In 2026, the fifth revision of the Rome criteria (Rome V) was published, reflecting the current concept of disorders of gut–brain interaction (DGBI) as an independent group of diseases associated with impaired visceral sensitivity, dysregulation of the gut-brain axis, and immune-inflammatory and psychophysiological mechanisms. The relevance of this review is determined by the high prevalence of DGBI, their frequent overlap, their substantial impact on patients’ quality of life, and the need to adapt new international diagnostic approaches to routine gastroenterological practice. The particular importance of Rome V is associated with the transition from a predominantly symptom-oriented description of functional disorders to a clinical and instrumental diagnostic model based on the combination of symptom criteria, criteria for excluding organic pathology, and modern instrumental standards. Publications were excluded if the full text was unavailable, if they were not relevant to DGBI, if they duplicated previously published data, or if their findings could not be correlated with current diagnostic criteria. The Lyon Consensus 2.0 and the Chicago Classification v4.0 are now considered essential components in the diagnosis of functional esophageal disorders. Functional impedance planimetry significantly improves the diagnostic specificity for functional dysphagia. In irritable bowel syndrome (IBS), the symptom of “discomfort” and a lower symptom-frequency threshold have been reinstated, which is expected to improve case identification in populations where pain is perceived or reported less intensely. Retrograde cricopharyngeal dysfunction (R-CPD), commonly referred to as the inability-to-burp syndrome, has been recognized as a distinct clinical entity with specific diagnostic and therapeutic criteria.

Helicobacter pylori infection represents a global public health problem, as the pathogen is associated with the development of gastric and duodenal ulcer disease, gastritis, gastric adenocarcinoma, and MALT lymphoma. The efficacy of eradication therapy is declining due to increasing antibiotic resistance, necessitating a revision of therapeutic strategies. The article presents the mechanisms of H. pylori survival in the aggressive gastric environment, its pathogenicity factors, current data on the mechanisms of action of the main antibacterial drugs used for treating the infection in Russia and worldwide: clarithromycin, metronidazole, amoxicillin, tetracycline, levofloxacin, rifabutin, bismuth tripotassium dicitrate, as well as the mechanisms of resistance development for these agents. Single-phase and two-phase eradication therapy regimens are examined in detail according to the 2022 Russian clinical guidelines and the Maastricht VI consensus, including first-line regimens: standard triple therapy, bismuth-enhanced and non-bismuth-enhanced, concomitant, sequential, hybrid, reverse hybrid, bismuth-based quadruple therapy, high-dose dual therapy, and vonoprazan-based dual therapy. For second-line therapy, regimens including levofloxacin and rifabutin are reviewed, and the principles of individualized therapy are outlined. A brief clinical and pharmacological characterization of each drug is provided. The reasons for failures in finding the optimal H. pylori eradication regimen are also analyzed. The World Health Organization's changing stance toward H. pylori as a pathogen requiring the development of new antibacterial drugs is mentioned. The concepts of the "post-antibiotic era" and the renaissance of antibiotics are discussed. The concluding section examines the risks associated with the choice of first-line therapy regimens and the drugs included in them. It is concluded that with proper assessment of H. pylori resistance, triple pharmacotherapy with or without bismuth is a relatively effective and safe eradication regimen for regions of the Russian Federation. Consideration of clarithromycin metabolism characteristics and adverse drug reactions allows for rational selection of first-line therapy that accounts for the physiological and clinical features of patients with H. pylori infection.

Introduction. The declining efficacy of the standard regimens for the eradication of Helicobacter pylori (H. pylori) and the development of adverse events when prescribed antibacterial therapy substantiates the search for strain-specific adjuvant approaches that can improve the tolerability and efficacy of treatments.

Aim. To systematize data on the effect of Limosilactobacillus reuteri (L. reuteri) DSM 17648 on the efficacy and safety of H. pylori eradication therapy.

Materials and methods. In accordance with PRISMA 2020 statement, a comprehensive literature search was conducted using MEDLINE/PubMed, Embase, Cochrane Library, Scopus, and the Russian Science Citation Index (RSCI) to identify relevant studies published between January 1, 2007 and March 10, 2026. The systematic review and meta-analysis protocol was entered into the PROSPERO database (CRD420261355068). The meta-analysis included the studies of L. reuteri DSM 17648 used as an adjuvant treatment to the standard eradication therapy, as well as studies exploring its effect on H. pylori bacterial load.

Results. Ten studies were included; the analysis of the efficacy of adjuvant therapy included seven comparative studies involving 1,217 patients. There was a significant increase in eradication efficacy as compared with the control group when L. reuteri DSM 17648 was given as part of H. pylori therapy (RR 1.088, 95% CI: 1.029–1.150; p = 0.003). The eradication rate was 93.6% versus 83.5% in the control group. The L. reuteri DSM 17648 group demonstrated a lower overall rate of incidence adverse events (RR 0.708, 95% CI: 0.591–0.850; p < 0.001), including the risk of diarrhea (RR 0.586, 95% CI: 0.387–0.886; p = 0.011). A separate analysis showed that the groups receiving L. reuteri DSM 17648 had a significant reduction in bacterial load as measured by the 13C-urea breath test (standardized mean difference: -0.416, 95% CI -0.749 to -0.083; p = 0.014).

Conclusions. This strain-specific systematic review and meta-analysis demonstrated that supplementation of L. reuteri DSM 17648 to H. pylori treatment regimens was associated with higher eradication efficacy and an improved safety profile.

This article presents case studies illustrating the management of patients with multimorbidity and confirmed Helicobacter pylori infection, who were recommended the Lactobacillus reuteri DSM 17648-based metabiotic. Particular attention is paid to the situations when the standard antibacterial eradication therapy was challenging or impossible due to contraindications, a high risk of side effects, or drug intolerance. The first clinical observation shows a patient treated with terbinafine for onychomycosis, who developed a complication in the form of mild hepatotoxicity. The Lactobacillus reuteri DSM 17648 metabiotic was chosen as an alternative to conventional therapy for the concomitant Helicobacter pylori­-associated gastritis, with good treatment outcomes. The second observation describes a case of drug-induced hepatotoxicity in a patient with liver disease, who received Helicobacter pylori eradication therapy. Due to discontinuation of antibiotics as part of the eradication regimen and introduction of the metabiotic into the treatment plan, the laboratory parameters returned to normal, and Helicobacter pylori eradication was achieved. The third case is a report of toxicoderma in a patient with Helicobacter pylori infection under treatment with bismuth quadruple therapy (BQT). The successful eradication of Helicobacter pylori without adverse events was achieved through replacement of the bismuth drug with the metabiotic. These observations demonstrate practical approaches to personalized therapy that expands patient management options with the introduction of Lactobacillus reuteri DSM 17648 in the therapy regimen when standard treatments are not possible. The options of using Lactobacillus reuteri DSM 17648 in highrisk patients and its potential role in preventing reinfection after treatment are discussed.

The review article systematises scientific data extracted from international and domestic electronic libraries (PubMed, Scopus, eLIBRARY.RU, RSCI). The information search was conducted using the following keywords: “rebamipide”, “Helicobacter pylori eradication”, “gastroprotection”, “antibiotic resistance”, and “randomised controlled trials”. At the initial stage, 134 publications were selected. After verification against the screening criteria, 86 studies were retained. These included results from randomised controlled trials, longitudinal studies, and cohort studies. A qualitative analysis was performed on 71 articles, while a quantitative synthesis included 4 meta-analyses aggregating data from 34 primary studies. The “Introduction” section is based on 22 sources covering epidemiology and resistance trends, while the “Conclusion” section draws on 47 publications detailing the inhibition of bacterial adhesion, NF-κB modulation, cytotoxicity protection against the CagA toxin, and acceleration of mucosal repair. A total of 16 studies were excluded from the analysis due to the use of outdated treatment regimens or non-compliance with current diagnostic criteria. The final systematic review includes 57 relevant articles. It was found that under conditions of steadily increasing antibiotic resistance— particularly to clarithromycin— the adjuvant use of rebamipide significantly enhances eradication efficacy (up to 82–96%). The drug stimulates prostaglandin synthesis, restores epithelial tight junctions, suppresses oxidative stress, and reduces the expression of pro-inflammatory cytokines. The analysis confirms that the findings align with international consensus statements and the recommendations of the Russian Gastroenterological Association. Rebamipide demonstrates a favourable safety profile: it minimises the incidence of dyspeptic reactions, normalises epithelial permeability, accelerates the healing of erosive and ulcerative lesions, and promotes the regression of intestinal metaplasia in the post-eradication period. This fully justifies its integration into current clinical protocols.

Introduction. Ursodeoxycholic acid (UDCA) significantly reduces markers of cytolysis and cholestasis in patients with nonalcoholic fatty liver disease (NAFLD); however, its role in improving non-invasive markers of steatosis and fibrosis remains a matter of discussion.

Aim. To evaluate the effect of UDCA therapy on changes in non-invasive calculated indices of steatosis and fibrosis in patients with NAFLD.

Materials and methods. This systematic review and meta-analysis was conducted in accordance with the PRISMA 2020 guidelines. The study protocol was prospectively registered in the international PROSPERO database (CRD420261396761). MEDLINE/PubMed, Embase, the Cochrane Library, Scopus, and the Russian Science Citation Index were searched through February 3, 2026. Studies evaluating changes in non-invasive markers of steatosis (FLI and St-index) or fibrosis (FIB-4, NFS, APRI, and FibroTest) in adult patients with NAFLD receiving UDCA therapy were included. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated for the quantitative synthesis.

Results. Eight studies involving a total of 729 patients were included in the meta-analysis. UDCA therapy was associated with statistically significant reductions in FLI (SMD = −0.58; 95% CI: −0.75 to −0.41; n = 7), FIB-4 (SMD = −0.63; 95% CI: −1.15 to −0.11; n = 4), APRI (SMD = −0.49; 95% CI: −0.93 to −0.05; n = 3), and FibroTest (SMD = −0.07; 95% CI: −0.13 to −0.01; n = 1). A trend towards improvement was observed for NFS, although the result did not reach statistical significance (SMD = −0.62; 95% CI: −1.32 to 0.08; n = 4). An additional pooled analysis of the full study set, with avoidance of double-counting, demonstrated a statistically significant reduction in non-invasive fibrosis indices after UDCA therapy (SMD = −0.16; 95% CI: −0.21 to −0.11; n = 7).

Conclusion. UDCA therapy in patients with NAFLD is associated with statistically significant reductions in non-invasive calculated indices of steatosis (FLI) and fibrosis (FIB-4 and APRI).

Metabolic dysfunction-associated steatotic liver disease (MASLD) is an umbrella term encompassing a spectrum of conditions ranging from steatosis to metabolic dysfunction-associated steatohepatitis (MASH), liver fibrosis, and cirrhosis associated with systemic metabolic dysfunction. The prevalence of MASLD continues to rise steadily and is closely linked to cardiovascular morbidity and mortality, making it one of the most relevant chronic noncommunicable diseases. This review analyzes data from clinical trials on the efficacy of essential phospholipids (EPL) as monoand adjuvant therapy for MASLD, taking into account the characteristics of their mechanisms of action, effects, and potential for pharmacological enhancement. The review was conducted using a narrative (non-systematic) approach based on a literature search performed in Russian and international specialized databases and clinical trial registries. EPL and their principal active component, 1,2-dilinoleoylphosphatidylcholine, enhance the stability and fluidity of cell membranes, support the transmembrane processes, reduce the severity of mitochondrial dysfunction and oxidative stress, inhibit lipogenesis, facilitate bile acid efflux, slow the activation of hepatic stellate cells, and reduce local inflammation and hepatocyte apoptosis. In addition to their own hepatotropic activity, EPL may also act as a pharmacological enhancer by increasing bioavailability, prolonging systemic circulation, and potentiating the effects of other drugs. When used as monotherapy for MASLD/MASH, EPL exert an anti-cytolytic effect, may reduce hepatic steatosis (assessed by ultrasonography), and improve lipid profile parameters; however, the available evidence is limited by the small statistical power and design flaws of the clinical trials. Special attention has been directed toward the potential use of EPL as part of combination pharmacotherapy for MASLD in comorbid patients. As evidenced by clinical trials, the addition of EPL to standard treatment regimens can enhance therapeutic efficacy regarding morphological liver changes, marker enzyme levels, lipid metabolism parameters, and patients’ quality of life.

Introduction. Currently, views on the potential for active interaction between adaptive and innate immunity are being revised, making the study of T-cell immunity parameters in patients with viral and parasitic pathologies of great interest.

Aim. To determine blood T-cell immunity indicators in patients with chronic viral hepatitis C (CHVHC), in patients with Opisthorchis felineus (O. felineus) infection, and in healthy individuals.

Materials and methods. We examined 67 patients with genotype 1 CHVHC, 41 patients with chronic opisthorchiasis, and 29 apparently healthy individuals. A study of the subpopulation composition of T-helper, cytotoxic T-cells, and T-regulatory cells (T-reg) was performed in all subjects using direct immunofluorescence of whole peripheral blood with monoclonal antibodies on a Navios flow cytometer (Beckman Coulter, USA). Diagnosis of chronic hepatitis C and opisthorchiasis was performed using standard clinical, laboratory, and instrumental methods.

Results. The levels of effector memory T-helper cells and TEMRA T-helper cells in the blood were significantly higher in patients with chronic hepatitis C compared to controls and patients with opisthorchiasis. Patients with chronic hepatitis C had a reduced proportion of naive T-killers in the blood compared to healthy individuals and patients with opisthorchiasis. In the groups with O. felineus invasion and chronic hepatitis C, higher levels of total T-reg, the proportion of naive T-reg, central memory and effector memory T-reg were recorded in the blood.

Conclusion. In patients with O. felineus infection and chronic hepatitis C, there was a significant increase in the levels of regulatory cells, the proportion of naive T-reg cells, central memory T-reg cells, and effector memory T-reg cells compared to healthy individuals. Blood levels of T-helper and T-killer cells did not differ significantly in patients with chronic hepatitis C and opisthorchiasis compared to the control group.

The review discusses the clinical significance of hyperammonemia and hyperammonihistia (tissue ammonia accumulation) in non-alcoholic (metabolic dysfunction-associated) fatty liver disease. Elevated blood and tissue ammonia levels can be observed already at pre-cirrhotic stages (in 40–78% of patients) and are not only a consequence but also a factor of disease progression, making it an independent pathogenetic target. Hyperammonemia exacerbates hepatocellular injury (through impairment of autophagy and epigenetic suppression of enzymes of the ornithine cycle), contributes to the development of sarcopenia, fatigue, cognitive and other neuropsychiatric impairments, and worsens the course of comorbid conditions. Key non-pharmacological approaches include the Mediterranean diet with adequate protein intake and regular physical activity combining aerobic and resistance exercise. From a pathogenetic pharmacotherapy perspective, the use of L-ornithine L-aspartate (LOLA) is justified, as it activates the urea cycle in the liver and the glutamine pathway in skeletal muscle. By reducing intracellular ammonia concentrations, LOLA helps alleviate mitochondrial dysfunction, restore autophagic processes, and slow the activation of hepatic stellate cells, which may in turn slow down the progression of steatosis, inflammation, and fibrosis. Course administration of LOLA at doses of 9–12 g per day for at least 12 weeks has been shown to reduce ammonia levels, decrease steatosis, improve cognitive function, enhance exercise tolerance, and improve patients’ quality of life. The experts emphasize that the decision to initiate therapy may be based on clinical manifestations (hepatogenic weakness, cognitive impairment, sarcopenia), even in the absence of routine monitoring of blood ammonia levels. The review was conducted in a narrative fashion without the use of systematic methodology. A targeted search of Russianand English-language publications was carried out using PubMed, eLIBRARY.RU, the Cochrane Library, and other databases.

The liver is a multifunctional organ that is central to regulating physiological processes including metabolism, detoxification, protein synthesis, and immune response. Liver diseases represent a wide array of pathological changes characterized by hepatocyte injury and hepatic stellate cells (HSC) activation, which cumulatively impair liver function and disrupt its architecture. Annually, liver diseases cause approximately 2 million deaths and account for 4% of global mortality. Chronic liver diseases typically arise from hepatitis B virus (HBV), and hepatitis C virus (HCV) infections, alcohol consumption, along with a rising incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) globally. Modern diagnosis of liver diseases typically requires a combination of clinical presentation, specific biomarkers, and liver biopsy. Currently, pathogenetic management of liver diseases largely focuses on cause elimination, liver function normalization, and symptom alleviation. Conventional treatments are often limited by adverse effects, high costs, and insufficient efficacy, prompting the search for alternative therapeutic strategies. Phytotherapy exploiting plant bioactive compounds (e.g., flavonoids, polyphenols, and alkaloids) offers a promising approach in harnessing the hepatoprotective, antioxidant, anti-inflammatory, and antifibrotic properties of herbal medicines. These multitargeted properties have the capability to combat oxidative stress and inflammation while promoting liver regeneration. Recent advances in medicine emphasize the synergy between phytotherapy and conventional drug strategies, with herbal medicines proving eventually more effective in restoring and stabilizing lipid and liver profiles. Integration of phytotherapy into conventional medicine has the potential to revolutionize the treatment of liver diseases, particularly in resource-limited settings.

Introduction. The review covers the epidemiology, pathogenesis, clinic, diagnosis, and treatment of polysyndromic nonalcoholic fatty liver disease (NAFLD) associated with obesity, type 2 diabetes, and cardiovascular pathology.

Aim. To assess the key pathogenetic links of cardio-reno-hepato-metabolic syndrome in patients, as well as the therapeutic efficacy of dual-incretin drugs, such as tirzepatid and its domestic analogue sejaro.

Materials and methods. The search for literature sources was carried out in the PubMed and Google Scholar databases. The selection of publications was carried out on the principle of open free access, on the analysis of abstracts and assessment of relevance.

Results. 60 articles were selected for the review: 5 Russian-language and 55 foreign sources. Most publications reflect an increase in the global burden of NAFLD due to an increase in the incidence of type 2 diabetes and obesity, in the pharmacological correction of which double agonists of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), such as tirzepatid and its analogue sejaro, which are effective for weight loss, fibrosis regression and resolution of Nonalcoholic Steatohepatitis (NASH), as well as for the complex treatment of chronic metabolic diseases outside of traditional diabetes care.

Conclusions. Based on a large number of clinical trials, the review evaluated the possibilities of outpatient drug therapy for NAFLD, focused on the use of GLP-1 and GIP agonists, as well as available pharmacological drugs with a dual mechanism of action of GLP-1/GIP – tirzepatide and its domestic analogue sejaro. At the same time, sejaro shows distinct effects on pathogenic metabolic dysregulation, inflammation and fibrosis.

A duet of non-alcoholic fatty liver disease (NAFLD) / metabolically associated fatty liver disease (MAFLD) and hyperammonemia in patients with metabolic dysfunction is still insufficiently studied, and elevated ammonia levels in this patient population remain an underestimated pathogenetic factor in routine clinical practice. This article presents two clinical observation reports demonstrating the role of hyperammonemia in the clinical picture of NAFLD/MAFLD in female patients of different ages and metabolic status, as well as the efficacy of introduction of L-ornithine-L-aspartate (LOLA) in the combination therapy regimen. Observation report 1: A 65-year-old female patient with MAFLD, metabolic dysfunction (obesity, diabetes), laboratory-confirmed cytolysis, and verified hyperammonemia (ammonia 190 μmol/L). A 12-week LOLA treatment resulted in normalization of ammonia levels (to 56 μmol/L), regression of cytolysis syndromes, and improvement of inflammatory and metabolic parameters. Observation report 2: A 42-year-old female patient with NAFLD/MAFLD, type 2 diabetes, and clinical signs of minimal hepatic encephalopathy (the time to complete the number connection test was 52 seconds). The 3-month treatment with LOLA resulted in improvement of mental status (the time to complete the number connection test was 37 seconds) and normalization of cytolysis and glycemia indicators. Key conclusion: Hyperammonemia is a clinically significant but often underdiagnosed component of NAFLD/MAFLD, and elevated ammonia levels in this patient population remain an underestimated pathogenic factor in routine clinical practice. Its correction with LOLA improves laboratory, cognitive, and functional parameters even without mandatory measurement of ammonia in blood.

Helicobacter pylori (H. pylori) infection affects 30–50% of the population in developing countries, reaching up to 90% in some regions. The infection is associated with chronic gastritis, peptic ulcer disease, gastric cancer, and MALT lymphoma. Standard eradication regimens (e.g., triple therapy) demonstrate declining efficacy (71–74.8%) due to antibiotic resistance and high rates of adverse effects (up to 50% of patients). The aim of this review was to evaluate the potential of probiotics – particularly multistrain formulations – as an adjunct therapy to a standart H.pylori eradication scheme. A narrative review of the current literature was conducted, including systematic reviews, meta-analyses (including 19 randomized controlled trials with n = 2 730), and clinical studies (including retrospective and double-blind, placebo-controlled trials), to evaluate the efficacy and safety of probiotic support. Multistrain probiotics (e.g., Lactobacillus acidophilus / Bifidobacterium animalis or 8-strain mixtures) significantly improve eradication rates (up to 90% vs 70% in controls) and reduce adverse effects, especially antibiotic-associated diarrhea. A meta-analysis of 40 studies (n = 8 924) showed a 14% increase in successful eradication with probiotics (relative risk 1.140, 95% CI 1.101–1.180; p < 0.001). Multistrain products exert synergistic effects via multiple mechanisms: immune modulation, antimicrobial activity (via short-chain fatty acids), mucosal barrier protection, competitive inhibition of H. pylori, and microbiota restoration. Clinical trials (e.g., with the multistrain probiotic Bac Set) confirm better stool normalization and microbiota preservation compared to monostrain options. Multistrain probiotics represent a promising strategy to optimize H. pylori eradication. They enhance treatment efficacy, reduce adverse effects, and support gastrointestinal microbiota recovery. Current guidelines (e.g., Maastricht VI/Florence and World Gastroenterology Organisation, 2023) endorse their use for minimizing side effects and improving outcomes, especially in combination with bismuth-containing quadruple therapy.

Inflammatory bowel diseases (IBD) – ulcerative colitis (UC) and Crohnʼs disease (CD) represent a significant medical and social problem, with the number of patients continuing to rise worldwide. Mesalazine (5-aminosalicylic acid, 5-ASA) has for several decades held a leading position in the pharmacotherapy of both conditions. However, the evidence accumulated to date indicates that its efficacy differs fundamentally between UC and CD, and mesalazine has been excluded from clinical guidelines for CD both in Russia and internationally. This review focuses on the etiology, pathogenesis, and classification of IBD; the history of mesalazineʼs development and its mechanisms of action; the characteristics of its dosage forms; and a comparative analysis of the composition of enteric coatings designed to release mesalazine either in the small intestine – typically affected in CD – or in the large intestine, affected in UC. Thus, in the manufacture of enteric coatings for medicinal products whose active substance is intended to be released in the small intestine, a number of pH-dependent polymers are used, among which the most widely applied is a copolymer of methacrylic acid and ethyl acrylate [1:1]. Release of active substances in the large intestine is achieved through the use of enteric coatings based on a copolymer of methacrylic acid and methyl methacrylate [1:1]. On the Russian pharmaceutical market, mesalazine formulations are available with both types of polymers, which was relevant when the drug was used in the treatment of Crohn’s disease and ulcerative colitis. At present, the restriction of mesalazine use in Crohn’s disease raises the question of the appropriateness of using mesalazine in enteric dosage forms with the methacrylic acid-ethyl acrylate copolymer [1:1] for any indications. Current clinical guidelines on IBD are also examined with regard to whether the mesalazine preparations registered in the Russian Federation are suitable for use in CD and UC.

Abdominal pain is a fairly common clinical problem encountered by clinicians. The causes of abdominal pain can be varied (both functional and organic). Abdominal pain is a fairly common clinical problem and is a serious issue in internal medicine and gastroenterology. Abdominal pain is the primary symptom of irritable bowel syndrome (IBS) and is primarily associated with intestinal smooth muscle spasm. However, abdominal pain caused by spasm can also occur with other conditions, such as biliary system disorders, specifically functional disorders of the gallbladder and sphincter of Oddi, and painful colonic spasms associated with IBS-like symptoms associated with underlying organic bowel pathology in remission (diverticular disease, inflammatory bowel disease in remission, and others). Antispasmodics are the drugs of choice for abdominal pain with a spastic component. The domestic pharmaceutical market offers various classes of antispasmodics, including selective calcium channel blockers. One such selective calcium channel blocker is otilonium bromide, which is widely used worldwide. It is effective, well-tolerated, and superior to placebo in reducing symptoms and preventing pain recurrence in patients with both IBS and other intestinal spasticity. The drug’s selective action and low intestinal absorption result in minimal side effects and the potential for otilonium bromide use in patients with comorbidities, including long-term use. This article presents two clinical cases of abdominal pain: a female patient with a long history of IBS and a patient with uncomplicated diverticular disease with IBS-like manifestations. These cases highlight the potential use of otilonium bromide.

Disorders of the intestinal microbiocenosis are considered to be one of the pathogenetic mechanisms of the occurrence and progression of not only diseases of the gastrointestinal tract, but also other diseases, exactly oncological, allergic, autoimmune, dermatological, neurological, neuropsychiatric and metabolic disorders. Modern methods, in particular, genomic sequencing, have revealed a large number of previously unknown species and genera of the intestinal microbiota, the role of which is only beginning to be clarified. In this regard, the metabolic activity of the microbiota is currently becoming increasingly important. The main metabolites of a healthy microbiota are short-chain fatty acids, which have metabolic and regulatory effects on both the host and the microbiota itself. There are various tools for correcting the microbiota, such as probiotics, prebiotics, and metabiotics. The combination of probiotics and prebiotics in symbiotics aims to improve their properties. This review focuses on the combination of the metabiotics calcium lactate and the prebiotics inulin and oligofructose. This combination can be considered as a separate subclass of agents metaprebiotic with a synergistic effect on the microbiota. The article examines the experimental effect of calcium lactate on colonization resistance, the protective effect on the normal microbiota, and the rate of restoration of the host microbiota in antibiotic-induced dysbiosis in animals. The article also evaluates the effect of a metaprebiotic on the metabolic function of the microbiota in patients with functional bowel disorders. The clinical efficacy of metaprebiotic use on symptoms and stool frequency has been demonstrated in patients with functional bowel disorders of different ages, as well as in dermatological diseases.

The relevance of this observation is due to the growing problem of morbid obesity and metabolic syndrome, which pose a serious threat to public health worldwide. The case demonstrates the difficulty of managing patients with severe obesity and polymorbidity. The clinical picture of a 60-year-old patient was characterized by morbid obesity (BMI 55.6 kg/m2); metabolic syndrome with type 2 diabetes mellitus, stage III hypertension, dyslipidemia, and fatty hepatosis; cardiovascular disorders with atrial fibrillation, myocardial hypertrophy, pulmonary hypertension; concomitant pathologies: osteoarthritis, chronic pancreatitis, gynecological diseases. The interventions performed included a comprehensive diagnosis of the condition with the involvement of doctors of various specialties, personalized diet therapy and physical therapy, as well as drug therapy with the inclusion of dietary fiber preparations, antihypertensive, hypoglycemic, etc. The outcome of the treatment showed positive dynamics in the form of stabilization of blood pressure, weight loss and improvement of the patient’s general condition. The main conclusions from the presented observation are as follows: the need for a multidisciplinary approach to the treatment of morbid obesity, the importance of personalized diet therapy, the importance of a combination of drug and non-drug treatment, the role of dietary fiber preparation in integrated weight management, the need for long-term patient support to achieve sustainable results. The demonstrated case highlights the complexity of managing patients with morbid obesity and metabolic syndrome, and also demonstrates the effectiveness of an integrated approach while observing all components of diagnosis, treatment, and prevention.

Introduction. Juvenile idiopathic arthritis, juvenile psoriatic arthritis, and Crohn's disease are progressive immune-mediated disorders carrying a high risk of early disability.

Aim. To analyze changes in serum cytokines to identify early molecular biomarkers of subclinical intestinal involvement in patients presenting with joint syndrome.

Materials and methods. The study enrolled children diagnosed with juvenile idiopathic arthritis, juvenile psoriatic arthritis, and Crohn’s disease, alongside healthy controls. The concentrations of serum cytokines were quantified using enzyme-linked immunosorbent assay. Data were evaluated using Tukeyʼs post-hoc test, principal component analysis, and heatmapping.

Results. Initial analysis revealed shared immunopathogenetic pathways across the examined cohorts. However, subsequent stratification of patients with juvenile idiopathic arthritis into clinical variants uncovered an atypical phenomenon: patients with the enthesitis form exhibited a profound, isolated elevation in the levels of proinflammatory cytokines IL-18, IL-27, and IL-31, as well as the anti-inflammatory cytokine IL-1ζ. Prospective follow-up demonstrated that comorbid Crohn's disease subsequently manifested in 80% of the patients within this specific subgroup. Multivariate statistical analysis enabled distinct visualization and spatial segregation of these patients into an independent cluster specific to the coexisting pathology.

Conclusions. The identified phenomenon of concurrent upregulation of IL-18, IL-27, IL-31, and IL-1ζ in children with joint syndrome is pathogenetically driven by the gut–joint axis. This specific cytokine panel, combined with multivariate statistical modeling, can serve as a molecular fingerprint for the early screening of subclinical intestinal inflammation. This approach facilitates the timely diagnosis of latent Crohn's disease prior to the development of severe systemic complications.

The review examines the issues of epidemiology, etiological factors, pathogenetic mechanisms, clinical and diagnostic approaches and principles of treatment of primary biliary cholangitis in women. The prevalence of primary biliary cholangitis is very variable and ranges from 0.9 to 58.2 per 100,000 people. Women account for up to 90% of all cases, so an important aspect is to characterize the course of this disease depending on the age period. Epidemiological data suggest that primary biliary cholangitis predominantly affects postmenopausal women and is more often diagnosed in this group at later stages. The development and progression of this pathology is associated with a number of genetic, autoimmune, and environmental factors. More than half of the patients have another autoimmune disease along with primary biliary cholangitis. During the reproductive age, patients often have a long latency period without pronounced clinical symptoms, an increased risk of anovulatory cycles and menstrual irregularities. Pregnancy in women with primary biliary cholangitis is associated with an increased risk of gestational hypertension, preeclampsia, and premature birth. After menopause, the clinical picture of this disease often becomes more pronounced, and the likelihood of developing cirrhosis and liver failure increases. There are gender differences in the prevalence, risk factors, and clinical outcomes of primary biliary cholangitis. The incidence reaches its peak among postmenopausal women. In pregnant women, this pathology is relatively rare, but it has significant clinical consequences for both the mother and the fetus.

Introduction. The study of the role of cytokines in cellular interactions in liver diseases is currently given great importance. However, studies in this area in patients with Opisthorchis felineus (O. felineus) invasion are still limited.

Aim. To study the relationship between laboratory and instrumental manifestations of pathology with polymorphisms of the genes IFNG (rs2069705) and IL28b (rs12979860) in patients with O. felineus invasion.

Materials and methods. A total of 360 patients with O. felineus invasion (170 men and 192 women, mean age 42.1 ± 0.7 years) and 124 control group individuals (65 men and 59 women, mean age 48.3 ± 1.1 years) were examined. O. felineus invasion was diagnosed using duodenal bile microscopy and coproovoscopy. All patients underwent complete blood count, biochemical blood test, abdominal ultrasound, and liver elastometry with liver fibrosis assessment using the METAVIR scale. Genotyping of single nucleotide polymorphisms of the genes IFNG (rs2069705) and IL28b (rs12979860) was performed using real-time PCR. Results. In patients with O. felineus invasion, liver fibrosis was associated with the heterozygous TC genotype for the rs2069705 IFNG polymorphism. Elevated alkaline phosphatase levels and an increased proportion of blood eosinophils were more prevalent in patients with the homozygous CC genotype of the rs2069705 IFNG polymorphism. We found no association between the rs12979860 IL28b polymorphism and manifestations of O. felineus invasion.

Conclusion. From our point of view, patients with opisthorchiasis who have the rs2069705 IFNG polymorphism should be identified during dispensary observation as a risk group to prevent the development of complications of parasitic invasion, which include liver fibrosis and hepatocellular carcinoma.

Endometriosis is a pathological process characterized by the presence of tissue outside the uterine cavity that has morphological and functional properties similar to the endometrium. Endometriosis affects 10% (190 million) of women of reproductive age worldwide. Intestinal endometriosis is a pathological condition characterized by infiltration of the intestine with ectopic endometrial tissue. The prevalence of intestinal endometriosis ranges from 3% to 37% of all women with endometriosis. A search of PubMed for references on various aspects of intestinal endometriosis research published before January 15, 2026, was conducted. The pathogenesis of endometriosis is multifactorial, with hormonal, immune, and microbiome components. In recent years, the role of intestinal microbiota and immune dysregulation in the development of endometriosis has been widely discussed. A new area of research is the study of the role of periodontal pathology. In the clinical picture of endometriosis, gastrointestinal symptoms are often present alongside typical gynecological symptoms. Abdominal pain and bowel disturbances in women of reproductive age suggest a wide range of differential diagnoses, including irritable bowel syndrome, inflammatory bowel disease, and a number of other conditions. Intestinal endometriosis can pose a diagnostic challenge for the physician. Difficulties in differential diagnosis may be associated with irritable bowel syndrome, inflammatory bowel disease, celiac disease, and intestinal cancers. The presence of gastrointestinal symptoms in genital and intestinal endometriosis can complicate their diagnosis over time. When conducting a differential diagnosis of intestinal diseases, the possible presence of intestinal endometriosis must also be considered.