Aim: to review current understanding of the role of intestinal microbiota in the pathogenesis of irritable bowel syndrome (IBS), anxiety and depressive disorders, and to present the materials of the Expert Council, which met on April 19, 2025, in Moscow.

Key points. A likely unifying factor in the development of IBS, anxiety, and depressive disorders is a change in the composition of the intestinal microbiota, which causes disruption of neuroendocrine, immune, and metabolic signaling pathways of interaction between the gut and brain (components of the gut-brain axis). The intestinal microbiota plays a coordinating role in maintaining the physiological constancy of these pathways. However, when its composition is disrupted, pathogenic mechanisms are activated, leading to the combined development of both IBS and anxiety and depressive disorders. Recent data have shown that patients with IBS, as well as those suffering from anxiety and depressive disorders, exhibit a unidirectional change in the composition of the intestinal microbiota, characterized by a decrease in the number of Bifidobacterium bacteria, suggesting their key role in the pathogenesis of these diseases. A pathogenetically substantiated therapeutic strategy for the combination of IBS and mental disorders includes modifying the gut microbiota using strain-specific pro biotics containing Bifidobacterium type species. Bifidobacterium longum 35624 and Bifidobacterium longum 1714 strains have demonstrated clinical efficacy in reducing the severity of IBS symptoms, anxiety, and depression.

Conclusion. Prescribing a combination of Bifidobacterium longum 35624 and Bifidobacterium longum 1714 probiotic strains to patients with IBS, including those with comorbid mental disorders, is clinically justified. This combination of strains holds promise for inclusion in clinical guidelines for the management of patients with irritable bowel syndrome and mental and behavioral disorders.

Introduction. Celiac disease is a chronic autoimmune disease requiring a lifelong gluten-free diet. Despite the effectiveness of the diet in controlling symptoms, patients’ quality of life remains at risk due to limitations in social, emotional, and gastronomic spheres.

Aim: to analyze current approaches to assessing the quality of life of patients with celiac disease in order to optimise strategies for providing care to this category of patients.

Key points. Current research emphasizes the importance of not only clinical control, but also of psychosocial support for patients This review describes validated tools for assessing life quality in patients with celiac disease, highlighting the differential impact of the disease on children and adults, the specifics of adherence to and perceptions of a gluten-free diet, and regional and cultural differences in access to support and gluten-free products. An unfavorable psychological state can reduce adherence to a gluten-free diet, creating a vicious cycle. A comparison with other chronic diseases showed that with strict adherence to a gluten-free diet, celiac disease may have a lesser impact on quality of life.

Conclusion. Optimizing quality of life requires a multidisciplinary approach — from cultural adaptation of life quality scales to psychological and social support for these patients and normalizing nutrition outside the home.

Aim: to assess the efficacy of dietary treatment regimens in eosinophilic esophagitis patients.

Materials and methods. Twenty-seven patients (1 woman and 26 men) aged 24 to 61 years with a previously confirmed diagnosis of eosinophilic esophagitis (according to esophagogastroduodenoscopy with esophageal biopsy: > 15 eosinophils per high-power field, ×400) off therapy were instructed on dietary exclusions as the only treatment method. Three patients were placed on a targeted diet based on allergy testing; 17 patients followed a two-food elimination diet; and 7 patients followed a six-food elimination diet. All patients underwent esophagogastroduodenoscopy with esophageal biopsy (6 specimens from the distal and middle/proximal portions) and histopathological examination of biopsy specimens, as well as questionnaire-based assessment of dysphagia severity before and after 12 weeks of dietary therapy.

Results. After 12 weeks of dietary therapy, histological remission was achieved in 3 of 7 (42.9 %) patients who followed the six-food elimination diet, in 7 of 17 (41.2 %) patients who followed two-food elimination diet, and in 1 of 3 (33.3 %) patients on a target diet (differences were not statistically significant). Complete resolution of dysphagia was ob served in 1 (33.3 %) patient who followed a target diet, in 8 of 14 (57.1 %) patients with dysphagia in the two-food elimination diet group, and in 3 of 5 (60 %) patients with dysphagia on the six-food elimination diet (differences were not statistically significant).

Conclusions. The efficacy of two-food and six-food elimination diets is comparable and allows histological remis sion to be achieved in 41.2–42.9 % of patients with eosinophilic esophagitis.

Aim: comprehensive assessment of the efficacy and safety of hymecromone in the treatment of biliary tract dysfunction.

Materials and methods. A systematic review and meta-analysis of observational studies (n = 1117) selected from 5 databases (Central Scientific Medical Library, eLibrary, PubMed, Google Academy, Cochrane Library) without restrictions on publication date, devoted to the study of the use of hymecromone in patients with biliary tract dysfunction, including gallstone disease.

Results. During the meta-analysis, it was found that three-week therapy with hymecromone, 1200 mg/day, was accompanied by a change in pain intensity by –48.51 mm (95 % confidence interval (95% CI): –56.97…–40.05) on the Visual Analog Scale. Improvement in quality of life was observed according to the “Bodily Pain” subscale of the 36-Item Short-Form Health Survey (SF-36) with a mean increase of 21.69 points (95% CI: 18.23–25.16). Following three-week therapy with hymecromone, 1200 mg/day, the proportion of patients with abdominal pain relief was 70.0 % (95% CI: 59.0–81.0), flatulence — 77.0 % (95% CI: 60.0–95.0), bitter taste — 74.0 % (95% CI: 54.0–93.0). The proportion of patients with improvement of gallbladder motility was 91.0 % (95% CI: 82.0–100.0), and the proportion of patients with restoration of bile homogenicity was 70.0 % (95 % CI: 43.0–98.0). The proportion of patients with normal stool frequency increased from 60.0 % (95% CI: 9.0–100.0) to 78.0 % (95% CI: 34.0–100.0) after 3 weeks of hymecromone therapy (1200 mg/day). Monotherapy with hymecromone at doses of 600–1200 mg/day had a favorable safety profile. The probability of persistent unformed stool after 3 weeks of therapy was dose-dependent: at the end of treatment, the symptom persisted in 23.0 and 0 % of patients receiving 1200 or 600 mg/day of hymecromone, respectively.

Conclusions. Course therapy with hymecromone at the full therapeutic dose of 1200 mg/day results in regression of key clinical manifestations, including biliary pain and dyspeptic symptoms. The drug contributes to the restoration of gallbladder motility and improvement of bile rheological properties while demonstrating a favorable tolerability profile. These findings support the pathophysiological rationale for the use of hymecromone in biliary tract disorders and reinforce its applicability in routine clinical practice.

Aim: to identify the frequency of secondary hepatosiderosis not related to hereditary hemochromatosis, depending on the etiology of chronic diffuse liver disease, in a retrospective study based on the results of morphological examination of liver biopsies.

Materials and methods. The study included 227 patients with chronic diffuse liver diseases of various etiologies (viral (HCV, HBV), metabolic, alcoholic), the average age of patients was 35.3 ± 11.9 years, among those examined there were 153 (67 %) men, 74 (33 %) women. All patients underwent laboratory and instrumental examination: clinical blood test, coagulation test, biochemical blood test (alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transpeptidase, alkaline phosphatase, total bilirubin, albumin, lipid phenotyping), virological research methods (HBsAg, HCV antibodies, HCV-RNA, HBV-DNA in blood serum and liver biopsies, expression of HCV non-structural proteins, HBsAg, HBcorAg in liver biopsies), markers of autoimmune liver diseases (ANA, AMA), iron metabolism indices (serum iron, ferritin), as well as hepatobiopsy with morphological examination of biopsy specimens and assessment of the histological activity index (Knodell, 1994), fibrosis stage (Desmet, 1994), Perls staining to detect iron deposits.

Results. Histological examination of hepatobiopsy specimens from patients with chronic liver diseases of various etiologies revealed the presence of iron overload syndrome in 36.1 % of cases. Most often, iron deposits in liver tissue were detected in a combination of viral and alcohol-associated liver diseases (chronic hepatitis C + alcoholic steatohepatitis — 69.6 %; chronic hepatitis B + alcoholic steatohepatitis — 66.7 %), in combination with chronic hepatitis C with metabolically associated fatty liver disease at the stage of steatohepatitis (50 %), with autoimmune hepatitis (50 %); with significant frequency — with alcohol-associated liver diseases (47.5 %), and virus-associated liver diseases — chronic hepatitis B (44.4 %), chronic hepatitis C (38.9 %). Iron overload syndrome in the liver was observed significantly less frequently in non-alcoholic steatohepatitis (25 %). Iron deposits in the form of hemosiderin in secondary hepatosiderosis against the background of chronic liver diseases were localized in hepatocytes of the I–II acinar zones, less often in Kupffer cells. Patients with hepatosiderosis, regardless of etiology, had higher histological activity of inflammation in liver tissue. More severe degrees of hepatosiderosis were detected in liver biopsies of patients with alcohol-associated liver diseases.

Conclusion. The high frequency of secondary hepatosiderosis detected in patients with chronic liver diseases of various etiologies indicates the need to improve treatment and diagnostic algorithms: conducting additional examinations to identify iron metabolism disorders, optimizing pathogenetic therapy.

Aim: to conduct a comprehensive analysis of the clinical-genetic database of patients with Wilson’s disease and to evaluate the possibilities of using it as a tool for epidemiological and clinical research.

Materials and methods. The study is based on data from 296 patients diagnosed with Wilson’s disease (WD), included in the clinical-genetic database for the period 2015–2025. The study involved a comprehensive assessment of results of clinical examinations of patients, including initial diagnosis and monitoring of their condition; laboratory test data, including molecular-genetic studies (performed using next generation sequencing and polymerase chain reaction); results of instrumental examinations.

Results. The analysis of the clinical genetic database of patients with Wilson’s disease included data on 296 patients: 120 males and 176 females. The age of the study participants ranged from 14 to 67 years, with a mean age of 30.0 ± 6.5 years. Among the examined patients, 281 (94.94 %) individuals reside in the Russian Federation.

Analysis of the distribution of patients by clinical forms of the disease revealed the following: abdominal form of WD was diagnosed in 140 (47.29 %) patients; neurological form — in 18 (6.09 %); mixed form — in 99 (33.45 %); asymptomatic form — in 39 (13.17 %) patients.

When studying the characteristics of disease onset, it was found that 67 (22.63 %) patients had no pronounced clinical manifestations at the time of diagnosis. Among them, 17 patients (25.37 % of those with asymptomatic onset) were diagnosed through family screening.

Molecular-genetic testing of the ATP7B gene was performed in 146 patients. Among the identified pathogenic variants, the most common was c.3207C>A (p.His1069Gln), detected in 114 (78.08 %) patients. The majority of patients (72.5 %) were compound heterozygotes, while rare variants of the ATP7B gene were found in 16.15 % of cases.

Additionally, an analysis of course in WD patients who had COVID-19 was conducted. The results showed that 41.1 % experienced worsening of neurological symptoms. Furthermore, 9.8 % of patients with initially asymptomatic WD developed the first clinical manifestations of the disease after COVID-19 infection.

Conclusions. The developed clinical-genetic database is an effective tool for studying WD, providing an informational basis for further epidemiological, clinical, and molecular genetic research.

Aim: to study the composition of the intestinal microbiota in patients with ulcerative colitis, focusing on its ability to produce functionally important metabolites.

Materials and methods. A metagenomic analysis of stool samples from patients with ulcerative colitis (n = 18) and a control group of healthy volunteers (n = 47) has been done using 16S ribosomal RNA sequencing.

Results. We observed decreased diversity in the gut microbiome of patients with ulcerative colitis; the Shannon index was lower in this group, indicating an uneven distribution of taxa compared to healthy volunteers. There were disproportions in the main phylotypes: a decrease in the proportion of Actinobacteria and Firmicutes, alongside an increase in Proteobacteria and Bacteroidota. We suppose that intensive protein and amino acid degradation could occur due to an increased proportion of proteolytic bacteria and bacteria producing indole, indole-acetic acid, phenol, bile acids, polyamines, and GABA in the intestines of patients with ulcerative colitis. Additionally, an increase in mucin-degrading bacteria was detected. On the contrary, the proportion of saccharolytic bacteria and butyrate producers decreased in patients with ulcerative colitis.

Conclusions. Patients with ulcerative colitis exhibited an imbalance in their intestinal microbiota composition, with increased proportions of bacteria involved in protein and amino acid metabolism and decreased saccharolytic bacteria, including butyrate producers.

Aim: to improve the surgical treatment outcomes for patients with chronic anal fissure through the new surgical ap proach application.

Materials and methods. A prospective study including 33 patients with chronic anal fissure undergoing a new surgical approach treatment was conducted. This approach involved the dissection of the internal and external anal sphincters, as well as the perianal tissues film from a thin, dense connective tissue film that envelops and fixes the lat ter structures, preventing the sphincter from fully relaxing and contracting. In 14 patients, the connective tissue film and surrounding tissues film were stained with aqueous dye — trypan blue 0.06 %, used in ophthalmic surgery for better fibrous tissue film identification. In 19 patients, the fissure was combined with a fistula originating from the fissure itself.

Results. The application of the new surgical approach in patients with chronic anal fissure results in complete sphincter’s relaxation and its contractile function restoration, significantly reducing the intensity of anal pain in postoperative period and creating conditions for surgical wound healing within acceptable time frames.

Conclusion. The new surgical approach aiming isolation of the anal sphincters from the connective tissue film and scars fully leads to the restoration and preservation of the sphincter function, thus enabling the complete avoidance of sphincterotomy in such patients.

Aim: to review the current literature on the potential link between Helicobacter pylori (H. pylori) infection and iron deficiency and vitamin B₁₂ deficiency anemia.

Key points. Published studies have shown that iron deficiency anemia of unknown cause may be due to H. pylori infection, especially in pediatric practice. This infection can lead to impaired iron absorption through various mechanisms. Eradicating H. pylori infection can contribute to restoring normal red blood cell parameters. Additionally, patients infected with H. pylori have lower blood levels of vitamin B₁₂ compared to uninfected individuals. The mechanisms contributing to impaired vitamin B₁₂ absorption in patients with H. pylori infection may be associated with the progression of multifocal atrophic gastritis, as well as the production of antibodies against parietal cells and intrinsic factor. Many national gastroenterology societies and consensus meetings recommend testing for H. pylori infection patients with iron deficiency anemia or B₁₂ deficiency anemia of unknown origin and, if positive, eradicating it.

Conclusion. There is a positive association between H. pylori infection and the development of unexplained iron deficiency anemia. The relationship between H. pylori infection and vitamin B₁₂ deficiency anemia has not been sufficiently studied and requires further research.

Aim: to demonstrate the utility of ultrasound in evaluating of Crohn’s disease with multiple extraintestinal manifestations after restorative proctocolectomy.

Key points: Patient S., a 40-year-old female, was admitted to the clinic presenting with frequent bloody stools, abdominal pain in left lower quadrant and fever. She had a history of ulcerative colitis diagnosed in 2005. In 2021, the disease was complicated by toxic megacolon requiring a colectomy and an end ileostomy. In 2022, the second stage of surgical treatment was performed: proctectomy with ileal pouch-anal anastomosis. In 2023, the patient developed extraintestinal manifestations: aphthous stomatitis, erythema nodosum, and left ankle arthritis. Examination revealed ultrasound signs of Crohn’s disease: significant thickening of the bowel wall (predominantly of the muscularis propria and submucosa) with loss of wall stratification, as well as pathological vascularization of the ileoanal anastomosis, indicating transmural inflammation. Ileoscopy revealed linear ulcers, and histology showed inflammatory infiltration extending to the muscular layer, confirming the diagnosis of Crohn’s disease. Therapy with ustekinumab was initiated with positive clinical response and disease remission.

Conclusion. Ultrasound has revealed signs of transmural inflammation of the ileal pouch and allowed to suspect Crohn’s disease, which has been subsequently confirmed by endoscopic and histological examinations.