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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.

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.

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.

In spite of the large diversity of diagnostic and interventional devices associated with gastrointestinal endoscopic procedures, there is little information on the impact of the biomaterials (metals, polymers) contained in these devices upon body tissues and, indirectly, upon the treatment outcomes. Other biomaterials for gastroenterology, such as adhesives and certain hemostatic agents, have been investigated to a greater extent, but the information is fragmentary. Much of this situation is due to the paucity of details disclosed by the manufacturers of the devices. Moreover, for most of the applications in the gastrointestinal (GI) tract, there are no studies available on the biocompatibility of the device materials when in intimate contact with mucosae and other components of the GI tract. We have summarized the current situation with a focus on aspects of biomaterials and biocompatibility related to the device materials and other agents, with an emphasis on the GI endoscopic procedures. Procedures and devices used for the control of bleeding, for polypectomy, in bariatrics, and for stenting are discussed, particularly dwelling upon the biomaterial-related features of each application. There are indications that research is progressing steadily in this field, and the establishment of the subdiscipline of “gastroenterologic biomaterials” is not merely a remote projection. Upon the completion of this article, the gastroenterologist should be able to understand the nature of biomaterials and to achieve a suitable and beneficial perception of their significance in gastroenterology. Likewise, the biomaterialist should become aware of the specific tasks that the biomaterials must fulfil when placed within the GI tract, and regard such applications as both a challenge and an incentive for progressing the research in this field.

Inflammatory bowel disease (IBD) remains difficult to manage in patients who fail multiple therapeutic lines, and growing evidence suggests that alterations in the gut microbiome contribute to persistent symptoms and inflammatory activity. This study evaluated a three-month, AI-guided, multi-omic personalized microbiome modulation program in adults with treatment-refractory IBD. Baseline stool metagenomic sequencing, blood biomarkers, micronutrient panels, and clinical data were integrated through an artificial intelligence platform to generate individualized plans combining dietary adjustments, targeted synbiotics, selective antimicrobials, and micronutrient correction. Clinical outcomes, inflammatory markers, and microbial signatures were reassessed after three months. Across 358 participants, stool frequency decreased substantially, urgency and rectal bleeding resolved in most patients, and over 70% reported a “much improved” overall condition. Inflammatory biomarkers showed marked normalization, with reductions in hs-CRP and fecal calprotectin observed in over 85% of cases. Micronutrient deficiencies, particularly iron and zinc, also improved, and beneficial microbial taxa such as Faecalibacterium prausnitzii, Bifidobacterium longum, and Akkermansia muciniphila increased significantly. These findings suggest that personalized, multi-omic microbiome modulation may support clinically meaningful improvements by targeting microbial, metabolic, and immune imbalances rather than symptoms alone. While encouraging, these results require confirmation in randomized controlled studies.

Background: Crohn’s disease (CD) is a chronic, relapsing and remitting inflammatory bowel disease that can be associated with significant bowel damage and disability. The Lémann Index (LI) is a validated tool for measuring cumulative bowel damage in CD patients through a comprehensive assessment of stricturing, penetrating and surgical lesions. However, prospective studies evaluating bowel damage progression in recently diagnosed CD patients remain limited. Objectives: To characterise the absolute and longitudinal variations in bowel damage progression, as measured by the LI, in a cohort of recently diagnosed CD patients, and to assess its association with relevant disease features, including disease phenotype, treatment strategies, biomarkers and disability. Design: Study protocol for the Crohn’s Disease Cohort Study (CROCO Study), a multicentre, European, prospective cohort study. Methods and analysis: Patients with recently diagnosed CD (within the previous 12 months) will be enrolled and followed up for 5 years. Patients will receive standard-of-care treatment determined by the practising gastroenterologist. Morphological assessments to measure the LI and to evaluate bowel damage progression will be performed at years 1, 3 and 5 after the diagnosis. Disability will be assessed annually using the Inflammatory Bowel Disease – Disability Index (IBD-DI). The primary outcome will be the absolute LI at year 3 following diagnosis. Predictors of bowel damage progression and the association between bowel damage and disability will be analysed. Discussion: The CROCO study represents a unique multicentre cohort of recently diagnosed CD patients, designed to advance the understanding of CD’s natural history and evolution. It will facilitate the development of composite scores for predicting bowel damage progression and provide valuable tools for designing future disease-modification trials. Trial registration: NCT05420233.

In the gastroenterology field, the impact of artificial intelligence was investigated for the purposes of diagnostics, risk stratification of patients, improvement in quality of endoscopic procedures and early detection of neoplastic diseases, implementation of the best treatment strategy, and optimization of patient prognosis. Computer-assisted diagnostic systems to evaluate upper endoscopy images have recently emerged as a supporting tool in endoscopy due to the risks of misdiagnosis related to standard endoscopy and different expertise levels of endoscopists, time-consuming procedures, lack of availability of advanced procedures, increasing workloads, and development of endoscopic mass screening programs. Recent research has tended toward computerized, automatic, and real-time detection of lesions, which are approaches that offer utility in daily practice. Despite promising results, certain studies might overexaggerate the diagnostic accuracy of artificial systems, and several limitations remain to be overcome in the future. Therefore, additional multicenter randomized trials and the development of existent database platforms are needed to certify clinical implementation. This paper presents an overview of the literature and the current knowledge of the usefulness of different types of machine learning systems in the assessment of premalignant and malignant esophageal lesions via conventional and advanced endoscopic procedures. This study makes a presentation of the artificial intelligence terminology and refers also to the most prominent recent research on computer-assisted diagnosis of neoplasia on Barrett’s esophagus and early esophageal squamous cell carcinoma, and prediction of invasion depth in esophageal neoplasms. Furthermore, this review highlights the main directions of future doctor–computer collaborations in which machines are expected to improve the quality of medical action and routine clinical workflow, thus reducing the burden on physicians.

Background: Up to one-third of patients with gastroesophageal reflux disease (GERD) have persistent symptoms despite proton-pump inhibitor (PPI) therapy. E-Gastryal® + MgAlg (Aurora Biofarma, Italy) is a mucosal protective agent that enhances barrier function against acid and non-acidic reflux. This study assessed its efficacy in combination with omeprazole versus omeprazole alone and as maintenance therapy. Methods: Patients with symptomatic GERD and Grade A reflux esophagitis confirmed by endoscopy were randomized to receive omeprazole 20 mg plus E-Gastryal® + MgAlg or omeprazole 20 mg alone. The primary endpoint was the number of rescue medications used over 28 days. Secondary endpoints included symptom relief and quality-of-life assessments using the Reflux Symptom Index (RSI), Gastroesophageal Reflux Disease Impact Scale (GIS), GERD-Health-Related Quality of Life (GERD-HRQL), and Global Assessment of Performance (IGAP). Results: Ninety-six patients were included. The combination group used significantly fewer rescue medications (mean: 21 vs. 40.9 tablets; p = 0.002). At week 4, the combination group showed greater improvement in RSI, GIS, and GERD-HRQL scores (p < 0.001). Symptom relief was sustained during weeks 5–26 with E-Gastryal® + MgAlg alone. Conclusions: E-Gastryal® + MgAlg combined with omeprazole improves symptom control compared to PPI monotherapy. Continued use as maintenance therapy supports its role in long-term GERD management (NCT04130659).

Background: Endoscopic retrograde cholangiopancreatography (ERCP) represents a major pivotal point in gastrointestinal endoscopy. Little is known about acute kidney injury (AKI) post-ERCP. This study analyses the incidence, risk factors, and prognosis of post-ERCP AKI. Methods: A total of 396 patients were prospectively studied. AKI was defined by an increase in serum creatinine (SCr) ≥ 0.3 mg/dL or by an increase in SCr ≥ 50% in the first 48 h post-ERCP. Logistic regression analysis was used to identify the predictors of AKI and in-hospital mortality. A two-tailed p value < 0.05 was considered significant. Results: One hundred and three patients (26%) developed post-ERCP AKI. Estimated glomerular filtration rate (adjusted odds ratio (aOR) = 0.95, 95% confidence interval (CI): 0.94–0.96, p < 0.001), nonrenal Charlson Comorbidity Index (Aor = 1.19, 95% CI: 1.05–1.35, p = 0.006), choledocholithiasis (aOR = 4.05, 95% CI: 1.98–8.29, p < 0.001), and bilirubin (aOR = 1.1, 95% CI: 1.05–1.15, p < 0.001) were associated with post-ERCP AKI. Post-ERCP AKI was associated with longer hospital stay (p < 0.001) and with increased in-hospital mortality (7.76% versus 0.36%, p < 0.001). Moderate-to-severe (stage 2 and 3) AKI was independently associated with in-hospital mortality (aOR = 6.43, 95% CI: 1.48–27.88, p < 0.013). Conclusions: Post-ERCP AKI represented an important complication associated with longer hospital stay. Moderate-to-severe post-ERCP AKI was an independent risk factor for in-hospital mortality.

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.