation occurs and scattered pigment spots appear on the skin of the body.

According to Gilbert’s own description, in the typical course of the disease a triad should be detected: hepatic mask, xanthelasma of the eyelids, yellow skin color.

Some clinicians consider urticaria, increased sensitivity to cold, and the phenomenon of “goose bumps” to be characteristic of this syndrome.

An objective examination reveals a moderate enlargement of the liver in 1/4 of patients. On palpation the liver is soft and painless. When pigmented stones form in the gallbladder, clinical manifestations of cholelithiasis and chronic calculous cholecystitis are possible

General blood test: in a third of cases of GS, an increase in hemoglobin content over 160 g/l, erythrocytosis, and a decreased ESR are detected (these changes are usually combined with increased acidity of gastric juice).

General urine test: normal color, no bilirubin.

Biochemical blood test: isolated unconjugated hyperbilirubinemia, which only in isolated cases exceeds the level of micromol/l, averaging about 35 micromol/l. All other biochemical parameters,

characterizing liver function are usually normal.

Instrumental methods (ultrasound, computed tomography, isotope scintigraphy) do not reveal any changes in the liver structure specific to GS.

Ultrasound often reveals pigmented stones in the gallbladder. Liver puncture biopsy: no signs of necrosis, inflammation, or activation of fibrosis processes. The presence of a pigment, lipofuscin, is determined in the liver cells.

Provocative tests with limited energy value of food and a load of nicotinic acid, which cause an increase in the level of unconjugated hyperbilirubinemia, help to detect Gilbert's syndrome:

Serum bilirubin is examined in the morning on an empty stomach. Then, for 2 days, the patient receives food with limited energy value - about 400 kcal/day. The serum bilirubin level is re-examined. If it turns out to be 50% or more greater than the original, then the sample is considered positive.

The initial content of serum bilirubin is recorded. 5 ml of a 1% solution of nicotinic acid is administered intravenously. After 5 hours, a control test of bilirubin is carried out. If its level increases by more than 25%, the sample is considered positive.

One of the most convincing diagnostic tests is a stress test with the patient prescribed phenobarbital or zyxorin - inducers of transport proteins and hepatocyte glucuronyltransferase:

10 days after the start of oral administration of phenobarbital 0 times a day or zyxorin 0.2 - 3 times a day after meals in persons with Gilbert's syndrome, the level of unconjugated bilirubin significantly decreases or normalizes.

It is carried out primarily with hemolytic jaundice, mainly with hereditary microspherocytosis. Such criteria are taken into account as the appearance of the first clinical symptoms (jaundice) of Gilbert's syndrome in adolescence, while hemolytic jaundice appears much earlier, in childhood. Microspherocytosis is characterized by splenomegaly and moderate anemia, which is not the case with GS. Serum bilirubin levels in GS are usually lower than in hemolytic jaundice.

Unlike chronic hepatitis, which may also have predominantly unconjugated hyperbilirubinemia, Gilbert's syndrome does not show signs of carriage of hepatotropic viruses. Unlike hepatitis, there are no laboratory findings in hepatomegaly indicating the presence of an active inflammatory process in the liver. Analysis of liver biopsies does not reveal signs of inflammation, necrosis of liver cells, or active fibrosis. The presence of a pigment, lipofuscin, is determined in hepatocytes.

General blood analysis.

Biochemical blood test: bilirubin, cholesterol, AST, ALT, gamma-glutamyl transpeptidase.

Ultrasound of the abdominal organs.

Liver puncture biopsy.

Provocative tests with limiting the energy value of food or taking nicotinic acid.

Load tests with glucuronyl transferase inducers - phenobarbital or zyxorine.

GS is not a reason to prescribe any specific treatment. Preventive complex vitamin therapy may be indicated. It should be remembered that such people need a nutritious, high-calorie diet with sufficient fat in the diet. They must stop drinking alcohol. During vocational guidance, the undesirability of emotional and physical overload is taken into account. It is necessary to avoid taking medications that can induce jaundice (nicotinic acid). In the presence of concomitant cholelithiasis, an effective way to treat it is cholecystectomy using minimally invasive, laparoscopic surgery.

In the classical course of the process, the prognosis is favorable.

Dubin-Johnson syndrome (DDS) is a genetically determined enzymopathy that causes disruption of bilirubin transport in the liver, which is manifested by an increase in the content of conjugated bilirubin in the blood, jaundice, and accumulation of melanin-like pigment in hepatocytes.

ICD10: E80.6 – Other disorders of bilirubin metabolism.

DDS is an inherited disease. Individuals with DDS have an autosomal recessive genetic defect that causes a disruption in the transport of organic anions, including the transport of conjugated bilirubin from hepatocytes to the bile ducts. DDS occurs more often in men than in women.

As a result of disruption of the mechanism of directed transport of bilirubin from hepatocytes into the lumen of the bile ducts, part of the conjugated bilirubin returns to the blood. Postmicrosomal hepatocellular jaundice occurs with a moderate increase in direct bilirubin in the blood. Pathogenetically, DDS is identical to Rotor syndrome, from which it differs in one feature - the accumulation in hepatocytes of a large amount of melanin-like pigment, which gives the liver a dark bluish-green, almost black color. In patients with DDS, stones from bilirubin salts may form in the gallbladder.

Complaints of periodically occurring yellowness of the sclera and skin, sometimes along with slight itching, are typical. During the period of jaundice, many patients experience general weakness, physical and mental fatigue, decreased appetite, mild nausea, bitterness in the mouth, and sometimes dull aching pain in the right hypochondrium. When jaundice appears, the urine becomes dark in color.

Jaundice can be provoked by physical and psycho-emotional stress, fever caused by a respiratory viral infection, alcohol excess, and the use of anabolic steroids.

Gallbladder cholelithiasis is usually asymptomatic, but sometimes manifests itself as biliary colic, symptoms of calculous cholecystitis, and in some cases can cause obstructive jaundice.

Objective manifestations include moderate icterus of the sclera and skin, and a slight increase in liver volume. On palpation, the liver is not hardened and painless.

Complete blood count: no abnormalities.

General urine analysis: dark color, high bilirubin content.

Biochemical blood test: increase in bilirubin content due to the conjugated fraction.

Tests with a load of bromsulfalein, radioisotope hepatography reveal a pronounced violation of the excretory function of the liver.

Ultrasound: liver of normal structure. Intra- and extrahepatic bile ducts are not dilated. Portal hemodynamics are not impaired. Dense, echo-positive stones may be detected in the gallbladder.

Laparoscopy: the surface of the liver is dark bluish-green or black.

Puncture biopsy: the morphological structure of the liver is not changed. Melanin-like pigment is detected in hepatocytes.

It is carried out with obstructive jaundice, from which DDD differs in the absence of an increase in the level of cholesterol in the blood, the activity of enzymes specific to cholestasis - alkaline phosphatase, gamma-glutamyl transpeptidase. Ultrasound with DDS does not show dilation of the intra- and extrahepatic bile ducts, a specific sign of obstructive jaundice.

General blood analysis.

General urine analysis with determination of bilirubin, urobilin, hemosiderin.

Coprogram with the determination of stercobilin.

Biochemical blood test: bilirubin, cholesterol, alkaline phosphatase, AST, ALT, gamma-glutamyl transpeptidase.

A test with bromsulfalein to assess the excretory function of the liver.

Radioisotope hepatography to assess the excretory function of the liver.

Immunological analysis: markers of infection with hepatitis B, C, G viruses.

Ultrasound of the abdominal organs.

Liver puncture biopsy.

No special treatment is required. Individuals with DDD should completely abstain from drinking alcohol. They should avoid any intoxication and limit medications as much as possible. They can be recommended to take complex multivitamin preparations. In the presence of cholelithiasis, especially if it occurs with attacks of colic, cholecystectomy using minimally invasive surgery methods is indicated.

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Fatty hepatosis

Description of the disease

Fatty hepatosis is the accumulation of fat in the liver cells, which is often a reaction of the liver to various intoxications (toxic effects).

Causes

The main causes of fatty hepatosis are:

alcohol abuse,
diabetes mellitus combined with obesity,
obesity,
Cushing's syndrome,
myxedema,
unbalanced diet (protein deficiency),
chronic diseases of the digestive system with malabsorption syndrome,
exposure to toxic substances.

Symptoms

Patients with fatty hepatosis usually have no complaints. The course of the disease is mild and slowly progressing. Over time, constant dull pain appears in the right hypochondrium, there may be nausea, vomiting, and stool disturbances.

Diagnostics

A general practitioner may suspect fatty degeneration during a clinical examination based on an increase in the size of the liver upon palpation of the abdomen. Liver enlargement is confirmed using abdominal ultrasound. A biochemical blood test reveals an increase in liver enzymes (AST, ALT, alkaline phosphatase). In some cases, CT, MRI, and liver biopsy are performed to confirm the diagnosis.

Treatment

Traditional medicine around the world, in the treatment of fatty hepatosis, hepatomegaly and cirrhosis of the liver, offers medicinal, replacement and syndromic therapy, which can slightly improve the patient’s well-being, but inevitably leads to the progression of diseases, since any presence of chemicals in the human blood has a detrimental effect on the patient’s health. altered liver.

However, proper nutrition, avoidance of alcohol, and correction of metabolic disorders usually lead to an improvement in the condition.

Fatty hepatosis in the ICD classification:

My son has hepatitis C. How can I get him treatment under the state program?

Drug treatment of fatty liver hepatosis

The main reason for the appearance of fatty liver hepatosis is a disruption in the functioning of metabolic processes. When the disease is activated, healthy liver cells are replaced with adipose tissue. The disease can be inflammatory or non-inflammatory in nature, but in any case, the disease, when the underlying causes manifest itself, must be treated appropriately.

Treatment of fatty liver hepatosis with drugs

When diagnosing fatty hepatosis, the patient must begin timely treatment with medications, which are prescribed by the doctor in each case only individually.

There is a general basis of therapy, which is aimed at eliminating the root causes of the emerging disease, as well as eliminating the factors that provoked the manifestation of fatty liver hepatosis. Therapy is necessarily prescribed, aimed at normalizing internal metabolic processes, as well as restoring the functions of the internal organ. The patient necessarily requires intoxication therapy aimed at cleansing the liver of harmful pesticides and hazardous substances.

What medications are indicated for patients with fatty liver hepatosis?

A group of medications that is aimed at protecting and restoring the basic functions of the liver - Phosphogliv, Essentiale;
Sulfoamino acids that stabilize internal processes - Methionine, Dibikor;
Herbal remedies - Karsil, Liv 52.

The most effective remedy for the treatment of fatty hepatosis

Any, even the most effective medicine for unpleasant fatty hepatosis, is prescribed to patients only on an individual basis. But it is important to remember that a high-quality cure for such a disease is impossible without fulfilling important conditions that apply to all patients with this disease:

complete elimination from everyday life of all factors that provoked the disease to activity;
careful correction of your usual diet, as well as adherence to only a healthy lifestyle;
taking prescribed medications that are actively aimed at normalizing metabolism, as well as protecting and cleansing the liver from harmful factors.

Metformin for fatty liver hepatosis

For fatty liver hepatosis, which is not provoked by the abuse of alcohol-containing liquids, Metformin is often prescribed to patients. This medication acts as a normalizer of metabolic processes and a protector of the internal organ from negative harmful factors.

Along with Metformin, patients may be prescribed medications such as Pioglitazone or Rosiglitazone.

Is it possible to cure fatty liver disease completely?

Most patients are confident that fatty hepatosis cannot be fully cured. But such an opinion is deeply erroneous. This process in the liver is reversible. And with the correct course of treatment, fatty hepatosis can be eliminated forever.

The further life activity of a person who has recovered from the underlying disease also plays a big role here. The latter must be regularly observed by the attending physician, as well as adhere to regular adherence to the rules of a healthy and wholesome diet.

Fatty hepatosis - ICD code 10

According to the International Classification of Diseases, fatty liver disease (fatty liver degeneration) is classified under code 76.0.

Non-alcoholic fatty liver disease ICD. What is steatosis? Etiology and pathogenesis

Symptoms

Etiology

Pathogenesis

Steatosis in the International Classification of Diseases

Diagnostics

Instrumental methods

Treatment of steatosis

Diet and recipes for fatty liver

Pilaf

Casseroles

Why is fatty liver disease dangerous?

general information

Short description

Classification

Etiology and pathogenesis

Epidemiology

Risk factors and groups

Clinical picture

Clinical diagnostic criteria

Symptoms, course

Diagnostics

Laboratory diagnostics

Differential diagnosis

Complications

Non-alcoholic steatohepatitis: from pathogenesis to therapy

Pathogenesis.

Clinical picture.

Diagnostics.

What is fatty hepatosis: ICD 10 code

Causes of fatty hepatosis and its prevalence

Treatment of fatty hepatosis

K70-K77 Liver diseases. V. 2016

K70-K77 Liver diseases

/ Internal diseases / Chapter 3 DISEASES OF THE LIVER AND BILIARY SYSTEM-r

Fatty hepatosis

Description of the disease

Causes

Symptoms

Diagnostics

Treatment

Fatty hepatosis in the ICD classification:

Drug treatment of fatty liver hepatosis

Treatment of fatty liver hepatosis with drugs

The most effective remedy for the treatment of fatty hepatosis

Metformin for fatty liver hepatosis

Is it possible to cure fatty liver disease completely?

Fatty hepatosis - ICD code 10

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