Oxana Yurievna Zolnikova

Aim: to summarize current clinical guidelines and meta-analyses data, and to present the main statements of the Expert Council of the Russian Gastroenterological Association regarding the optimization of endoscopic diagnosis, morphological verification, pharmacotherapy, and management strategies for patients with gastroesophageal reflux disease (GERD) and Barrett’s esophagus. Key points. In the Russian Federation, GERD is a highly prevalent disease: according to a meta-analysis involving over 30,000 individuals, the frequency of heartburn and/or regurgitation occurring once a week or more is 25 %. Proton pump inhibitors (PPIs) represent the cornerstone drug class for the treatment of GERD. Rebamipide targets altered epithelial permeability and mucosal inflammation. Combination therapy with PPIs and rebamipide improves symptoms in patients with non-erosive reflux disease, leading to positive morphological changes in the esophageal mucosa and improved control of nocturnal esophageal acid exposure. Ursodeoxycholic acid (UDCA) may be added to GERD therapy in the presence of biliary reflux or reflux gastritis. The clinical significance of GERD is determined not only by its high prevalence, chronic relapsing course, and impaired quality of life, but also by its precancerous potential. In individuals with GERD, the prevalence of Barrett’s esophagus is approximately 7 %, while the incidence of adenocarcinoma and/or high-grade dysplasia in the presence of low-grade dysplasia is 1.73% annually. Risk factors for the development of Barrett’s esophagus include male sex, age over 50 years, frequent GERD symptoms, tobacco smoking, obesity, and a positive family history. The management of patients with Barrett’s esophagus requires strict adherence to endoscopic and histological diagnostic protocols. Long-term PPI pharmacotherapy remains the standard of chemoprevention against neoplastic progression, demonstrating superiority over surgical treatment. Timely screening of high-risk individuals and adherence to endoscopic surveillance intervals enable the detection of dysplasia and esophageal adenocarcinoma at early, treatable stages. Conclusion. The Expert Council members proposed algorithms for the treatment of acute GERD exacerbation and maintenance therapy, as well as for the diagnosis and surveillance of patients with Barrett’s esophagus, taking into account current evidence and principles of evidence-based medicine. The literature review and the proposed algorithms aim to provide informational support for general practitioners, internists, gastroenterologists, and endoscopists in order to improve the quality of healthcare delivery and ensure effective prevention of esophageal adenocarcinoma.

Potassium is the predominant intracellular cation and plays a fundamental role in maintaining membrane potential, cellular metabolism, enzyme activity, protein synthesis, acid–base homeostasis, and mitochondrial bioenergetics. Although hypokalemia is readily identified by decreased serum potassium concentration, serum potassium represents only a small fraction of total-body potassium stores and therefore may not accurately reflect intracellular potassium status. Consequently, chronic total-body potassium depletion and intracellular potassium deficiency may remain clinically unrecognized despite serum potassium concentrations within the reference range. Growing experimental and clinical evidence suggests that disturbances of potassium homeostasis are associated with multiple metabolic abnormalities involving the cardiovascular, neuromuscular, endocrine, renal, and gastrointestinal systems. Intracellular potassium depletion has been associated with mitochondrial dysfunction, oxidative stress, impaired insulin secretion and insulin sensitivity, metabolic alkalosis, chronic low-grade inflammation, and anabolic resistance. However, these relationships are complex and frequently bidirectional, indicating that potassium deficiency should be regarded as one component of an integrated metabolic network rather than an isolated pathogenic mechanism. This narrative review critically summarizes current evidence regarding the physiological regulation of potassium homeostasis, distinguishes hypokalemia from total-body potassium depletion and intracellular potassium deficiency, and discusses the mechanisms through which potassium depletion may contribute to systemic metabolic dysfunction. Particular attention is given to the clinical manifestations, diagnostic evaluation, and current therapeutic approaches to disorders of potassium homeostasis. Finally, important knowledge gaps are highlighted, including the need for reliable biomarkers of intracellular potassium deficiency and prospective studies evaluating whether correction of chronic potassium depletion improves long-term metabolic and clinical outcomes beyond normalization of serum potassium concentration.

Aim: to present the results of an interdisciplinary international expert council on addressing the challenges of managing patients with non-alcoholic (metabolic dysfunction-associated) fatty liver disease in connection with the creation of a new nomenclature, the definition of diagnostic criteria, and the development of approaches to the diagnosis and treatment of fatty liver disease. Key points. The key role of metabolic dysfunction in non-alcoholic (metabolic dysfunction-associated) fatty liver disease has been proven. Therefore, in the nomenclature, non-alcoholic fatty liver disease (NAFLD) has been replaced by metabolic dysfunction-associated fatty liver disease, and non-alcoholic steatohepatitis has been replaced by metabolic dysfunction-associated steatohepatitis. It is noted that, according to research, the prevalence of fatty liver disease in Russia is high: one-third of patients seeking primary care have this diagnosis. The results of a study of two incretin mimetics, semaglutide and tirzepatide, are presented, along with an opinion on their rational combination with ursodeoxycholic acid. The comorbidity of fatty liver disease with cardiovascular, endocrine, and oncological diseases, chronic kidney disease, and other conditions is discussed. Conclusion. The expert council included leading specialists: gastroenterologists-hepatologists, cardiologists, internists, and endocrinologists. There were confirmed that treatment for fatty liver disease should be comprehensive and integrated into the overall concept of metabolic health. Algorithms for diagnosis and personalized treatment of fatty liver disease have to be developed for the Russian medical community.

Small intestinal bacterial overgrowth (SIBO) refers to an abnormal increase in the number of bacteria in the small intestine and is observed in various diseases. SIBO can also develop after long-term use of proton pump inhibitors (drug-induced SIBO), bariatric surgery, gastrectomy, and other surgeries (postoperative SIBO). The aim of this narrative review is to summarize all of the published information on the treatment of SIBO in as much detail as possible and present it separately for each specific disease and intervention associated with SIBO. The most extensively studied drug for the treatment of SIBO is rifaximin. It eliminates SIBO in 63% of cases; however, most studies lack a control group. Small RCTs assessing the effects of this antibiotic on SIBO have reported conflicting results, and a meta-analysis showed no effect. A large RCT is required to verify the results of uncontrolled studies. Neomycin and norfloxacin showed efficacy in the treatment of SIBO in single RCTs, with elimination rates of 20 and 100%, respectively. Ciprofloxacin, rifamycin, metronidazole, and other antibiotics, as well as ursodeoxycholic acid, showed positive effects for the treatment of SIBO, but only in uncontrolled studies or in comparison with rifaximin or other drugs. The reported elimination rates were 54%, 67%, 79%, and 75%, respectively. Eradication therapy for Helicobacter pylori infection eliminated SIBO at a rate of approximately 70%. Probiotics have been tested for treatment of SIBO in various diseases. VSL#3 and Saccharomyces boulardii CNCM I-745 were effective in RCTs, with elimination rates of 58% and 80%, respectively. In conclusion, when selecting SIBO treatment regimens, those that have demonstrated the greatest efficacy for a specific concomitant disease should be preferred, despite the generally low level of evidence supporting these approaches in most cases.

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.

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 examine current evidence on the key metabolic alterations that reflect the major pathogenetic axes of metabolic syndrome (MS) and to assess their potential for the diagnosis and stratification of MS. Key points. The review highlights five major metabolomic pathogenetic axes of MS: anabolic resistance, mitochondrial dysfunction, systemic inflammation, insulin resistance, and lysosomal insufficiency. Each represents an essential pathogenic link influencing the development of MS complications. Characteristic alterations of low-molecular-weight metabolites (such as amino acids and organic acids) and lipids identified through modern metabolomic analytical methods are described for each axis, and their clinical significance is discussed. Special attention is given to the role of combined metabolite panels, which improve early diagnosis of MS and prediabetes, allow risk stratification for complications (type 2 diabetes, atherosclerosis, nonalcoholic fatty liver disease, etc.), and enable monitoring of treatment effectiveness. It is noted that metabolomic biomarkers possess high diagnostic and prognostic value, complementing standard clinical indicators. Evidence is presented showing that integrating metabolomic data with clinical parameters increases diagnostic accuracy (for example, combining metabolomic markers with the glucose tolerance test improves its predictive value). The development of integrated metabolomic indices (such as MetSCORE) provides high accuracy in identifying MS (AUROC ~0.9). Metabolomic studies confirm the heterogeneity of MS and allow subclassification according to predominant pathophysiological disturbances, opening prospects for precision medicine. Conclusion. Thus, the metabolomic approach substantially expands the possibilities for diagnosis and personalized therapy in patients with MS. It enables the detection of latent metabolic disturbances at the preclinical stage of disease, complementing routine diagnostic methods. Implementation into clinical practice requires standardization of metabolomic analytical protocols, validation of metabolomic biomarkers, and integration of multi-omics approaches, which will ensure the reproducibility of results and their broad application in medicine.

Background. On May 20, 2025, a Council of Experts was held in Moscow. The aim of the meeting was to discuss current understanding of the pathogenesis and clinical significance of biliary sludge. Key points. The following definition of biliary sludge has been established: echogenic fluid within the gallbladder cavity without a clear acoustic shadow, which shifts with changes in body position without fragmentation into fine particles. The absence of an acoustic shadow distinguishes sludge from gallstones. The International Consensus of Experts in Pancreatobiliary Diseases (2023) proposed distinguishing between biliary sludge, microlithiasis (echogenic stones ≤ 5 mm with acoustic shadowing), and larger gallstones in the gallbladder and/or ducts. When managing a patient with biliary sludge, it is important to identify the underlying disease or condition predisposing to the development of sludge. The most important factors are genetic and demographic ones, dietary habits, conditions associated with rapid weight loss, and medications that affect bile composition or gallbladder function. Biliary sludge can be asymptomatic, with dyspeptic symptoms, or lead to complications typical of gallstones. Some data suggest that sludge is associated with idiopathic pancreatitis. The primary diagnostic method for sludge is transabdominal ultrasound. If clinical manifestations characteristic of cholelithiasis complications develop, the common bile duct becomes dilated, or stones are detected in the common bile duct, additional diagnostic testing using magnetic resonance cholangiopancreatography and/or endoscopic ultrasound is recommended. Clinical observations also suggest the potential for sludge to transform into gallstones. However, the view that biliary sludge is the first stage of gallstone disease was not shared by all Council members due to the high incidence of reversible sludge. At this stage, it is proposed to consider biliary sludge more as a risk factor or a specific form of gallstone disease. The only medication shown to dissolve biliary sludge is ursodeoxycholic acid. Conclusion. The Expert Council adopted a resolution, the provisions of which emphasize the need for accurate diagnosis, individual assessment of risk factors for the development of biliary sludge, the feasibility of developing a scoring system for assessing biliary sludge, determining the location of ursodeoxycholic acid therapy for sludge, and the need to supplement the Clinical Guidelines of the Russian Ministry of Health for the diagnosis and treatment of cholelithiasis with sections devoted to the diagnosis and treatment of biliary sludge.

Aim: to present key data on the role of gastrointestinal motility dysfunction in the pathogenesis of functional and organic diseases and the importance of acotiamide in the correction of these disorders and to introduce a resolution of the expert council of the Russian Gastroenterological Association and the Russian Society of Neurogastroenterology and Motility.Key points. Gastrointestinal motility dysfunction represents a key pathogenetic factor that determines the development and clinical course of a broad range of diseases. Functional dyspepsia and gastroesophageal reflux disease are highly prevalent conditions, and motility impairments, such as impaired gastric accommodation and delayed gastric emptying, account for their frequent co-occurrence in the same patient. For the pharmacotherapy of these diseases, drug products with a prokinetic effect are of substantial importance. Acotiamide has a proven prokinetic effect, improves gastric accommodation and emptying, and reduces the severity of symptoms of postprandial distress syndrome and overlapping manifestations of gastroesophageal reflux disease. In a multicenter Russian study, a response to acotiamide therapy was noted in 74.1 % of patients with postprandial distress syndrome versus 51.9 % in the placebo group (p < 0.001). Dysmotility and its association with gastrointestinal symptoms in H. pylori-associated dyspepsia, reflux gastritis, and autoimmune gastritis, as well as therapeutic measures to correct these disorders and alleviate symptoms, require further research.Conclusion. Further research into motility disorders of the gastrointestinal tract will help to elucidate the pathogenesis of a number of functional and organic gastroenterological diseases. The body of evidence from international and local studies confirms the clinical efficacy and safety of acotiamide. Its inclusion in national clinical guidelines justifies the use of the drug product in patients with functional dyspepsia and gastric motility disorders, including cases in combination with gastroesophageal reflux disease.

Aim: to investigate the metabolomic profile of patients with alcoholic liver disease and non-alcoholic fatty liver disease.Materials and methods. The present study included patients diagnosed with non-alcoholic fatty liver disease (NAFLD) (n = 44), patients diagnosed with alcoholic liver disease (ALD) (n = 40) and 14 healthy volunteers. The level of metabolites in the blood serum were determined via high-performance liquid chromatography and tandem mass spectrometry.Results. In this study, a cross-sectional targeted metabolomic analysis of 96 serum metabolites was performed in patients. Statistical analysis using the principal component method identified six main factors, comprising metabolites from various metabolic pathways. Comparative analysis between patient groups and the control group revealed statistically significant differences in the metabolic activity of individual factors, collectively reflecting alterations in the metabolomic profile. Levels of acylcarnitines, uridine, metanephrine, asymmetric and total dimethylarginine were elevated in patients with NAFLD and ALD compared to the control group. Carnitine, short chain acylcarnitines, valine, leucine, lysine, and alanine were significantly higher in patients with NAFLD compared to those with ALD. In contrast, levels of tyrosine, epinephrine, and methionine were significantly increased in ALD patients compared to both NAFLD patients and healthy volunteers. Among patients with liver cirrhosis (both ALD and NAFLD), there was a noticeable trend toward altered metabolic activity of factors correlating with liver failure indicators and the FIB-4 index. As liver cirrhosis progressed, statistically significant changes in metabolite levels were observed across Child — Pugh classes, taking into account hypocoagulation, hypoalbuminemia, hyperbilirubinemia, the presence of ascites, and hepatic encephalopathy.