Explore the vast range of titles available.

Inflammatory bowel disease (IBD) is a complex disorder influenced by genetic, environmental, and microbial factors, with emerging evidence highlighting the gut microbiome’s role in disease pathogenesis. This study investigates the impact of microbiome-targeted interventions in pediatric IBD by integrating multi-omics analysis, including metagenomics, metabolomics, transcriptomics, and clinical biomarkers, to identify microbial dysbiosis patterns and potential therapeutic targets. A cohort of pediatric IBD patients underwent a personalized intervention involving dietary modifications, probiotic supplementation, and selective antibiotic therapy. Microbiome composition, inflammatory markers (fecal calprotectin, CRP), and disease activity scores (PCDAI/PUCAI) were assessed before and after treatment. At the 3-month follow-up, patients showed significant clinical improvement, with reduced stool frequency (p = 0.004) and improved stool consistency (p < 0.001). Symptoms such as bloating and abdominal pain decreased, while energy levels increased (p < 0.001). Dietary changes included higher fruit, meat, and dairy intake, and lower fast-food and sweets consumption (p < 0.001). Physician assessments classified 90% as “improved”, reinforcing the effectiveness of personalized microbiome interventions. Microbiome-targeted interventions (diet, probiotics, and selective antibiotics) improved pediatric IBD outcomes by reducing pathogenic bacteria and increasing short-chain fatty acid (SCFA)-producing species, lowering inflammation and symptoms. Early-life factors (cesarean birth, and formula feeding) influence IBD risk. Personalized diets enhanced microbial balance. Integrating multi-omics supports precision medicine, offering microbiome-based biomarkers and reducing immunosuppressive reliance.

Background: Few studies have evaluated the efficacy of butyric acid in treating children with inflammatory bowel disease (IBD). In children and adolescents with recently diagnosed IBD, the purpose of this research was to assess the efficacy of oral sodium butyrate (the product-patented, sustained and targeted-release form of butyrate MSB®) as an adjunct to conventional treatment. Methods: This trial was unicentric, prospective, randomized, and placebo-controlled. An amount of 150 mg sodium butyrate once a day (Group A), or a placebo (Group B) were randomly assigned to patients with ulcerative colitis or Crohn’s disease, aged 7–18 years, who were receiving conventional medication based on the severity of their conditions. Disease activity, C-reactive protein (CRP), and fecal calprotectin concentration differences between the two study groups at 12 weeks of the trial were the main outcomes. Results: With 44 patients in Group A and 44 in Group B, 88 individuals with initially active illness finished the research. Most patients experienced remission by week 12 of the study (36 patients in Group A with sodium butyrate, 81.82%; 21 patients in Group B with placebo, 47.73%). Between the two groups, a significant difference in disease activity was seen (p < 0.001). The sodium butyrate group appeared to have less systemic inflammation than the other group, as evidenced by the significantly lower CRP levels in Group A (18.14 ± 11.19 mg/L) compared to Group B (57.00 ± 33.28 mg/L) at 12 weeks (T2) (p < 0.001). No negative effects were recorded by any of the patients. Fecal calprotectin in Group A dropped much more after 12 weeks (T2) (p < 0.001), suggesting that the sodium butyrate group was better able to regulate intestinal inflammation. Conclusions: In newly diagnosed children and adolescents with IBD, a 12-week sodium butyrate supplementation did demonstrate effectiveness as an additional treatment.

Background/Objectives: Inflammatory bowel disease (IBD), encompassing ulcerative colitis and Crohn’s disease, is characterized by chronic gut inflammation driven by microbial dysbiosis and immune dysfunction. Current therapies primarily involve anti-inflammatory and immunomodulatory strategies; however, many patients experience an inadequate response or a gradual loss of efficacy over time. This study evaluates the clinical efficacy of personalized microbiome modulation (PMM)—an AI-driven intervention designed to restore microbial balance and improve key treatment outcomes such as symptom control and remission rates. Methods: This was a single-arm, open-label validation trial involving 27 patients with moderate-to-severe IBD who had experienced prior treatment failure. Participants underwent three months of PMM, which included personalized dietary modifications, targeted probiotic supplementation, and antimicrobial interventions based on gut microbiome sequencing. Primary outcomes included stool frequency and consistency as well as inflammatory markers (C-reactive protein and fecal calprotectin), while secondary outcomes assessed nutritional status, metabolic function, and quality of life. Statistical analyses included paired t-tests and repeated measures ANOVA to determine significant changes over time. Results: PMM led to significant clinical improvements, including a 58% reduction in stool frequency (p < 0.001) and improved stool consistency. CRP and fecal calprotectin levels decreased markedly (p < 0.001), suggesting reduced systemic inflammation. Additionally, iron, vitamin B12, and vitamin D deficiencies improved (p < 0.001), alongside weight gain and increased energy levels. Notably, patients on anti-TNF biologics showed enhanced response rates, suggesting potential synergistic effects between microbiome modulation and biologic therapy. Conclusions: This study highlights PMM as a promising adjunctive therapy for IBD, demonstrating benefits across clinical, inflammatory, and metabolic parameters. While findings support the role of microbiome-targeted interventions in disease management, larger randomized controlled trials are required to confirm the long-term efficacy and applicability in broader patient populations.

Gastric cancer (GC) remains a major global health burden, with high morbidity and mortality rates, particularly in regions with prevalent Helicobacter pylori (H. pylori) infection. While H. pylori has long been recognized as a primary carcinogenic agent, recent research has underscored the broader contribution of the gastric microbiota to gastric carcinogenesis. Alterations in the microbial community, or dysbiosis, contribute to chronic inflammation, immune modulation, and epithelial transformation through a range of mechanisms, including disruption of mucosal integrity, activation of oncogenic signaling pathways (e.g., PI3K/Akt, NF-κB, STAT3), and epigenetic alterations. Furthermore, microbial metabolites, such as short-chain fatty acids, secondary bile acids, and lactate, play dual roles in either promoting or suppressing tumorigenesis. Oral and gut-derived microbes, translocated to the gastric niche, have been implicated in reshaping the gastric microenvironment and exacerbating disease progression. The composition of the microbiota also influences responses to cancer immunotherapy, suggesting that microbial profiles can serve as both prognostic biomarkers and therapeutic targets. Emerging strategies, such as probiotics, dietary interventions, and fecal microbiota transplantation (FMT), offer new avenues for restoring microbial balance and enhancing therapy response. This review synthesizes current knowledge on the complex interplay between microbiota and gastric cancer development and emphasizes the potential of microbiome modulation in both preventive and therapeutic frameworks.

Background and objective: The incidence of inflammatory bowel disease (IBD) over the past years in Romania has been on the rise, but epidemiologic data are lacking. The aim of this study was to define the characteristics of IBD, the trends and phenotype among IBD patients in Romania. Material and methods: We conducted a prospective study over a period of 12 years, from 2006 to 2017. All patients diagnosed with IBD on clinical, radiological, endoscopic and histological features were included. We divided the country into eight regions: west (W), north-east (NE), north-west (NW), south-east (SE), south-west (SW), south (S), central (C) and Bucharest-Ilfov (B), and data were analyzed accordingly. Results: A total of 2724 patients were included in this database, but only 2248 were included in the final analysis, with all data available. Of the 2248 patients, 935 were Crohn’s disease (CD), 1263 were ulcerative colitis (UC) and 50 were IBD-undetermined. In UC phenotypes we observed more frequent left-sided colitis (50.5%, p < 0.0001), and in CD phenotype we observed more frequent colonic and ileo-colonic localization (37.8% and 37.6%, p < 0.0001). The region with the most IBD cases was NE (25.1%) and with the least IBD cases was SW (4.9%). UC was found more frequently in NE (32%), while CD was found more frequently in Bucharest (28.6%). Conclusions: In Romania, ulcerative colitis is more frequent than CD. UC is predominant in the northern part of Romania, while CD has become predominant in the southern part of the country. IBD occurs more in the male population, and in urban and industrialized areas. There are differences between the regions in Romania regarding IBD phenotypes, gender distributions, age distribution, treatment, smoking status and complications.

Objective To compare the diagnostic accuracy of endoscopic retrograde cholangiopancreatography (ERCP), magnetic resonance pancreatography (MRCP) and histological examination for malignant biliary obstruction. Methods This retrospective study included patients admitted for biliary obstruction caused by biliary tree malignancy that underwent ERCP, MRCP and histological examination. Data were collected from the medical records. The primary endpoints were the area under the receiver operating characteristic (AUROC) curve value, sensitivity, specificity and overall diagnostic accuracy of the three procedures in terms of a final diagnosis of obstructive biliary malignancy; and the agreement between ERCP, MRCP and histological examination with the final diagnosis. Results A total of 160 patients were included in the study (85 males, 53.1%; mean ± SD age, 69.31 ± 10.96 years). Considering the final diagnosis, the performance of MRCP, ERCP and histology in assessing biliary tumours produced AUROC values of 0.88 (95% confidence interval [CI] 0.75, 0.90), 0.94 (95% CI 0.85, 0.99) and 0.80 (95% CI 0.70, 0.82), respectively. ERCP presented higher sensitivity, overall diagnostic accuracy and agreement with the final diagnosis than MRCP and histological examination. Conclusion These current data suggest that invasive methods such as ERCP with biopsy remain more reliable than non-invasive methods.

Colorectal cancer (CRC) is the third most diagnosed cancer in men (after prostate and lung cancers) and in women (after breast and lung cancer). It is the second cause of cancer death in men (after lung cancer) and the third one in women (after breast and lung cancers). It is estimated that, in EU-27 countries in 2020, colorectal cancer accounted for 12.7% of all new cancer diagnoses and 12.4% of all deaths due to cancer. Our study aims to assess the opportunistic colorectal cancer screening by colonoscopy in a private hospital. A secondary objective of this study is to analyse the adenoma detection rate (ADR), polyp detection rate (PDR), and colorectal cancer (CRC) detection rate. We designed a retrospective single-centre study in the Gastroenterology Department of Saint Mary Hospital. The study population includes all individuals who performed colonoscopies in 2 years, January 2019–December 2020, addressed to our department by their family physician or came by themselves for a colonoscopy. One thousand seven hundred seventy-eight asymptomatic subjects underwent a colonoscopy for the first time. The mean age was 59.0 ± 10.9, 59.5% female. Eight hundred seventy-three polyps were found in 525 patients. Five hundred and twenty-five had at least one polyp, 185 patients had two polyps, 87 had three polyps, and 40 patients had more than three polyps. The PDR was 49.1%, ADR 39.0%, advanced adenomas in 7.9%, and carcinomas were found in 5.4% of patients. In a country without any colorectal cancer screening policy, polyps were found in almost half of the 1778 asymptomatic patients evaluated in a single private center, 39% of cases adenomas, and 5.4% colorectal cancer. Our study suggests starting screening colonoscopy at the age of 45. A poor bowel preparation significantly impacted the adenoma detection rate.

Filgotinib (GLPG0634, GS-6034) is a once-daily, orally administered, Janus kinase 1 (JAK1)-selective inhibitor. The FITZROY study examined the efficacy and safety of filgotinib for the treatment of moderate-to-severe Crohn's disease. We did a randomised, double-blind, placebo-controlled phase 2 study, which recruited patients from 52 centres in nine European countries. We enrolled eligible patients aged 18–75 years with a documented history of ileal, colonic, or ileocolonic Crohn's disease for 3 months or more before screening, as assessed by colonoscopy and supported by histology, and a Crohn's Disease Activity Index (CDAI) score during screening between 220 and 450 inclusive. Patients were randomly assigned (3:1) to receive filgotinib 200 mg once a day or placebo for 10 weeks. Patients were stratified according to previous anti-tumour necrosis factor alpha exposure, C-reactive protein concentration at screening (≤10 mg/L or >10 mg/L), and oral corticosteroid use at baseline, using an interactive web-based response system. The primary endpoint was clinical remission, defined as CDAI less than 150 at week 10. After week 10, patients were assigned based on responder status to filgotinib 100 mg once a day, filgotinib 200 mg once a day, or placebo for an observational period lasting a further 10 weeks. The filgotinib and placebo treatment groups were compared using ANCOVA models and logistic regression models containing baseline values and randomisation stratification factors as fixed effects. Analyses were done on the intention-to-treat non-responder imputation set. The trial was registered at ClinicalTrials.gov, number NCT02048618. Between Feb 3, 2014, and July 10, 2015, we enrolled 174 patients with active Crohn's disease confirmed by centrally read endoscopy (130 in the filgotinib 200 mg group and 44 in the placebo group). In the intention-to-treat population, 60 (47%) of 128 patients treated with filgotinib 200 mg achieved clinical remission at week 10 versus ten (23%) of 44 patients treated with placebo (difference 24 percentage points [95% CI 9–39], p=0·0077). In a pooled analysis of all periods of filgotinib and placebo exposure over 20 weeks, serious treatment-emergent adverse effects were reported in 14 (9%) of 152 patients treated with filgotinib and three (4%) of 67 patients treated with placebo. Filgotinib induced clinical remission in significantly more patients with active Crohn's disease compared with placebo, and had an acceptable safety profile. Galapagos.

Background: Metabolically associated fatty liver disease (MASLD) constitutes a major burden. Glucagon-like peptide-1 agonists (GLP-1) could improve hepatic steatosis as well as weight loss. However, the effect of GLP-1 agonists on patients with and without diabetes and the effect of newer drugs (dual and triple agonists) are unclear. Objective: To investigate the effect of GLP-1 agonists, including dual and triple agonists, in patients with metabolic-associated liver steatosis and steatohepatitis, while exploring their effect on patients with and without type 2 diabetes. Methods: We searched PubMed, Scopus, and Web of Science in October 2025 for randomized parallel controlled trials that investigated the effect of GLP-1 agonists in patients with MASLD or metabolic-associated steatohepatitis (MASH). We assessed the quality of the included studies using Cochrane ROB2. We performed the analysis using RevMan 5.4. We performed subgroup analysis based on the status of diabetes, the control group, and the class of GLP-1 agonist (single, dual, or triple). Results: We included twenty studies. Compared to the control group, GLP-1 agonists were associated with a statistically significant increase in the resolution of MASH without worsening fibrosis (RR 3.03, p < 0.0001) and at least one stage of liver fibrosis without the worsening of MASH compared to the control group (RR: 1.45, p < 0.00001). GLP-1 agonists were associated with a statistically significant weight reduction (SMD −1.11, p < 0.0001), glycosylated hemoglobin (SMD −0.81, p < 0.00001), levels of aspartate aminotransferase (SMD −0.48, p = 0.008), and alanine aminotransferase (SMD −0.54, p = 0.008). However, in patients without type 2 diabetes, GLP-1 agonists had no significant effect on weight loss (SMD −0.97, p = 0.12) or improvement in fibrosis (RR 1.54, p = 0.24). There was a statistically significant increase in the overall adverse events (RR 1.10, p < 0.00001), while there was no significant difference in serious adverse events (p = 0.35). Conclusions: GLP-1 agonists improved liver fibrosis, steatohepatitis, weight loss, HbA1c, and liver enzymes in patients with MASLD or MASH. Overall, GLP-1 agonists were associated with a significantly higher risk of adverse events compared to the control, while serious adverse events were comparable between both groups. There was no significant effect on weight loss or improvement in fibrosis in patients without type 2 diabetes. However, there was a limited number of studies in this population. Thus, further research is needed before recommendations can be made for this subgroup.

ObjectiveThe Epi-IBD cohort is a prospective population-based inception cohort of unselected patients with inflammatory bowel disease from 29 European centres covering a background population of almost 10 million people. The aim of this study was to assess the 5-year outcome and disease course of patients with Crohn’s disease (CD).DesignPatients were followed up prospectively from the time of diagnosis, including collection of their clinical data, demographics, disease activity, medical therapy, surgery, cancers and deaths. Associations between outcomes and multiple covariates were analysed by Cox regression analysis.ResultsIn total, 488 patients were included in the study. During follow-up, 107 (22%) patients received surgery, while 176 (36%) patients were hospitalised because of CD. A total of 49 (14%) patients diagnosed with non-stricturing, non-penetrating disease progressed to either stricturing and/or penetrating disease. These rates did not differ between patients from Western and Eastern Europe. However, significant geographic differences were noted regarding treatment: more patients in Western Europe received biological therapy (33%) and immunomodulators (66%) than did those in Eastern Europe (14% and 54%, respectively, P<0.01), while more Eastern European patients received 5-aminosalicylates (90% vs 56%, P<0.05). Treatment with immunomodulators reduced the risk of surgery (HR: 0.4, 95% CI 0.2 to 0.6) and hospitalisation (HR: 0.3, 95% CI 0.2 to 0.5).ConclusionDespite patients being treated early and frequently with immunomodulators and biological therapy in Western Europe, 5-year outcomes including surgery and phenotype progression in this cohort were comparable across Western and Eastern Europe. Differences in treatment strategies between Western and Eastern European centres did not affect the disease course. Treatment with immunomodulators reduced the risk of surgery and hospitalisation.