Non-alcoholic fatty liver disease (NAFLD) is considered not only as a disease with poor hepatic prognosis. The problem has acquired a multidisciplinary problem. The variety of concomitant diseases and pathological conditions are united by common pathophysiological mechanisms.

This review summarizes and presents the data available in the modern literature on the association of NAFLD with cardiovascular diseases, type 2 diabetes mellitus, polycystic ovary syndrome, chronic kidney disease, etc. The role of the liver in the homeostasis of the organism and the pathogenetic mechanisms of the formation of NAFLD-associated comorbidity are discussed.

Purpose. To assess the parameters of lipid and carbohydrate metabolism, insulin resistance, chronic low-intensity systemic inflammation, structural and functional parameters of the liver in patients with hypertension (AH) and non-alcoholic fatty liver disease (NAFLD) compared with patients with isolated AH, as well as the impact of changes in these parameters on reducing the elasticity of the main arteries and increasing the risk of cardiovascular complications in patients with comorbid pathology.

Material and methods. A comparative cross-sectional study was carried out, which included 120 patients, aged 45 to 65, with AH grade I-II, stages 1-2 (with (FLI≥60) and without NAFLD). During the initial examination, a clinical examination was carried out, the parameters of lipid, carbohydrate and structural-functional parameters of the liver were assessed. The severity of chronic systemic inflammation and insulin resistance were also assessed. Pulse wave velocity (PWV), central aortic pressure (CAP), vascular age and total cardiovascular risk were measured according to the SCORE scale.

Results. The data obtained indicate a more pronounced insulin resistance, chronic systemic inflammation, as well as significantly higher lipid metabolism in patients with AH and NAFLD in comparison with patients with isolated AH. In addition, in patients of this group, the indicators of PWV and CAP were significantly higher, and patients with AH and NAFLD had a higher 10-year fatal risk (p=0.013). The performed ROC analysis showed that at FLI≥60, a high risk of PWVm>10m/s is predicted. Multiple regression analysis found that an increase in VLDL cholesterol leads to an increase in the values of both PWVe (p<0.001) and PWVb (p=0.048). The 10-year fatal risk (SCORE) in patients with AH and NAFLD increased with an increase in PWVe (p=0.021), FLI (p=0.013), and visceral obesity (p<0.001).

Conclusion. The study shows that in patients with AH and NAFLD, compared with patients with isolated AH, the indicators of insulin resistance and chronic low-intensity systemic inflammation are significantly higher, the highly atherogenic type of hyperlipidemia and visceral obesity are more often found. Also, in comorbid patients with AH, statistically significant higher values of CAP and augmentation index are determined. Stiffness indices of the great arteries were also significantly higher in patients with comorbid pathology. The ROC analysis showed that at FLI≥60, a high risk of PWVm>10 m/s was predicted, which is associated with the development of cardiovascular complications. Also, multiple regression analysis showed that the increase in PWVe and PWVm was mainly due to an increase in VLDL cholesterol, and the 10-year fatal cardiovascular risk of complications had the greatest increase with an increase in the values of PWVe, FLI and visceral obesity.

Non-alcoholic fatty liver disease (NAFLD) is a pressing public health problem affecting up to a third of the world's adult population. The main reasons for its high mortality rate are cardiovascular diseases. They are caused by subclinical atherosclerosis characteristic of NAFLD, venous thromboembolic complications, functional and structural myocardial disorders, calcification of heart valves, heart rhythm and conduction disturbances. At the same time, NAFLD can serve as an independent factor of the cardiometabolic risk of their development, which is associated with atherogenic dyslipidemia, as well as the release of numerous pro-inflammatory mediators both from the pathologically altered liver and as a result of systemic endotoxemia, which is the result of disturbance of the intestinal microbiota, accompanied by a decrease in intestinal microbial gene richness., a change in its composition and function, followed by bacterial translocation. Considering that most patients with NAFLD die from cardiovascular complications, it becomes obvious that exclusively “liver-oriented” principles of their treatment cannot be sufficient, but require a multidisciplinary team approach involving cardiologists, cardiac surgeons and doctors of other related specialties.

Aim: to study the functional state of the kidneys in patients with chronic heart failure (CHF) and non-alcoholic fatty liver disease (NAFLD).

Materials and methods. 144 patients with CHF aged 45-70 years were divided into two groups: group 1 — persons with CHF and NAFLD, group 2 — CHF without NAFLD. A clinical examination was performed, the indices of FLI steatosis and NFS liver fibrosis were calculated, the functional state of the kidneys and the adipokine status were evaluated.

Results. The main group of patients with CHF and NAFLD is mainly represented by people with grade I obesity (73 (84%) vs 5 (9%), p<0.05). Among patients with CHF and NAFLD, a clinically significant decrease in GFR<60 ml/min/1.73 m2 was significantly more often detected compared to patients with CHF without NAFLD (37% vs 21% in groups 1 and 2, respectively). The level of albuminuria was significantly higher in the group of patients with CHF and NAFLD (200.7±22.3 [54.7;390] vs 92.6±23.4 [10.2;188.7] mg/g in groups 1 and 2, respectively). The percentage of individuals with an AU/CR. urine ratio >30 mg/g was statistically significantly higher in group 1 compared to group 2 (82.1 vs 51.1% in groups 1 and 2, respectively). The level of serum leptin was significantly higher and the concentration of serum adiponectin was significantly lower compared to group 2 in the main group of patients with CHF and NAFLD compared to the control group. There was a significantly higher occurrence of insulin resistance in patients with CHF and NAFLD. Correlation analysis revealed the presence of statistically significant associations between the parameters characterizing the functional state of the kidneys and the indices of FLI, NFD, adipokines, and the severity of insulin resistance.

Conclusion. In patients with CHF and NAFLD, a significant deterioration in the functional state of the kidneys was found, in comparison with patients with “isolated” CHF with comparable FC.

The goal. To determine the value of the triglyceride glucose index (TGI) for the diagnosis of insulin resistance (IR) in early forms of non-alcoholic fatty liver disease (NAFLD).

Materials and methods. 99 patients with NAFLD were examined: 38 (38.4%) with liver steatosis (LS) and 61 (61.6%) with steatohepatitis (SH). TGI was determined by the formula — In [fasting TG (mg / dl) × fasting glucose (mg / dl) / 2], patients with LS and SH were divided into quartiles (Q₁-Q₄) by increasing TGI levels with an assessment of liver tests, insulin levels (“Insulin TEST System”, Monobind Inc., USA), HOMA-IR, fragments of cytokeratin-18 (FCK-18) ("TPS ELISA, Biotech”, Sweden) and TNF-α (“Human TNFα Platinum” ELISA, eBioscience, Austria).

Results. In patients with LS with a TGI increase from Q₁ to Q₄, HOMA-IR increased from 1.12 ± 0.48 to 6.02 ± 3.15 (p <0.05), a direct relationship was found between these indicators — r = 0.52 (p = 0.03). TGI also correlated with waist circumference — r = 0.81 (p = 0.01), cholesterol — r = 0.51 (p = 0.002), alkaline phosphatase — r = 0.41 (p = 0.02). In patients with SH, from Q₁ to Q₄, HOMA-IR increased from 3.15 ± 1.8 to 6.2 ± 3.04 (p <0.05), but there was no significant correlation between HOMA-IR and TGI. The levels of FCK-18 increased from Q1 to Q4-139.82 ± 72.45 to 359.75 ± 189.03 U / L (p <0.05) and TNF-α — from 6.38 ± 1.25 pg / ml up to 7.75 ± 1.09 pg / ml (p <0.05). There was a connection between TGI and the level of a marker of hepatocyte apoptosis — FCK-18 — r = 0.43 (p = 0.004).

Conclusion. In liver steatosis, TGI has demonstrated its diagnostic role as a surrogate marker of insulin resistance, correlating with HOMA-IR. In steatohepatitis, TGI reflected the degree of hepatocytic apoptosis, correlating with fragments of cytokeratin-18.

The aim of the study was to study the cardiometabolic characteristics in individuals with an associated course of non-alcoholic fatty liver disease (NAFLD) and gastroesophageal reflux disease (GERD) in comparison with isolated cases of diseases.

Materials and methods. The study included 120 patients (30 — with GERD, 30 — with NAFLD, 30 — with GERD + NAFLD. Work design — prospective parallel comparative study with 2 stages. Stage I — inclusion in the study, assessment of the main cardiometabolic, cardio vascular rice (CVR) according to the SCORE scale and the Framingham scale. Stage II — follow-up of the participants for 5 years, re-examination and riskmetry.

Results. It has been shown that with a combination of NAFLD and GERD, the pathogenetic mechanisms involved in the formation of NAFLD (especially in steatohepatitis) affect the key characteristics of the metabolic profile and the state of the CV system to a greater extent than GERD. The total CVR values in this category of patients were: 4.8 — SCORE; 13.4 — on the Framingham scale. Over 5 years in this group, 10 (33% of the initial) newly diagnosed cases of CVD were verified: 6 — AH, 3 — IHD, 1 — AH + IHD. CVR for the NAFLD and GERD group increased: according to the SCORE scale — from low risk (4.8) to high (8.9), and according to the Framingham scale, the dynamics was even more negative (from 13.4 to 18.6).

Conclusion. Kinds of cardiometabolic disorders in persons with comorbidity of NAFLD and GERD have been proven, which can form the prerequisites for structural cardiovascular changes, including the risks of CVD. This can be a rationale for carrying out additional preventive measures for the groups of patients under discussion, especially in the case of their associated course, as measures for the early preclinical diagnosis of CVR factors and for timely correction of the identified disorders.

Non-alcoholic fatty liver disease (NAFLD), being a marker of significant changes in the hepatobiliary system against the background of metabolic syndrome and other endocrine pathologies, has a significant impact on the course of psoriatic disease. The presence of common mechanisms in the pathogenesis of these diseases suggests a very close relationship between them. This requires a multidisciplinary approach to studying the mechanisms of the pathogenesis of psoriasis and NAFLD, which will improve the methods of diagnosis and treatment of both diseases.

Aim: Evaluate the relationship of Smoking with fatty liver disease (FLD) of various etiologies.

Materials and Methods: Out of1568 residents of the rural therapeutic area agreed to participate in the study of 1123 residents of the rural medical area with negative markers of hepatitis B and / or C. The survey included the collection of anamnesis for smoking and alcohol consumption. An objective, laboratory (complete blood count, biochemical liver function tests) and instrumental examination, including ultrasound examination of the abdominal organs, were carried out.

Results: Non-alcoholic fatty liver disease (NAFLD) was detected in 247 (22.0%) people, alcoholic liver disease (ALD) — in 276 (24.6%) (p>0.05). 542 people smoked of the surveyed. Among patients with NAFLD, Smoking was 20.2%, their Smoking experience was 35.1±11.5 years, and the Smoking index was 24.5±10.9. Among patients with ALP, Smoking is higher-93.1% (p<0.05), Smoking experience is less — 29.5±9.8 years (p<0.05), as is the Smoking index of 21.8±7.7 (p<0.05). Among smokers, 56.8% had FLD, 83.8% of them were of alcoholic etiology, and 16.2% were non — alcoholic (p<0.05). Among non-smokers, compared with smokers, FLD was detected less frequently — in 37.2% of people (p<0.05), of which alcohol etiology — in 8.8% (p<0.05), non — alcoholic-in 91.2% (p<0.05).

Conclusion: In the rural therapeutic area, 93.1% of ALD sufferers smoke, and 20.2% of NAFLD patients smoke (p<0.05). In patients with NAFLD, the duration of smoking was longer (35.1 ± 11.5) than in patients with ALD — 29.5 ± 9.8 years (p <0.05); the smoking index was 24.5 ± 10.9 and 21.8 ± 7.7 pack-years (p<0.05), respectively. In smokers, FLD was more common (56.8%) than in non-smokers (37.2%) (p<0.05). FLD in smokers was of alcoholic etiology more often (83.8%) than non-alcoholic (16.2%) (p<0.05), in non-smokers non-alcoholic etiology prevailed (91.2%) (p<0.05).

The aim of the study was to assess the role of hepatocellular death and systemic inflammation in the development of acute kidney injury (AKI) in acute decompensation of alcoholic liver cirrhosis (AD ALC).

Materials and methods. 125 patients with ALC were examined: 20 (16.0%) (group I) with signs of hepatorenal syndromeacute kidney injury (HRS-AKI) at the age of 57.13 ± 9,08 years, 13 men (65.0%) and 105 (84.0%) patients (group II) without such a syndrome at the age of 56.30 ± 9.6 years., 62 men (59.0%). Along with liver tests, a markers of hepatocyte apoptosis and cytokines were determined by ELISA: fragments of cytokeratin-18 (FCK-18) ("Biotech" Sweden), cytokines — TNF-α, IL-1β, IL-4, IL-6, IL-8 (“Vector-Best”, Russia). Grade and index of acute on chronic liver failure (ACLF) were determined using an on-line calculator (www.efclif.com/scientific-activity/score-calculators/clif-c-aclf).

Results. The hepatocellular death indicators were significantly higher in patients of group I with HRS-AKI compared with patients of group II without HRS-AKI: FCK-18-1609.44 ± 542.79 U / l versus 975.77±607.59 U / l, bilirubin — 242.64 ± 98.14 pmol/l versus 145.09 ± 79.35 pmol/l, inflammation indicators — TNF-α — 9.28 ± 3,11 pg/ml versus 6.59 ± 2.21 pg/ml, IL-6-54.79 ± 17.7 pg/ml versus 36.71 ± 18.05 pg/ml, CRP — 49.68 ± 23.23 mg/l versus 22.07 ± 20.40 mg/l, leukocytes — 12.23 ± 3.28x109/l versus 8,66 ± 2,31x109/l (everywhere p <0.05). ACLF developed in all (100.0%) patients of group I, its grade was 2.73±0.76 and score — 56.33 ± 4.01; ACLF developed only in 37 (35,2%) patients of group II, its grade was1.05±0.24 (p<0,05) and score was 47.45 ± 4,80 (p <0.05).

Conclusion. The development of HRS-AKI in patients with acute decompensation of ALC was associated with significantly higher rates of hepatocytic apoptosis, hyperbilirubinemia, systemic inflammation, frequency and severity of ACLF.

In the strategy of managing patients with chronic diffuse liver diseases, the priority areas are the determination of the diagnosis with the determination of the main risk factors, the activity of the process (steatosis, steatohepatitis), as well as the degree of fibrous transformation. The rate of progression of liver fibrosis is a decisive factor that will determine the prognosis, treatment tactics and the likelihood of severe complications. The “gold standard” for diagnosing chronic liver pathology is a puncture liver biopsy with morphological examination of the liver tissue. At the same time, potential complications, contraindications to the procedure, low patient compliance, as well as errors in the interpretation of the results obtained due to various reasons are significant limitations of this diagnostic method. These shortcomings were the reason for the search for reliable non-invasive methods for diagnosing liver fibrosis both during the initial examination and during subsequent monitoring in dynamics. Modern methods of liver elastography are widely used for non-invasive assessment of fibrosis, demonstrating good diagnostic capabilities and significantly reducing the need for liver biopsy. Various elastography methods, which have their own advantages and disadvantages, effectively complement each other, which is successfully used in clinical practice in the diagnosis of fibrous transformation. The combined use of elastographic methods and commercial predictive diagnostic panels will increase the diagnostic accuracy in the determination of liver fibrosis.

Objective. Comparison of the effects of liraglutide and dulaglutide on the dynamics of scales and markers of hepatic fibrosis.

Materials and methods. 35 patients with NAFLD were included in the study and received liraglutide 1.8 mg or dulaglutide 1.5 mg once daily for 6 months.

Results. Body weight and glycated hemoglobin (HbA1C) decreased significantly and comparable after 6 months of treatment in both groups. Serum aspartate aminotransferase (AST) levels decreased only in the dulaglutide group. The decrease in the AST level in the dulaglutide group was from 31.9 ± 26.8 to 30.8 ± 10.6 U / L (p = 0.04). The dynamics of the risk of fibrosis reached statistical significance only when assessed on the FIB-4 scale in the liraglutide group when comparing the baseline values and values after 6 months of treatment — 1.18 ± 0.51 and 0.97 ± 0.40, respectively (p = 0.022). In the dulaglutide group, there was also an insignificant positive dynamics of 1.31 ± 0.53 and 1.11 ± 0.23 (p = 0.865), which can be explained by the minimal severity of changes at baseline.

Conclusions. The study demonstrated comparable effects of liraglutide and dulaglutide on metabolic parameters and, at the same time, the advantage of liraglutide in influencing the dynamics of the risk of fibrosis, assessed on the FIB-4 scale. To unequivocally confirm the benefits of liraglutide in the treatment of patients with NAFLD, randomized prospective comparative studies of various aGPP1 on large samples of patients with different stages of NAFLD are needed.

The aim. To assess the relationship between body mass index (BMI) and gut bacteria in men and women with obesity.

Materials and methods. The study included 56 overweight patients, divided into 2 groups. The first group consisted of 27 women (the average age was 62 ± 2.2 years), the second group — 29 men (the average age was 55 ± 9 years). The Quetelet index (kg / m²) was calculated for all patients. To study the gut microbiome, the method of polymerase chain reaction in real time (RT-PCR) and metagenomic sequencing were used. DNA from feces was isolated using the Express-DNA-Bio DNA isolation kit (AlkorBio, Russia). To carry out RT-PCR, a set of reagents “Colonoflor-16” (“Alfalab”, Russia) was used. For microbiome sequencing, DNA libraries were prepared using the Illumina Nextera Sample Preparation Kit with DNA primers corresponding to the V3 — V4 regions of the 16S rRNA gene. The study of fecal samples was carried out using 16S rRNA gene sequencing on the Illumina platform (MiSeq sequencer).

Results. It was revealed that a higher total number of bacteria, an increased content of Bacteroides fragilis group and Faeca-libacterium prausnitzii, is statistically significantly more common in women than in men. Strong negative correlations were found between BMI and total bacterial mass, between BMI and the number of Bacteroides fragilis group among women with grade I obesity. In overweight men, a correlation was found between BMI and the Bacteroides fragilis group / Faecalibacterium prausnitzii ratio.

Conclusions. The total number of bacteria, the content of Bacteroides fragilis group and Faecalibacterium prausnitzii in the gut of patients have statistically significant associations with BMI, and probably can affect the formation of metabolic disorders to a greater extent in women than in men. To clarify the identified trends and patterns in this pilot study, further study of the microbiome with a large number of patients and additional analyzes of the metagenome (16S rRNA) and metabolome, a transcriptome, allowing to control the expression of key metabolic enzymes, largely associated with the compositional features of the gut microbiocenosis, is required.

Aim of investigation: to assess the effectiveness and tolerance of dietary supplements (BAA) STIM and STIM Lax

Materials and methods: The analysis of the treatment of 73 patients who were divided into 2 groups. Group 1-32 patients with functional constipation (8 men and 24 women; mean age — 45.7 ± 12.4 years), Group 2-41 patients with functional diarrhea (19 men and 22 women; mean age — 41.0 ± 15,8 years). The study of clinical symptoms was carried out according to the data of an individual diary, using specialized questionnaires with a scoring of symptoms before and after the course of treatment, before and after treatment, the result of the carbolene test, the content of short-chain fatty acids in the feces was assessed. Tolerability was assessed by recording side effects and adverse events.

Monotherapy was carried out with STIM LAX for patients with functional constipation at a dose of 1 tablet 3 times a day for 30 days. STIM for patients with functional diarrhea was prescribed in a dose of 2 tablets 3 times a day for 30 days.

Results of the study: The results of the study showed that FC therapy with StimLax effectively reduces the frequency and intensity of symptoms such as difficulty / pain, discomfort during defecation, feeling of incomplete emptying, abdominal pain, time spent in the toilet and the number of failed bowel movements. We observed the normalization of transit time according to the carbolene test and an increase in stool frequency up to 5 times a week.

Treatment of patients with FD with Stim led to a significant decrease in the intensity of abdominal pain, rumbling, flatulence, stool frequency, an increase in the time of the carbolene test and the normalization of its consistency.

Adverse events were observed in 8 (10.9%) patients (4 patients with FD and 4 patients with FD). On the 3-5th day of treatment, there was an increase in flatulence, rumbling in the abdomen. A temporary decrease in the dose of the drug to 1-2 tablets per day removed these phenomena and the symptoms that appeared were resolved within 1-3 days. After that, the dose of the drug was gradually increased to the initial (effective), which the patients tolerated normally.

Conclusions: The results of this study indicate high clinical efficacy and good tolerability of treatment with drugs StimLax and Stim in patients with FC and FD. In some cases, it is necessary to titrate the dose of the drug (downward), but this is not accompanied by a decrease in the effectiveness of therapy. The use of these drugs with metaprebiotic properties helps to modify the microbiota of patients with functional bowel diseases. With constipation, the number and activity of both lactic acid flora and microorganisms that produce butyric acid are stimulated; in addition, calcium lactate is an additional source of butyric acid due to metabolism. With diarrhea, along with the stimulation of the number and activity of the lactic acid flora, there is an improvement in the utilization of butyrate by intestinal cells.

Metabolically associated fatty liver disease is a widespread disease (MAFLD).

The main treatment strategy for MAFLD is the correction of metabolic factors, changes in lifestyle, normalization of body weight, which is achieved by the use of diet therapy and physical activity.

The purpose of this review is to present the characteristics of diets that have been studied in the treatment of patients with MAFLD.

Results. The greatest evidence base on the effectiveness of treatment of MAFLD and the safety profile is the use of the Mediterranean diet and the diet with a low glycemic index. Patients should be advised to reduce their sugar intake, reduce their intake of saturated fatty acids and trans fats, and increase their intake of dietary fiber. Eating a balanced, calorie-restricted diet can help to provide healthy lifestyle and healthy eating habits, which are essential for the prevention and treatment of MAFLD. Hereditary factors, the composition of the intestinal microbiota, comorbid pathology can affect the results of diet therapy, which emphasizes the urgent need for an individualized approach in the treatment of this disease.

The aim of the study was to evaluate the effectiveness of a standard reduced-calorie diet in elderly subjects with obesity and nonalcoholic fatty liver disease (NAFLD).

Materials and Methods: 60 women with I-III degree obesity and NAFLD were examined. Metabolic status was assessed by indirect calorimetry and body composition indices using bioimpedance spectroscopy. Biochemical indices in blood serum were determined on a biochemical analyzer “KONELAB Prime 60i”. SPSS Statistics 23.0 program was used for statistical data processing.

Results and Discussion: It was found that resting energy expenditure was significantly higher in middle-aged women (1896.8±46.5 kcal/d) with obesity and NAFLD than in elderly women (1691.6±34.2 kcal/d). Fat oxidation rate was significantly lower in elderly women (66.8±7 g/day) than in middle-aged women (70.8±9 g/day). The elderly patients received a variant of the standard diet with reduced caloric content for 10 days. Against the background of diet therapy, a significant decrease in glucose, total cholesterol, LDL, triglycerides, as well as fat mass, total fluid and visceral fat area was observed in elderly patients with obesity and NAFLD. However, the use of a standard reduced-calorie diet resulted in a slight elevation of serum uric acid levels and a significant decrease in muscle mass.

Conclusions: the selection of specialized diets is recommended for elderly patients with obesity and NAFLD when prescribing diet therapy, which will not only prevent the decrease of muscle mass and increase of uric acid but also improve the effectiveness of treatment measures in obesity by preventing the development and progression of its complications.

Hepatoprotectors and prebiotic molecules that promote the growth of intestinal flora differ significantly in their effects on different representatives of the human microbiome. This work presents the results of a comparative chemomicrobiomic analysis of ornithine and reference molecules (S-ademetionine, ursodeoxycholic acid, lactulose, and fructose). For each of the studied molecules, estimates of the values of the area under the growth curve were obtained for a representative sample of human microbiota, which included 38 commensal bacteria (including bifidobacteria and lactobacilli) and the values of the minimum inhibitory concentrations (MIC) for 152 strains of pathogenic bacteria. It has been shown that ornithine, to a lesser extent than the reference molecules, stimulates the growth of pathogenic bacteria of the genera Aspergillus, Klebsiella, Pseudomonas, Staphylococcus and Candida fungi. Ornithine is also less likely to stimulate the growth of more aggressive bacteria (Biosafety Level 2) and to a greater extent less aggressive bacteria (Biosafety Level 1). By stimulating butyric and other short-chain fatty acid-producing microorganisms, ornithine can improve the profile of gut microbiota.

The aim of the study was to study the effect of hepatoprotective drugs on the expression of the Sod1 gene in rats with ethanol liver damage.

Materials and methods. Male outbred white rats were used in the experiment. Five groups of animals were formed, 14 individuals each. Distilled water was administered to rats of the 1st group (control); Group 2 — ethanol at a dose of 5 g/kg of body weight; Group 3 — ethanol and heptor at a dose of 72 mg/kg; Group 4 — ethanol and mexidol at a dose of 50 mg/kg; Group 5 — ethanol and OMU at a dose of 50 mg/kg. The drugs were administered 1 hour before the introduction of ethanol. 24 and 72 hours after the introduction of ethanol (7 individuals), the animals were decapitated and the liver was removed. The expression level of the Sod1 gene was assessed using real-time reverse transcription PCR.

Results. The fold change in Sod1 expression in rat liver after 24 h practically did not change in response to the introduction of ethanol to the animals. A tendency to a slight decrease was observed in relation to changes in the expression of Sod1 with the use of heptor and mexidol, while under the influence of OMU, the expression level increased moderately. After 72 h, the exposure to ethanol was accompanied by a slight decrease in the frequency of expression of the Sod1 gene. A similar trend was observed with respect to changes in Sod1 expression with the use of heptor, mexidol, and OMU.

Conclusion. The results obtained indicate that the introduction of both ethanol and the prophylactic use of hepatoprotective drugs did not lead to significant changes in the level of Sod1 gene expression in rat liver. Additional studies are needed to identify the mechanisms of regulation of the antioxidant system, as well as the search for drugs that affect the transcriptional activity of genes.

The article presents the results of a review of publications devoted to the study of the problems of drug-induced liver damage in inflammatory bowel diseases (IBD). The hepatotoxic effect of thiopurines (azathioprine and 6-mercaptopurine) — hepatotoxicity from 0% to 17%; sulfasalazine and mesalamine (hepatotoxicity from 0% to 4%); methotrexate (hepatotoxicity from 15% to 50%); tumor necrosis factor inhibitors (hepatotoxicity up to 75% of cases.), anti-integrins (hepatotoxicity from 2% to 5%); an interleukin 12/23 inhibitor (hepatotoxicity from 0,5% to 2%); Janus-kinase inhibitors is considered (hepatotoxicity from 1% to 2%).

Conclusion. The drugs currently used to treat IBD require periodic liver function tests to rule out drug-induced lesions that require therapy correction. As the range of new drugs is rapidly expanding, this requires special observation and discussion in terms of their adverse effects on the liver.

The article presents a rare clinical case of Gaucher's disease, a hereditary disease that belongs to lysosomal accumulation diseases. A 36-year-old patient was admitted to the clinic with complaints of pain in the left half of the abdomen, pain in the chest, cough with yellow sputum, difficulty breathing due to pain, general weakness. The mental underdevelopment, hepatosplenomegaly, anemia, thrombocytopenia, and the threat of rupture of the spleen were revealed in the process of collecting anamnesis and examination. The patient was transferred to the surgical department, and a splenectomy was performed. Histological examination of the spleen and genetic examination confirmed the diagnosis of Gaucher's disease.

A rare clinical case of thyrotoxic hepatitis detected in a pregnant woman is presented. A diagnostic search was carried out to clarify the cause of hepatitis, during which the pathology of the thyroid gland was revealed. The patient was prescribed adequate therapy with a thyrostatic drug, which in a short time allowed to achieve a significant decrease in the activity of the hepatic pathological process, which made it possible to prolong pregnancy.

The article presents clinical case of the jaundice development and severe hyperenzymemia in GAM-Covid-VAK (Sputnik V) vaccination against COVID-19 in a 69-year-old patient. History — systematic use of non-steroidal anti-inflammatory drugs due to persisting pain after knee arthroplasty in 2018; frequent trips for several years to another region for sanatorium treatment, the use of mineral water. The diseases caused by hepatitis viruses, drug damage and post-vaccination reaction were included in diagnostic search. The markers of hepatitis B and C infection viruses were not detected during the enzyme immunoassay and polymerase chain reaction. The indicator for determining the relationship of a drug with the liver damage development was 6 points (borderline value) and only indicated the likelihood of drug hepatotoxicity. At the same time, it is known from history that repeated administration of the drug did not cause liver dysfunctions. The diagnosis of coronavirus infection was established based on the identification of SARS-CoV-2 in the hospital with repeated laboratory testing and competing diagnosis of hepatitis A has been confirmed on the basis of hepatocellular damage and the presence of serological marker of hepatitis A virus (immunoglobulin M antibodies). The treatment was continued in the infectious hospital, where the diagnosis of co-infection was confirmed. The pneumofibrotic changes in the S5 region of the left lung were revealed according to computed tomography. The normalization of aminotransferase activity and bilirubin was noted during dynamic observation. Apparently HAV infection led to a decrease in the immune response, the formation of an insufficient level of neutralizing antibodies in vaccinated against COVID-19 patient M. and contributed to the development of a new coronavirus infection with minimal manifestations in contact with SARS-CoV-2.