Vol 12, No 5 (2026)

The high prevalence of Gilbert’s syndrome (GS) in the Russian population and its clinical polymorphism necessitate a thorough study of associated conditions and diseases. The most common complaints with which patients seek medical care, as well as possible correlations between bilirubin levels and comorbidities, require clarification. The question of the presence of gender differences in the structure of concomitant clinical symptoms in GS is of particular interest.

The aim: to identify the clinical features, frequency, and spectrum of comorbidities in adult patients with GS.

Material and methods. A retrospective study included 53 patients (24 male and 29 female individuals, median age 40 years) with benign hyperbilirubinemia (GS).

Results. All subjects with GS had gastrointestinal complaints. Approximately half of the patients had GS combined with gastroesophageal reflux disease and irritable bowel syndrome (56.6 and 47.2%, respectively). Dyspeptic symptoms were present in 90.6% of the subjects. Association between biliary sludge and gallbladder dysfunction was statistically significant (p < 0.05). Hepatic steatosis was diagnosed in 20.8% of patients, with a significant association with obesity (p <  0.01). GS was combined with cholelithiasis in a third of the cases, and 7 subjects (13.7%) had a history of cholecystectomy. Chronic gastritis associated with Н. рylori was diagnosed in 12 patients (22.6%), and gastric ulcer and duodenal ulcer were diagnosed in 3 (5.7%) persons. Individuals with the homozygous GS genotype (7TA/7TA) had higher bilirubin levels (38.2 versus 27.4 μmol/L in heterozygous carriers; p < 0.01).

Conclusion. GS is a common hereditary condition that requires dynamic monitoring. In adult patients with GS, episodes of jaundice are accompanied by a variety of clinical manifestations of dyspeptic nature, and among gastrointestinal diseases, gastroesophageal reflux disease, irritable bowel syndrome, gallbladder dysfunction, and cholelithiasis are most often diagnosed. No gender differences in the pattern of complaints were identified in patients with GS.

The factor uniting independent nosologies (hiatal hernia, cholelithiasis, and intestinal diverticulosis) into a consistent multimorbidity – Saint’s triad (ST) – is not obvious, which complicates the development of treatment and preventive measures that minimize the risk of complications and the need for repeated surgical interventions.

The aim: to evaluate the totality of clinical manifestations and possible combinations of components of ST in terms of multimorbidity in patients with a dysplasia-dependent phenotype.

Material and methods. In a clinical cohort of 77 patients with at least two components of ST, as determined by gastrointestinal imaging, the clinical manifestations, phenotypic, and visceral stigmas of connective tissue dysplasia (CTD) were studied using a diagnostic screening set of its features. The comparison group (70 patients) consisted of patients with hiatal hernia (HH) in whom other components of ST were excluded.

Results. Complete ST was detected in 6.5% of cases; in the remaining cases, its components in various combinations formed comorbid pairs. Clinical manifestations at the time of presentation were determined by reflux syndrome in half of the cases, biliary dysfunction in a third, and intestinal disorders in a fifth of the cases. Among the phenotypic signs of CTD, the most prevalent were cutaneous, musculoskeletal, osteoarticular, and cranial; among visceral manifestations – HH, gallbladder anomalies, and colonic diverticula. Quantitative indices established a statistically significant predominance of the number and severity of CTD signs in patients with ST compared to patients with HH (p < 0.001), corresponding to the level of moderate CTD.

Conclusion. Diagnosis of ST requires an active diagnostic search for its components using instrumental verification of the digestive system. CTD is a structural predictor of ST; identification of a dysplasia-dependent phenotype may prompt an active diagnostic evaluation of the components of multimorbidity.

Key goals in the treatment of inflammatory bowel diseases today include not only control of symptoms but also achieving endoscopic healing of the intestinal mucosa and normalizing laboratory markers of inflammation.

The aim: to prospectively evaluate the dynamics of clinical symptoms, laboratory markers, and endoscopic activity in patients with Crohn’s disease (CD) over 52 weeks of observation, also to find the correlation between the nature of performing therapy and achievement of remission in accordance with the treat-to-target strategy.

Material and methods. The study included 66 patients with CD. Clinical activity was assessed using the PRO2 scale (stool frequency, abdominal pain). Laboratory examinations included complete blood counts and biochemical blood tests with calculation of hematological phlogosis index. Endoscopic activity was assessed using SES-CD scale. Clinical observation was performed at checkpoints of 0, 3, 6, and 12 months.

Results. By the 12th month of observation, the participants showed a statistically significant decrease in the mean stool frequency score (from 1.74 ± 0.91 to 1.05 ± 0.83; p = 0.008) and abdominal pain (from 1.86 ± 0.87 to 1.05 ± 0.87; p = 0.001). The proportion of patients with normal stool frequency reached 74.1%, with a complete absence of pain – 31.0% (a 4-fold increase comparatively to the baseline level). There was a decrease in the level of C-reactive protein (CRP) (from a peak of 24.8 ± 6.6 to 10.9 ± 3.8 mg/L), leukocytes, neutrophils, platelets and fibrinogen (p < 0.05), as well as an increase inhemoglobin content (p = 0.02). The proportion of patients with endoscopic remission increased from 1.5 to 10.3% (p = 0.02). A strong correlation was found between CRP (ρ = 0.892; p <  0.001) and platelet (ρ = 0.721; p = 0.008) levels and the degree of endoscopic CD activity. Patients also experienced a sharp reduction in glucocorticoid use (from 45.5% to 5.2%; p < 0.001) and an increase in the proportion of genetically engineered biological drugs in therapy (from 40.9 to 70.1%; p < 0.001), with a change in their structure toward agents with alternative mechanisms of action (different from TNF-α inhibition).

Conclusion. Treat-to-target strategy in patients with Crohn’s disease demonstrates high efficacy, resulting in regression of clinical symptoms, normalization of laboratory markers of inflammation, and improvement of the endoscopic picture of the disease. The identified correlations support the use of CRP and hemoglobin levels as surrogate markers of endoscopic healing in real-world clinical practice.

Comorbidity between gastroesophageal reflux disease (GERD) and obstructive sleep apnea syndrome (OSAS) is a pressing interdisciplinary problem. Pathophysiological mechanisms underlying their mutual influence remain incompletely understood, and data on the clinical and functional characteristics of the combined course are contradictory.

The aim: to determine the clinical peculiarities, pH-impedance data, and cardiorespiratory monitoring parameters in patients with GERD and OSAS comorbidity.

Material and methods. A cross-sectional analytical study was performed involving 203 patients divided into three groups: Group 1 – patients with isolated GERD (n = 79), Group 2 – with isolated OSAS (n = 94), and Group 3 – with comorbid GERD and OSAS (n = 30). All patients underwent a clinical examination with questionnaires (GERDQ, Berlin Questionnaire, SF-36), esophagogastroduodenoscopy with biopsy, 24-hour esophageal pH-impedance monitoring, and cardiorespiratory monitoring. The diagnosis of GERD was established according to the recommendations of the Russian Gastroenterological Association (2024) and Lyon Consensus 2.0, while OSAS was diagnosed according to the recommendations of the Eurasian Association of Cardiology and the Russian Society of Somnologists (2024).

Results. In the group of patients with comorbidities, compared to participants with isolated GERD, nocturnal symptoms (86.6 vs. 36.7%, p = 0.00001), regurgitation (93.3 vs. 60.8%, p = 0.0009), erosive esophagitis (50 vs. 22.8%, p = 0.006), papillary elongation (89.5 vs. 57.9%, p=0.04), and intraepithelial cell infiltration (73.7 vs. 44.7%, p=0.04) were more frequently detected. In addition, pH-impedance monitoring revealed an increase in esophageal AET (6.9 vs. 1.9%, p = 0.01), a predominance of nocturnal weakly acidic and mixed reflux episodes, and a decrease in the PSPW index (31.5 vs. 54.6%, p = 0.00001) and mean nocturnal baseline impedance in the proximal segment (2.9 vs. 5.3 kOhm, p = 0.000001) in comorbid patients.

Conclusion. The comorbidity of GERD and OSAS creates a phenotype that is qualitatively different from either of these pathologies, characterized by a specific symptom complex, a distinct reflux pattern, and impaired esophageal defense mechanisms. Comparatively with patients with isolated OSAS, comorbid patients had less severe obesity (BMI 28.7 vs. 37.2 kg/m², p = 0.00001) and less severe apnea (AHI 9.7 vs. 13.9, p = 0.03), but more often associated apnea with food intake (60%) and GERD symptoms.

Non-alcoholic fatty liver disease (NAFLD) is an important component of the cardio-renal-hepato-metabolic continuum, requiring timely diagnosis. Available diagnostic tools do not always accurately detect liver steatosis at early stages. A promising solution in this case is the use of the cardiometabolic index (CMI), which can improve the accuracy of screening and risk stratification.

The aim: to evaluate the diagnostic utility of CMI as a potential NAFLD predictor and analyze its dynamics during therapy with ursodeoxycholic acid (UDCA – Ursosan Forte).

Material and methods. The study included 120 patients (68 female and 52 male individuals, median age 55 [47; 63] years) with confirmed NAFLD based on abdominal ultrasound and magnetic resonance imaging with proton density adipose tissue evaluation (MRI-PDFF). CMI was calculated basing on anthropometric and laboratory parameters. A subgroup of 30 participants who were prescribed UDCA at a dose of 12 mg/kg of body weight were then followed for 6 months. After 6 months, CMI and MRI-PDFF were recalculated.

Results. CMI demonstrated diagnostic value for the early detection of hepatic steatosis. In 84.6% of male and 86.8% of female patients with proven hepatic steatosis, the index values were above the cutoff figures, allowing its use for NAFLD screening. A statistically significant correlation between CMI values and the degree of steatosis was revealed (r_s = 0.296, p < 0.001), gender differences of this correlation were identified. UDCA therapy (12 mg/kg/day for 6 months in combination with non-pharmacological measures for NAFLD correction) significantly reduced liver fatty infiltration according to MRI-PDFF from 10 to 6.5% (p = 0.008), as well as a decrease in CMI as an integral indicator of cardiometabolic disorders.

Conclusion. CMI can be used as an auxiliary tool not only for identifying patients with NAFLD but also for assessing the efficacy of therapy. The use of UDCA promotes steatosis regression and reduces cardiovascular risks.

Functional gastrointestinal disorders occupy leading positions of applying for medical care to general practitioners, therapists, and gastroenterologists. However, managing this cohort of patients is challenging. Among the many clinical variants of functional gastrointestinal disorders, the most common are irritable bowel syndrome (IBS) and functional dyspepsia (FD), with a significant proportion of patients experiencing comorbidity. It is supposed that this comorbidity is based on common risk factors and the universality of the pathogenetic links of IBS and FD, the study of which is of great importance, including for the subsequent development of highly effective treatment regimens that can achieve sustained remission of these diseases. Current review is devoted to analysis and systemization current scientific data concerning the key pathogenesis links underlying the development of the comorbid course of IBS and FD.

The article presents a literature review of current data on Parkinson’s disease, focusing on two promising areas of research: methods for stimulating deep brain structures and the influence of the gut microbiota on the development of the disease. The main types of neuromodulatory interventions (including deep brain stimulation), their mechanisms of action, clinical efficacy, and limitations of use are discussed. A separate analysis of current understanding of the role of the gut microbiome in Parkinson’s disease pathogenesis, including possible pathways of gut-brain interaction (via vagal nerve, immune system, microbial metabolites, etc.), as well as data from preclinical and clinical studies in this area is provided. The results of key publications from recent years are systematized; promising areas for further research, and potential opportunities for developing new therapeutic strategies combining neuromodulation and microbiota modification are identified in the article.

The association between gastroesophageal reflux disease (GERD) and obesity has been proved in epidemiological studies. Accurate diagnosis of various GERD phenotypes (erosive and non-erosive, hypersensitive esophagus) and functional heartburn helps improve the effectiveness of therapy for patients with refractory heartburn. It is a known fact that 24-hour pH-impedance monitoring is an important part of the diagnostic algorithm for GERD. It allows the recording of all types of reflux into the esophagus, regardless of pH, and to make an assessment of their correlation with symptoms. Current article presents clinical observations of obese patients with GERD. A detailed examination demonstrated a link between symptoms and both acidic and non-acidic refluxes, enabling treatment adjustments and long-term remission.

Current study is devoted to the analysis of clinical and laboratory approaches to diagnosing extraintestinal manifestations of inflammatory bowel disease (IBD). According to the review, IBD diagnosis is currently based primarily on clinical assessment, physical examination data, instrumental research methods, and the use of standardized classification criteria, while laboratory methods are auxiliary and primarily used for differential diagnostic purposes. Moreover, data of scientific literature demonstrates the systemic nature of IBD and points out to the potential for further exploration of non-invasive biomarkers reflecting the activity of extraintestinal manifestations and disease prognosis. Studying immune-inflammatory mechanisms underlying systemic lesions in case of IBD, as well as assessing the potential of extraintestinal manifestations as predictors of the underlying disease, may contribute to the improvement of diagnostic and therapeutic strategies in this patient population.

Triple therapy with amoxicillin, clarithromycin, and omeprazole is one of the basic regimens for Helicobacter pylori eradication. This article discusses pharmacological peculiarities of this drug combination in terms of drug interactions, convenience of treatment, and increased adherence to anti-Helicobacter therapy, as well as the relevance of its use in the setting of H. pylori resistance. The article discusses international and Russian guidelines for the management of patients with H. pylori-associated diseases, emphasizing the importance of an individualized approach, 14-day treatment duration, and adherence to therapy. The pharmacokinetic aspects of the omeprazole + amoxicillin + clarithromycin combination, their role in achieving effective acid suppression, and antibiotic stability in the acidic environment of the stomach are presented. Particular attention is paid to the problem of H. pylori resistance to clarithromycin: molecular mechanisms, regional data on resistance, and strategies for overcoming it, including the choice of alternative treatment regimens, are described.

Comorbidity between cardiovascular diseases (CVD) and gastroesophageal reflux disease is a common clinical situation that complicates therapy selection. Patients with CVD are often receiving long-term antiplatelet therapy (in particular, clopidogrel), which increases the risk of gastrointestinal complications and requires the use of proton pump inhibitors. A number of drugs from this class inhibit CYP2C19 isoenzyme involved in the bioactivation of clopidogrel. This potentially reduces its antiplatelet activity and increases the risk of cardiovascular events. However, this interaction is not a class effect. Current review analyzes the pharmacokinetic properties of rabeprazole, whose metabolism is minimally dependent on CYP2C19. Results from clinical trials, systematic reviews, and meta-analyses are presented, demonstrating that rabeprazole does not have a clinically significant effect on the antiplatelet response of clopidogrel and does not increase the risk of cardiovascular events.