Introduction. The etiological aspects of functional dyspepsia (FD) and irritable bowel syndrome (IBS) are not clear; the epidemiology of diseases in age groups and societies can help in understanding the starting causes of the pathology.

Aim. To assess the risk factors for the development and prevalence of abdominal symptoms characteristic of FD and IBS among active users of Internet communities.

Materials and methods. An anonymous online survey was conducted among medical university students. The questionnaire contains questions about complaints typical of FD and IBS over the past week, “alarm” symptoms, personal characteristics of the respondent and possible risk factors: smoking, family history, taking antibiotics, iron pills, non-steroidal anti-inflammatory drugs (NSAIDs).

Results and discussion. The study included 983 respondents aged 18−26 years, 279 men and 704 women. Symptoms of unstudied regular (>1 time per week) postprandial dyspeptic disorders, bloating and abdominal pain were identified in 391 (39.8%) people, of which 29% were men and 44% were women (p < 0.001). Risk factors for regular unstudied disorders were having relatives with chronic gastrointestinal diseases (OR 2.05 [1.56, 2.70]); female gender (OR 1.92 [1.43, 2.59]); taking NSAIDs (OR 1.48 [1.14; 1.91]); for women – smoking (OR 2.24 [1.57; 3.18]). 6.5% of respondents met the criteria for FD, of which 23.4% had isolated epigastric pain, 26.6% had isolated postprandial distress syndrome, and 50% had combined FD. 2.5% of respondents met the criteria for IBS, 64% of whom had overlap syndrome with FD. The presence of FD was associated with NSAIDs use: r = 0.081; p = 0.011 (OR 1.95 [1.16; 3.30]).

Conclusions. The prevalence of FD and/or IBS among people aged 18−26 years is 7.4%, with no significant differences between men and women. Taking NSAIDs can be considered as a factor contributing to the development of FD.

Due to increasing prevalence of functional diseases of the colon in obese patients, the mechanisms by which the intestinal microbiota affects the development of symptoms of irritable bowel syndrome (IBS) in the setting of metabolic activity of adipose tissue should be investigated. The quantitative and qualitative changes in the pool of synthesized short-chain fatty acids, which have a multidirectional impact on the colonic motility is one of the key mechanisms by which the intestinal microbiota affects the occurrence and features of the course of irritable bowel syndrome. But as regards the issue of whether individual short-chain fatty acids have an impact on the severity of abdominal pain and characteristics of colonic motility dysfunction, it remains a subject of discussions. The study of the mechanisms of impact of short-chain fatty acids on the development and progression of obesity deserves special attention. Increased serum and faecal short-chain fatty acid levels in obese patients can either be a result of changes in the intestinal microflora composition associated with special eating habits and lifestyle, or have an independent effect on the development of obesity in individuals due to intestinal microflora composition disorders that have been already developed. Due to special features of the course of irritable bowel syndrome associated with overweight and obesity, studying the intestinal microbiota composition and the short-chain fatty acids produced by it in this cohort of IBS patients is of particular interest. This publication has been prepared to describe and systematize the possible mechanisms of impact of short-chain fatty acids on the development of abdominal pain and impaired colonic motility in IBS patients with overweight and obesity. The literature search was conducted in the databases Embase, PubMed and Google Scholar using the keywords “irritable bowel syndrome”, “obesity”, “short-chain fatty acids”, “gut microbiota”.

Introduction. There is a debate about the significance of intestinal metaplasia (IM) subtypes for the development of gastric cancer. Therefore, determining the indicators of cellular renewal in individuals with complete and incomplete IM is certainly a topical issue.

Aim. To study the proliferative activity of epithelial cells of the gastric antrum in patients with Helicobacter pylori-positive antral atrophic gastritis depending on the subtype of IM.

Materials and methods. The study included 20 people with chronic antral non-atrophic gastritis (CNG; group A), 20 patients with chronic antral atrophic gastritis (CAG) without IM (group B), 20 patients with CAG with complete IM (group C) and 20 people with CAG with incomplete IM (group D). The stage of chronic gastritis was assessed by the morphological method in accordance with the modified Sydney classification. Typing of IM foci in the gastric mucosa was performed using the PAS reaction. Proliferation activity was studied by the expression of nuclear protein Ki67 using immunohistochemistry.

Results. The proliferation index in the foci of complete BM in group C was 5%, and in group D in the foci of incomplete BM the Ki67 expression index was significantly higher and was 39% (p < 0.001). Outside the foci of metaplasia, the proliferation index was 23.5% in group C and 19% in group D (p = 0.06).

Conclusion. We have registered significantly higher proliferation indicators of gastric epithelial cells in foci with incomplete IM compared to foci with complete IM. Determination of proliferation indicators in foci of incomplete intestinal metaplasia may be a marker of an increased risk of developing gastric cancer.

Gastroesophageal reflux disease (GERD) is a common chronic disease leading to a spontaneous and regular retrograde flow of gastric and/or duodenal contents into the esophagus. Reflux of the gastric contents into the oral cavity refers to the extraesophageal presentation of the disease, which, in the absence of timely treatment, can result in erosion of dental hard tissue (EDHT) through repeated exposure of the dental tissue to acidic contents. EDHT are non-carious lesions of the dental hard tissues (mainly enamel, and in some cases dentin), induced by a chemical reaction involving acids, which results in demineralization processes. The incidence rates of EDHT in adult patients with GERD are 32.5–51.5%. The EDHT in GERD develops in stages. Initially, the gradual degradation of tooth pelicula happens when it gradually becomes decayed by repeated acidic attacks. The loss of the pelicula results in direct contact of hydrochloric acid refluxate with the enamel surface and initiation of its demineralization at pH < 5.5 with dissolution of hydroxyapatite crystals. Given the high prevalence of GERD in the population, it seems important to update an integrated approach to the treatment of such patients, which involves pharmacotherapy provided by the gastroenterologist, as well as prevention and minimally invasive treatment of presentations in the oral cavity by the dentist. Patients with EDHT due to GERD need to maintain individual oral hygiene (use mouth washes with a neutral pH level, avoid abrasive toothpastes), use remineralization therapy at home applying remogels (Tooth Mousse), and also be observed by a dentist as part of the follow-up care. Minimally invasive treatment by the dentist involves restorations using composite tooth filling materials and ceramic veneers. It is reasonable to empirically use proton pump inhibitors twice a day for 3 months for the direct treatment of GERD in patients with EDHT.

Helicobacter pylori (H. Pylori), microaerophilic spiral-shaped Gram-negative bacteria which colonize the gastric mucosa of human population, is the leading causal factor in the development of a whole range of diseases of the gastroduodenal region (chronic gastritis, gastric and duodenal ulcer disease, MALT lymphoma and gastric adenocarcinoma). Since the discovery of H. pylori infection and the identification of its leading role in the development of a range of gastroenterological diseases, researchers have begun to actively study the potential trigger significance of this pathogen in the development of extragastric pathology. At the epidemiological level, H. pylori infection has been shown to be frequently associated with skin diseases such as rosacea, acne, chronic urticaria and psoriasis, although the clinical significance of these associations remains clouded. In fact, recent meta-analytic studies (2019–2024) demonstrate an increased risk of developing the above diseases in H. pylori-infected individuals with odds ratios ranging from 1.19 to 3.00. On the other hand, not all studies have showed that eradication therapy of this microorganism helps reduce the clinical severity of symptoms of skin diseases, which is hypothetically explained only by the trigger role of infection within the complex pathogenesis. In a modern light, such associations can be viewed in terms of pathogenetic findings through the implementation of the syndrome of increased epithelial permeability (SIEP). The chronic gastritis caused by H. pylori infection is believed to lead to increased permeability of the epithelial lining of the stomach, as well as the walls of the mucosal vessels and a higher exposure of bacterial and nutritional antigens in the systemic circulation, which can induce both local release of inflammatory mediators in tissues and systemic immunological reactions (autoimmune and inflammatory processes, formation of molecular mimicry-induced immune complexes and cross-reactive antibodies).

Introduction. Nowadays, a multifactorial model of the pathogenesis of NAFLD is recognized. It is interesting to study the contribution of changes in the composition of the intestinal microbiota and its metabolites in the development of the disease.

Aim. To evaluate the contribution of research into the qualitative composition of the intestinal microbiota in relation to the risk of progression of NAFLD to reduce the loss of health- saving potential of the population.

Materials and methods. An open comparative study of 83 mature-aged patients (56.6 years (46–63)) suffering from NAFLD was conducted. The levels of insulin, leptin, its receptor, adiponectin in blood serum, zonulin in feces were studied, and SCFA in feces

was determined. The analysis was carried out depending on the phenotypes of NAFLD: the degree of steatosis (1 – 40 patients, degree 2 – 18 and degree 3 – 25), the presence of NASH (43 patients), the presence of fibrosis (fibrosis was found in 35 patients). The degree of steatosis and fibrosis was assessed using elastometry. The results of the study were analyzed using the Microsoft Excel, STATISTICA 12.0 software package.

Results. In patients with NAFLD, the absolute number of all SCFA in the feces was reduced. The anaerobic index was deviated towards sharply negative values (-0,711 (-0,576-(-0,830)). A high level of propionic acid was noted among the patients with fibrosis (p < 0.05). Anaerobic index, relative content of isoC4 + isoC5 + isoC6, relative content of butyric acid had a positive relationship with the St-index (r_s = 0.254, r_s = 0.269, r_s = 0.240, p≤ 0.05). An increase in the relative amount of propionic acid was statistically significantly associated with a decrease of FLI (r_s = -0.229, p ≤0.05). A positive correlation was found between the level of insulin and the absolute amount of butyric acid C4 (r_s = 0.228, p ≤ 0.05). There was an inverse relationship of the absolute and relative amounts of isoC4+ isoC5 + isoC6 and Iso Cn/Cn with zonulin in the feces (r_s = -0.231, p ≤ 0.05, r_s = -0.380, p ≤ 0.05 and r_s = -0.332, p ≤ 0.05, respectively).

Conclusion. There is the anaerobic flora among the patients with NAFLD. Modification of the content of SCFA in feces may affect to the progression of NAFLD. The effect of SCFA on the development and progression of NAFLD may be mediated by the development of insulin and leptin resistance, as well as an integrity violation of the intestinal barrier.

Diseases of the hepatobiliary system today remain an urgent health problem worldwide. A significant percentage of gastroenterological patients are people suffering from cholestasis syndrome. In gastroenterology, there are a number of nosological forms accompanied by the development of cholestasis syndrome. This pathological condition has many etiological factors, but in general, the mechanisms of its formation for various reasons are largely similar. When working with this group of patients, it is necessary to take into account the peculiarities of the clinical picture, which may vary depending on the etiology of the cholestatic syndrome. The fact of the economic burden in this pathology is also important, because sometimes it is necessary to resort to high-tech examination methods and expensive laboratory screening to perform high-quality differential diagnosis. As for the treatment of cholestatic syndrome, at the moment there are many drugs with different mechanisms of action, the predominant part of which, according to randomized clinical trials and meta-analyses, has proven effectiveness. In this article, based on literature sources taken from foreign and domestic databases, the etiology and pathogenesis of the development of cholestasis syndrome, the clinical picture and approaches to the diagnosis of this condition are considered. When considering the treatment of cholestatic syndrome, this article focuses on therapy with ursodeoxycholic acid drugs, in particular Ecurochol. A clinical case is also considered on the example of a patient with cholestasis syndrome who was prescribed treatment with Ecurochol and who showed positive dynamics due to improvements in the ultrasound picture of the abdominal organs.

Introduction. The search for simple and informative markers for predicting positive outcomes in patients with liver cirrhosis (LC) does not affect its relevance.

Aim. To study the possibility of using the “neutrophil to lymphocyte ratio” indicator as a predictor of development of LC complications and death.

Materials and methods. For a retrospective clinical study, 225 case histories of patients with LC were selected from 2008 to 2018. Three groups were formed from them: group 1: patients with LC class A according to Child- Pugh (24n); Group 2: patients with LC class B and C according to Child- Pugh (201n); and group 3: healthy individuals (50n). A correlation analysis of the NLR indicator with the Child- Pugh and MELD scales was carried out. The prognostic value of NLR in the development of complications and death was analyzed.

Results. Patients with LC had statistically significantly higher values of NLR compared to healthy individuals (p < 0.001). NLR had a statistically significant positive correlation with the Child- Pugh (p < 0.001) and MELD (p < 0.001) scales. NLR is a statistically significant predictor of the development of complications in patients with LC (p = 0.003). A NLR value > 2.3 had a sensitivity of 0.97 [95% CI: 0.92; 0.99] and specificity 0.19 [95% CI: 0.11; 0.29]. NLR statistically significantly correlated with the number of complications of LC (p<0.001) and served as a statistically significant predictor of death (p<0.001). A NLR value > 4.5 had a sensitivity of 0.24 [95% CI: 0.15; 0.36] and specificity 0.97 [95% CI: 0.92; 0.99].

Conclusion. An NLR value of more than 2.3 increases the risk of complications in patients with LC, and an NLR value of more than 4.5 increases the risk of death.

Gilbert’s syndrome, also known as benign hyperbilirubinemia, was described more than 100 years ago. It has usually been considered a physiological abnormality characterized by a mild elevation of the systemic level of unconjugated bilirubin, in the absence of any underlying liver or overt RBC hemolysis. The molecular basis of Gilbert’s syndrome lies in the impairment of the conjugation of bilirubin with glucuronic acid in the hepatocytes, which is mediated by a specific hepatic enzyme named bilirubin-UDP-glucuronosyl transferase 1A1 that forms bilirubin diglucuronoside. Clearance of various xenobiotics, which are not substrates for glucuronosylation, is impaired in patients with Gilbert’s syndrome; their detailed list is provided in the article. Fatigue, asthenia, and various vaguely defined dyspeptic complaints attributed to Gilbert’s syndrome in the past are no longer considered a part of this condition, and proper evaluation of possible causes is required in these cases. Since the re-discovery of the potent antioxidant effects of bilirubin in the late 1980s, as well as the multiple intracellular signalling pathways affected by bilirubin, an ever-increasing body of evidence suggests that individuals with Gilbert’s syndrome may benefit from the mild hyperbilirubinemia and are actually protected from the development of a wide range of “diseases of civilization”, such as cardiovascular diseases, certain cancers, and autoimmune or neurodegenerative diseases. Gilbert’s syndrome is defined phenotypically, and therefore not according to predisposing genetic markers, as the elevation of serum unconjugated bilirubin concentration above the upper limit of normal, with no laboratory signs of hemolysis or liver damage. This review analyses the current state of medical knowledge given recent discoveries in this rapidly developing field, as well as their possible clinical significance, and provides a new perspective on this condition.

Introduction. Violation of metabolic processes in the gastrointestinal tract in patients with chronic hepatitis C (HCV) leads to the accumulation of toxic metabolic products in the intestine, negatively affecting both the balance of the microbiota and the functional state of hepatocytes. The sorption of toxins released by opportunistic anaerobic bacteria contributes to the restoration of the population of bifidobacteria and lactobacilli, which has a beneficial effect on the functional state of the liver.

Aim. To evaluate the clinical and laboratory efficacy and safety of Polysorb as part of complex pathogenetic therapy in patients with HCV with severe liver fibrosis.

Materials and methods. The study included 62 patients with HCV in the stage of severe liver fibrosis (F3 according to METAVIR) of both sexes aged 18 to 65 years who were not receiving antiviral therapy. In the study group, pathogenetic therapy was supplemented with Polysorb. Clinical and laboratory parameters were evaluated before and after the course of treatment. The study of the intestinal microbiota was carried out by determining the concentration of volatile fatty acids (VFA) in the intestinal contents: acetic, propionic, butyric, the total content of isoC4 + isoC5 + isoC6 and the value of the anaerobic index by gas-liquid chromatography (chromatograph “Tsvet 100”, Russia).

Results and discussion. Complex pathogenetic therapy of patients with HCV (F3), including the enterosorbent Polysorb, increases the effectiveness of treatment for clinical syndromes: right hypochondrium by 35.8%, asthenovegetative – by 13.6%, dyspeptic – from 8 to 22.5% (according to individual symptoms), cholestatic – by 8%, and also improves the biochemical parameters of liver function: p = 0.060; GGTP, p = 0.014 and it helps to stabilize the composition of the microbiota, increasing the total level of LVH (p < 0.05), mainly due to normalization of acetic acid values, improvement of the anaerobic index: before treatment -0.858 ± 0.152, after -0.601 ± 0.163 (p < 0.05).

Conclusion. The inclusion of Polysorb in the pathogenetic therapy of patients with HCV (F3) helps to stabilize the composition of the microbiota, while no side effects or adverse events have been recorded.

The review examines the epidemiology and risk factors of non-alcoholic fatty liver disease (NAFLD) for women. According to various sources, the global prevalence of NAFLD ranges from 20 to 40% of the adult population in the world. In Russia, 37.3% of polyclinic patients have NAFLD. NAFLD can occur at any age and has differences in prevalence and severity depending on ethnicity and gender. Over the past 10 years, there has been a trend towards an increase in the prevalence of NAFLD among women, as well as a sharper increase in mortality compared to men. Regardless of gender, prognostically significant risk factors for NAFLD include age, obesity, type 2 diabetes mellitus, insulin resistance, dyslipidemia. The clinical course and prognosis of NAFLD in women depends on age, reproductive stage and use of synthetic hormones. Premenopausal women have less pronounced liver fibrosis and a better life prognosis compared to postmenopausal men and women. The article describes the features of the course of NAFLD in the reproductive period, pre- and postmenopausal period, characterizes the effect of liver steatosis on the course and outcome of pregnancy, the perinatal condition of the mother and fetus. Thus, there are gender differences in the prevalence, risk factors, fibrosis, and clinical outcomes of NAFLD. The prevalence and severity of NAFLD in reproductive age is higher in men, but after menopause, there is an increase in this pathology in women, especially those with metabolic disorders. Liver steatosis can affect the course of pregnancy, labor and postpartum periods.

Alcoholic hepatitis is a progressive inflammatory-dystrophic lesion of the liver, the pathogenetic mechanism of which is based on alcoholic damage. Acute alcoholic hepatitis is defined primarily as an exacerbation of the chronic process of alcoholic liver disease. Two mechanisms are defined as the basis for the formation of alcohol-associated liver damage: primary (direct effect of ethanol on hepatocytes and oxidative stress provoked by it) and secondary (through changes in the gut-liver axis with dysbacteriosis and increased permeability of the intestinal wall). For the treatment of acute alcoholic hepatitis, mainly glucocorticosteroids are used, the action of which is directed at cytotoxic and inflammatory mechanisms of the pathogenesis of this disease. Also, phosphodiesterase inhibitors, broad-spectrum antibiotics (rifaximin), probiotics, prebiotics, synbiotics, enterosorbents and hepatoprotectors are actively used. Choosing a hepatoprotector that is effective and safe for patients is still a challenge. At the moment one of the most promising and optimal in terms of “price-quality” ratio drug from this group is a domestic drug from the group of combined hepatoprotectors – Remaxol (inosine + meglumine + methionine + nicotinamide + succinic acid). A clinical case of application of this drug in a patient diagnosed with acute alcoholic hepatitis combined with chronic alcoholic hepatopathy is presented. Not severe course (MELD: 16. Maddrey’s index: 14.04). Ademetionine was prescribed. On the background of the prescribed treatment slight improvements were noted, no significant changes in laboratory data were registered (MELD: 16, Maddrey index: 12.54). After replacement of the hepatoprotector by Remaxol, the following was observed: correction of the general condition, correction of the mental status, reduction of the severity of hepatosplenomegaly, normalization of laboratory parameters (MELD: 10. Maddrey’s index: 6.06). Based on the review of Russian and foreign literature, as well as personal experience in the use of Remaxol, we can conclude that this pharmacological agent contributes to a more favorable course of acute alcoholic hepatitis, a significant reduction in the risk of complications, as well as reducing the length of hospital stay and the cost of treatment.

Introduction. Relapses occur in 30–50% of patients IgG₄-related sclerosing cholangitis. Relapses may act an independent risk factor for malignancy development and the need in maintenance therapy for relapse prevention is still uncertain. Thus, studying relapse predictors and developing reliable preventive approaches is an important area of research for this condition.

Aim. To determine relapse predictors of IgG₄-related sclerosing cholangitis.

Materials and methods. A single- center dynamic bidirectional observational study was conducted in patients aged 18 years and older with verified IgG₄-related sclerosing cholangitis (n = 32). We searched for possible factors influencing the relapse of IgG₄- related sclerosing cholangitis. The development of a prognostic model for the relapse probability was carried out using logistic regression. ROC analysis was used to assess the diagnostic performance of quantitative variables in predicting of relapse.

Results. The median follow-up period was 33 (16–60) months. The majority of patients with IgG₄-related sclerosing cholan- gitis were male (71.9%), median age was 59 ± 13 years. In most patients, delayed diagnosis (median 10.5 [4.8; 22.5] months) was associated with overdiagnosis of primary sclerosing cholangitis (41.2%) or bile duct malignancy (43.8%). Surgical interventions were performed in 50% of patients. Median serum IgG₄ level was 2.70 g/L [1.92; 6.48], and 21.9% of patients had normal serum IgG₄ level. Disease relapse developed in 34.4% (n = 11) of patients. Serum IgG₄ level before glucocorticosteroid therapy ≥ 2.24 g/L and a delay in diagnosis by ≥ 17 months were associated with the relapse (p = 0.040 and p = 0.049 respectively). Multi-organ involvement, and extrahepatic localization of biliary strictures in the patients with the history of surgical interventions increased the risk of relapse 85 (p = 0.001) and 12 (p = 0.047) fold, respectively. The presence of biliary strictures below the confluence reduced the risk of relapse 7.5 fold (p = 0.032).

Conclusions. Possible predictors of IgG₄-related sclerosing cholangitis relapse may include multi- organ involvement, intrahepatic and proximal extrahepatic strictures, prior surgical interventions in patients with extrahepatic strictures, high serum IgG₄ level, and delayed diagnosis.

Introduction. Non-alcoholic fatty liver disease (NAFLD) is caused by excess accumulation of fats in hepatocytes. An increasing percentage of adipose tissue is associated with chronic inflammation and developing oxidative stress. These pathological conditions can lead to the progression of steatosis to steatohepatitis with the further development of fibrosis and cirrhosis.

Aim. To evaluate the indicators of lipid peroxidation and antioxidant defence factors in steatosis and steatohepatitis in patients with NAFLD.

Materials and methods. During the work, 116 patients with NAFLD were examined, of which 65 had steatosis, and 51 had steatohepatitis. The study of biochemical markers of metabolism of proteins, fats and carbohydrates was performed on a Mindray BS-380 biochemical analyzer. The indicators of the LPO-AOD system (MDA, SOD, catalase, ceruloplasmin) were assessed using spectrophotometric methods. Statistical data processing was carried out in the STATISTICA and SPSS 26 programs using nonparametric tests.

Results. Patients with steatohepatitis had more severe dyslipidemia, blood triglyceride, total cholesterol levels and LDL were significantly higher (p > 0.05). Impaired cholesterol metabolism was reflected by a high atherogenic index of 3.46. In patients with steatosis, changes in the lipid profile were less pronounced. No disturbances in protein and carbohydrate metabolism were detected. Increased levels of liver markers were noted only in patients with steatohepatitis. The change in the balance in the LPO- AOD system was more pronounced in patients with steatohepatitis; they had a high level of MDA, a high concentration of catalase; in patients with steatosis, only a decrease in the level of MDA and an increase in the level of ceruloplasmin were noted.

Conclusion. Dyslipidemia, hepatocyte cytolysis and liver fibrosis are detected in patients with steatohepatitis. Disturbances in the LPO-AOD system have been identified in both forms of NAFLD, but in steatosis they are compensated. In steatohepatitis, disturbances in “LPO-AOD” in the form of an increase in pro-oxidants and a decrease in antioxidants cause the development of oxidative stress.

Introduction. Non-alcoholic fatty liver disease (NAFLD) is caused by excess accumulation of fats in hepatocytes. An increasing percentage of adipose tissue is associated with chronic inflammation and developing oxidative stress. These pathological conditions can lead to the progression of steatosis to steatohepatitis with the further development of fibrosis and cirrhosis.

Aim. To evaluate the indicators of lipid peroxidation and antioxidant defence factors in steatosis and steatohepatitis in patients with NAFLD.

Materials and methods. During the work, 116 patients with NAFLD were examined, of which 65 had steatosis, and 51 had steatohepatitis. The study of biochemical markers of metabolism of proteins, fats and carbohydrates was performed on a Mindray BS-380 biochemical analyzer. The indicators of the LPO-AOD system (MDA, SOD, catalase, ceruloplasmin) were assessed using spectrophotometric methods. Statistical data processing was carried out in the STATISTICA and SPSS 26 programs using nonparametric tests.

Results. Patients with steatohepatitis had more severe dyslipidemia, blood triglyceride, total cholesterol levels and LDL were significantly higher (p > 0.05). Impaired cholesterol metabolism was reflected by a high atherogenic index of 3.46. In patients with steatosis, changes in the lipid profile were less pronounced. No disturbances in protein and carbohydrate metabolism were detected. Increased levels of liver markers were noted only in patients with steatohepatitis. The change in the balance in the LPO- AOD system was more pronounced in patients with steatohepatitis; they had a high level of MDA, a high concentration of catalase; in patients with steatosis, only a decrease in the level of MDA and an increase in the level of ceruloplasmin were noted.

Conclusion. Dyslipidemia, hepatocyte cytolysis and liver fibrosis are detected in patients with steatohepatitis. Disturbances in the LPO-AOD system have been identified in both forms of NAFLD, but in steatosis they are compensated. In steatohepatitis, disturbances in “LPO-AOD” in the form of an increase in pro-oxidants and a decrease in antioxidants cause the development of oxidative stress.

This review presents the main extraintestinal manifestations (EIMs) in patients with inflammatory bowel diseases (IBD), in particular ulcerative colitis (UC) and Crohn’s disease (CD), describes the modern potential mechanisms, classification, characteristics and frequency of the main EIMs (rheumatological, skin, ophthalmological and orofacial manifestations). The issues of the mechanism of action, indications for prescribing ustekinumab are also covered in detail, the place of ustekinumab in the treatment of IBD is highlighted, the effectiveness of this drug in relation to the treatment of IBD is assessed – summarizes the results of a retrospective analysis of data from the UNITI-1, UNITI-2, IM-UNITI clinical trial program, prospective cohort studies, retrospective cohort studies and a registry study on the effect of ustekinumab on the course of various EIMs and the outcomes of immune-mediated diseases (IMDs) in patients with CD and UC. Ustekinumab is a fully monoclonal human immunoglobulin G1k that binds to the common p40 subunit of interleukin (IL)-12 and IL-23, which are actively involved not only in the development of intestinal symptoms, but are also triggers in the development of various EIMs. A review of the literature showed that ustekinumab may be effective for the treatment of EIMs in patients with UC and CD, especially in relation to dermatological and rheumatological manifestations, and is effective against psoriasis and psoriatic arthritis. A literature search of MEDLINE®, EMBASE®, BIOSIS Previews® and DERWENT® and/or other resources, including internal/external databases was conducted on April 15, 2024.

Symptoms of constipation such as derangements of the motor, secretory and/or evacuation functions of the colon are recorded occasionally or for a long period in at least 20% of the population in economically developed countries. QoL is significantly impaired in patients with chronic constipation. The frequency, time of bowel movement and stool consistency is, in large part, determined by the motor function of the colon. The primary approach to the treatment algorithm for chronic constipation (CC) is modification of a lifestyle and a diet rich in dietary fiber. If dietary measures provide poor efficacy, laxatives are prescribed to the patients. According to the current guidelines, therapeutic approaches to the treatment of CC should include the sequential administration of laxatives that increase the volume of contents and stimulate the motor function of the colon. According to the Russian Gastroenterological Association guidelines for the diagnosis and treatment of chronic diseases in adult patients, it is reasonable to use stimulant laxatives as second-line drugs. Contact laxatives, which increase intestinal peristalsis due to stimulation of nerve endings in the intestinal mucosa, have been shown to be more effective in treating chronic constipation than placebo. Among the drugs in this group, Bisacodyl®, a diphenylmethane derivative, and Regulax® Picosulfate, a sodium picosulfate derivative, are the most studied ones. These substances are hydrolyzed into bis-(p-hydroxyphenyl)-pyridyl-2-methane in the intestine, which, on contact with the receptors in colonic mucosa, stimulates propulsive activity and increases intestinal secretions. Regulax® Picosulfate is effective and safe in patients with acute and chronic constipation of various origin.

Diarrhoea is one of the most common gastroenterological complaints made by patients who seek medical attention. It can be a manifestation of the whole range of different diseases, although not exclusively of the digestive tract, which requires a thorough examination of the patient and often is a challenge for the clinician, especially in the limited time settings during an outpatient visit. The cause of diarrhoea should be identified early to begin treatment of the patient in a timely and rational manner. In managing a patient with diarrhoea, a diagnostic search must begin with the following actions: working out complaints in detail, identification of symptoms of anxiety and taking a medical history, including epidemiological, pharmaceutical, hereditary, allergic, as well as analysis of dietary preferences. A physical examination is an integral part of the patient management; it allows to assess the general health condition, identify signs of dehydration and clinical stigmas of the underlying condition, which may manifest itself as diarrhoea. After an initial examination and exclusion of anxiety symptoms, a number of laboratory and instrumental examination methods is prescribed to determine the cause of diarrhoea. Given the polyetiology of diarrhoea syndrome, the range of methods for examining the patient can be quite wide, therefore the choice of area for the diagnostic search and the scope of the necessary diagnostic procedures is carried out on an individual basis, taking into account the features of the clinical picture, history data and physical examination findings. Treatment of a patient with diarrhoea at the pre-examination stage must include rehydration, timely detection and correction of electrolyte disturbances and other possible complications. Once the cause of diarrhoea has been established, the patient is treated due to the identified etiological factor in accordance with the current clinical guidelines. The article presents a step-by-step algorithm for making a differential diagnosis in a patient with diarrhoea, and also presents our own clinical observations.

Russia and most countries of the world are currently facing pressures on their health services because of the growing number of diseases associated with unhealthy lifestyles: type 2 diabetes, obesity, non-alcoholic fatty liver disease, etc. Lifestyle modification is the first prerequisite in the treatment of non-alcoholic fatty liver disease and other diseases associated with unhealthy lifestyle. The use of lactitol provides the opportunity to make this process more effective, as it is able to increase the production of butyrate, reduce the damage to the intestine barrier structure, and interact with sweet-taste receptors. Lactitol has a low glycaemic index, it is not absorbed in the intestine and is fermented like dietary fibres. The results of the studies showed that the metabolic response to this drug corresponds to a lower increase in plasma glucose, insulin and C-peptide levels compared to the use of glucose in healthy, non-obese men. It has been shown through various experiments in animals and in humans that lactitol also reduces the plasma triglyceride levels, probably due to reduced triglyceride absorption as a result of accelerated transit of intestinal contents. An important property of the drug is its ability to increase the glucagon-like peptide-1 (GLP-1) and PYY levels, which is accompanied by delayed gastric emptying and reduced hunger, which is essential in the treatment of obesity, type 2 diabetes mellitus and non-alcoholic fatty liver disease. A 120-day randomized controlled trial was conducted to assess the efficacy, safety, and tolerability of lactitol in 139 patients with nonalcoholic fatty liver disease. Twice-daily administration of lactitol 6 g in addition to lifestyle modification events has been shown to increase their efficacy expressed as a significant decrease in ALT levels and an increase in the AST/ALT ratio compared to control subjects. Lactitol can be considered as a metabolic corrector and used in the treatment of diseases associated with an unhealthy lifestyle.

Introduction. Russia is among the leaders in incidence and mortality from gastric cancer (GC). The incidence of gastric cancer in the Republic of Tyva is especially abnormally high. Currently, there is interest in studying genetic factors in various types of cancer. But for GC, such research is not enough.

Aim. To study the polymorphism of the apoptosis marker genes CASP9 (rs1052576), TP53 (rs1042522), FAS/APO-1 (rs2234767) in the blood of indigenous people with GC in the Republic of Tyva.

Materials and methods. 107 Tuvinians were examined (47 people with GC and 60 persons in the control group). The diagnosis of GC was established on the basis of a comprehensive laboratory, instrumental and morphological examination by oncologists at the Republican Oncology Dispensary. Genotyping of polymorphisms rs1052576 CASP9, rs2234767 FAS/APO-1 and rs1042522 TP53 was carried out in all 47 patients with GC and in 60 people in the control group using the polymerase chain reaction method from DNA samples isolated from venous blood.

Results. In patients with GC, compared with healthy individuals, the mutant allele G (44.7% versus 27.5%; p = 0.01) and the homozygous genotype GG (23.4% versus 6.7%; p = 0.03) of polymorphism rs1042522 TP53, as well as mutant allele A (57.4% versus 32.5%; p < 0.001) and homozygous genotype AA (31.9% versus 15.0%; p = 0.05) of polymorphism rs2234767 FAS/ APO-1 were more often registered among indigenous inhabitants of the Republic of Tyva. The frequency of various genotypes and alleles of the polymorphism rs1052576 CASP9 did not differ significantly between patients with GC and healthy individuals.

Conclusion. Based on these results, it can be assumed that the A allele of rs2234767 FAS/APO-1 and the disruption of the anti-oncogenic function of the p53 protein produced by the G allele of rs1042522 TP53 are associated with GC and can be used as markers to determine increased risk in the population of indigenous residents of the Republic of Tyva.