Fatty degeneration of the liver is a chronic liver disease characterized by fatty degeneration of the liver cells. It occurs quite often, develops under the influence of alcohol, toxic substances (medicines), diabetes mellitus, anemia, lung diseases, severe pancreatitis and enteritis, malnutrition, obesity.
According to the mechanism of development, hepatoses appear due to excessive intake of fats in the liver, overload of the liver with dietary fats and carbohydrates, or due to impaired excretion of fats from the liver. Violation of the excretion of fat from the liver occurs with a decrease in the amount of substances involved in the processing of fats (protein, lipotropic factors). The formation of phospholipids, beta-lipoproteins, lecithin from fats is disrupted. And excess free fats are deposited in the liver cells.
Patients with hepatosis usually do not complain. The course of the disease is blurred, slowly progressing. Over time, constant dull pains in the right hypochondrium, nausea, vomiting, and stool disorders are found. The patient is concerned about weakness, headache, dizziness, fatigue during exercise. Very rarely observed hepatosis with a pronounced clinical picture: severe pain, weight loss, itching, bloating. On examination, an enlarged, slightly painful liver is found. The course of the disease is traditionally not severe, but sometimes fatty hepatosis can turn into chronic hepatitis or cirrhosis of the liver.
Ultrasound of the abdominal cavity – an increase in the echogenicity of the liver, an increase in its size. In a biochemical study of blood, a non-cardinal increase in the activity of liver tests and changes in protein fractions.
First of all, it is necessary to either eliminate or minimize the effect of the factor that led to the deposition of fat in the liver. This is almost always the case with alcohol, unless it is an addiction that requires the help of a narcologist. Patients with diabetes mellitus and hyperlipidemia should be observed jointly by an endocrinologist and a cardiologist, respectively. All patients require a low-fat diet and sufficient daily physical activity.
In patients with obesity, doctors traditionally consider it necessary to reduce the patient’s body weight. The effect of weight loss on the course of fatty hepatosis is ambiguous. Rapid weight loss naturally leads to an increase in inflammation activity and progression of fibrosis. Reducing the weight by 11-20 kg/year has a positive effect on the severity of steatosis, inflammation and the degree of liver fibrosis. The most effective weight loss is considered to be no more than 1.6 kg / week, which is achieved with a daily caloric intake of 25 cal / kg / day. and active physical exercise.
When these measures are not enough, the doctor prescribes special medicinal products that affect the metabolism of fat in the liver. Most patients with fatty liver are characterized by a mild, favorable course of the disease. Such patients are shown therapy that combines antioxidant protection, stabilization of hepatocyte membranes, immunomodulation, providing anti-inflammatory activity, also aimed mainly at stopping the manifestations of biliary dyskinesia.
Among the products that improve the functional state of the liver, the leading place is occupied by heptral (ademethionine), which is a complex product consisting of 2 natural substances – adenosine and methionine. Heptral is involved in the restoration of destroyed cell membranes, interferes with fat oxidation, stimulates the formation of protein in the liver. Its use is indicated primarily for alcoholic liver damage, and not only at the stage of fatty hepatosis, but also hepatitis and even cirrhosis. An additional therapeutic effect of heptral is represented by its mild antidepressant effect, which helps in overcoming alcohol dependence, and therefore this product has entered the arsenal of not only gastroenterologists, but also psychiatrists.
Another leading product in the treatment of fatty hepatosis is ursodeoxycholic acid (ursosan, ursofalk) at a dose of 10-15 mg / kg / day, which has a cytoprotective, immunomodulatory and anti-apoptotic effect, has a positive effect on biochemical parameters and steatosis, improves the rheological properties of bile.
Patients with hyperlipidemias should be monitored and specific lipid-lowering therapy (statins and/or fibrates) may be considered. It should be taken into account that the isolated use of lipid-lowering products is not effective and requires constant medical supervision.
Insulin resistance plays a fundamental role in the pathogenesis of fatty liver. This served as a prerequisite for studying the effectiveness of the use of insulin sensitizers (biguanides, glitazones). A lot of experience has been accumulated in the use of biguanides in insulin-resistant diabetes mellitus, which served as the basis for its use in fatty hepatosis. Thiazolidinediones (glitazones) are a new class of products that selectively improve insulin susceptibility (insulin sensitizers). Glitazones improve insulin susceptibility by activating certain enzymes in the liver, resulting in improved glucose uptake by peripheral tissues, reduced concentrations of glucose, insulin, triglycerides and lipids in the blood.
Combination therapy with insulin sensitizers of different classes seems to be the most promising: metformin (biguanides) and rosiglitazone (glitazones) for 6-12 months. At the same time, the positive dynamics of functional liver tests is combined with the correction of the main manifestations of the insulin resistance syndrome: a decrease in the degree of obesity, arterial hypertension, dyslipidemia, hyperuricemia.
Each patient will need to remember that the appointment of any product used for the treatment of fatty hepatosis is made by a doctor, with an individual approach to each patient, with the definition of indications and contraindications of the drugs taken and under the strict control of the prescribed treatment!