World Journal of Gastroenterology最新文献

Background: Inflammatory bowel disease (IBD) is a chronic, gastrointestinal condition including ulcerative colitis and Crohn's disease. Patients diagnosed with IBD are more susceptible to infections and frequently require antibiotics.

Aim: To analyze the antibiotic consumption of IBD inpatients and project future relevant trends.

Methods: We retrospectively collected the demographic and antibiotic usage data from the IBD patients hospitalized between 2015 and 2024. The antibiotics were classified, and the consumption intensity was calculated. The appropriate statistical methods were applied to compare the differences between groups. The Monte Carlo simulation was used to forecast the antibiotic consumption from 2025 to 2027.

Results: A total of 1985 hospitalizations and 372 antibiotic prescriptions were included in this work. The antibiotic-exposed patients were older, had longer hospital stays, and higher costs. Males and ulcerative colitis patients showed a higher antibiotic usage. The highest consumption was observed in 2019, 2022, and 2024. The common indications were intestinal infections and perioperative prophylaxis. Cephalosporins and β-lactam antimicrobials were most commonly used, while carbapenems and glycopeptide antibacterials increased during 2022-2024. Although the antibiotic usage rates decreased in 2020-2024 when compared to 2015-2019, the consumption intensity significantly increased. The Monte Carlo simulation projected a 170.0% (95% uncertainty interval: -42.1% to 689.7%) consumption increase by 2027.

Conclusion: These findings highlight the need to strengthen antibiotic stewardship and infection control strategies in IBD inpatient management to prevent further escalation of antimicrobial resistance.

This letter comments on a web-enabled, dynamic nomogram developed for early sepsis-risk estimation in adults with acute liver failure (ALF) admitted to the intensive care unit. The study successfully established and validated the sepsis in ALF model using five routinely available variables: Age, total bilirubin, lactate dehydrogenase, albumin, and mechanical ventilation. Across cohorts, the model demonstrated strong discrimination and outperformed traditional scores. We commend the inclusion of both Western and Chinese intensive care unit cohorts, which enhances the cross-population generalizability of the findings. This letter highlights the strengths of the model, including its web-based dynamic calculator and effective risk stratification, while also acknowledging limitations such as reliance on baseline admission data, restriction to intensive care unit populations, and the absence of infection-related biomarkers. We encourage further prospective, multicenter investigations to refine the sepsis in ALF model and expand its clinical utility.

Colonic diverticular hemorrhage is a major cause of acute lower gastrointestinal bleeding, particularly in aging populations with increasing prevalence of diverticulosis. Its pathogenesis is multifactorial, involving vascular fragility of the vasa recta, mechanical stress, and patient-related factors such as comorbidities and use of antithrombotic agents. Diagnosis remains challenging due to the intermittent nature of bleeding, with colonoscopy serving as the primary tool and computed tomography angiography providing complementary value for source localization. Endoscopic therapy, especially band ligation, has demonstrated superiority over clipping in reducing rebleeding, while transcatheter arterial embolization has emerged as an effective salvage approach when endoscopic treatment fails. Surgical intervention is reserved for refractory or complicated cases. Recent advances include risk stratification models to guide management and early feeding strategies to accelerate recovery. Despite these improvements, challenges remain in recurrence prevention and individualized treatment selection. This editorial synthesizes current evidence on the etiology, diagnostic modalities, and evolving therapeutic strategies of colonic diverticular hemorrhage, aiming to support clinical decision-making and optimize patient outcomes.

Background: Screening for latent tuberculosis (LTB) before initiating advanced therapy for inflammatory bowel disease (IBD) helps reduce the risk of tuberculosis (TB) development. However, there is limited data on screening practices from TB-endemic regions.

Aim: To study the practices of screening for LTB and study the incidence of TB in patients with IBD on biological and small molecule inhibitors.

Methods: This retrospective multicentre study analyzed LTB screening practices in IBD patients starting advanced therapies between 2018 and 2022. We included patients who were initiated on biologics (infliximab, adalimumab, vedolizumab) or small molecule inhibitors (tofacitinib). We assessed compliance with LTB screening methods, including the tuberculin skin test, interferon-gamma release assay (IGRA), chest X-ray, and computed tomography chest, both at initiation and annually. We also evaluated the incidence of active TB and its predictors.

Results: Of 378 patients (mean age: 36.9 ± 14.9 years, males: 56.9%), 158 (41.8%) and 216 (57.1%) had ulcerative colitis and Crohn's disease, respectively. Advanced therapy used were anti-tumor necrosis factor in 309 (81.74%), tofacitinib in 41 (10.84%) and vedolizumab in 28 (7.40%). Standard screening and diligent screening strategy was employed in 59% and 33% of patients, respectively. Compliance with tuberculin skin test and IGRA was noted in 261 (69.04%) and 298 (78.83%) patients, respectively. Chest X-Ray and computed tomography chest were performed in 300 (79.36%) and 242 (64.02%), respectively. Annual screening in those on advanced therapy for > 1 year was performed in 27.2% (50/184). Active TB developed in 17 (4.49%); 15 (88.23%) were on anti-tumor necrosis factor. LTB was detected in 40 (10.72%), with most diagnosed on the basis of IGRA (21/40, 52.50%). Among 17 patients who developed active TB, LTB screen was negative in 12 (70.58%).

Conclusion: Standard screening practices for LTB, prior to starting advanced therapy, remain suboptimal (< 60%) in India despite high TB endemicity.

Bile salts are essential molecules that have evolved beyond their digestive surfactant properties to act as relevant pathophysiological signalling modulators. In the gastroesophageal reflux disease (GERD), recurrent exposure of the oesophagus to harmful agents of gastric and duodenal origin, including bile salts, results in chronic inflammation and damage to the oesophageal mucosa, ultimately promoting the progression of the normal oesophageal epithelium to pre-malignant or malignant lesions, such as Barrett's oesophagus and adenocarcinoma. Although the acidity of the refluxed material has long been considered the leading cause of pathological features in GERD, some patients do not respond adequately to conventional therapy with proton pump inhibitors, implicating non-acidic components of the gastroesophageal reflux originating in the stomach and/or duodenum. Oesophageal motor activity is an essential protection against GERD symptoms, as it directly determines the contact time of the refluxed material inside the oesophagus. Oesophageal dysmotility profiles are documented in GERD, and bile salts appear to contribute to this dysfunction. In this work, we highlight the involvement of bile salts in the pathogenesis of GERD, particularly their effect on oesophageal motility and their potential signalling pathways.

This commentary provides a critical evaluation of the study by Wang et al, which focuses on rhapontin activating colonic nuclear factor erythroid 2-related factor 2 (NRF2) to explore its therapeutic potential for Parkinson's disease (PD)-associated gastrointestinal dysfunction. The commentary acknowledges the academic value of the study: It has not only validated intestinal NRF2 as a therapeutic target for PD but also provided experimental support for the "enteric pathology hypothesis". However, several key gaps remain unresolved in the study. At the gut microbiota level, the exploration of the causal relationship of the microbiota is insufficient, with no validation conducted via methods such as fecal microbiota transplantation; additionally, it fails to systematically integrate the gut-brain axis with PD and does not assess the impact of rhapontin on the composition or function of the gut microbiota. At the pathway mechanism level, it lacks an analysis of the crosstalk between NRF2 and other rhapontin-targeted pathways, including nuclear factor kappa-B, mitogen-activated protein kinase, adenosine monophosphate-activated protein kinase, and sirtuin 1. At the experimental method level, the behavioral testing methods for PD mouse models and the limitations of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse models need attention. Additionally, certain flaws exist in some experimental result figures. Furthermore, this commentary puts forward improvement suggestions for the study. Future research should prioritize multi-omics analysis, encompassing combined metabolomics and metagenomics detection, while conducting mechanistic validation of NRF2-interacting molecules (KEAP1 and p62). In addition, it is necessary to improve refined behavioral tests, focusing on incorporating cognitive function and anxiety-related assessment items.

Intraductal papillary mucinous neoplasms (IPMN) are pre-malignant tumours of the pancreas with variable malignant potential. Imaging often fails to map the disease extent accurately and guidelines differ on surgical thresholds. Pancreatoscopy, providing direct visualisation of the pancreatic duct and the option of targeted biopsies, may be able to delineate disease boundaries and improve preoperative and intraoperative decision-making. This mini-review appraises the current role, evidence base, and technical application of pancreatoscopy in the management of suspected or confirmed IPMN, with particular focus on its impact on the extent of pancreatic resections. Reported data show detection of additional lesions in about 20%-40% of cases and changes to operative strategy in roughly one third of patients, with low complication rates and high concordance between visual features and histology. Limitations include restricted availability, learning requirements, heterogeneity of technique, absence of a standardised visual classification, and a paucity of prospective outcome data; current international guidelines remain cautious. Pancreatoscopy is a promising adjunct to refine patient selection and the extent of resection in IPMN, particularly for delineating ductal spread and guiding margins. Routine adoption will require robust prospective studies to define diagnostic accuracy, impact on recurrence and survival, and cost-effectiveness.

Background: Prior studies indicate that allyl isothiocyanate (AITC) alleviates metabolic dysfunction-associated steatotic liver disease (MASLD). The vitamin D receptor (VDR) is known to exert protective effects in MASLD; however, whether AITC alleviates MASLD through VDR remains unclear.

Aim: To clarify the function and underlying mechanisms of AITC in MASLD via VDR.

Methods: AML-12 cells were exposed to 300 μM palmitate acid (PA) for 24 hours to establish an in vitro MASLD model, followed by treatment with AITC (20 μM). We quantified intracellular lipid content using oil red O staining and biochemical triglyceride assays, and measured the expression of key regulators of hepatic de novo lipogenesis, fatty-acid (FA) β-oxidation, and insulin-resistance-related signaling by immunoblotting and quantitative real-time polymerase chain reaction.

Results: To establish an in vitro MASLD model, AML-12 cells were treated with 300 μM PA for 24 hours. In this model, AITC significantly reduced protein levels associated with lipid synthesis and insulin resistance while upregulating those involved in FA β-oxidation. AITC enhanced VDR expression and increased the expression of hepatocyte nuclear factor 4 alpha (HNF-4α) and the downstream targets microsomal triglyceride transfer protein (MTTP) and apolipoprotein B (ApoB). These changes mitigated PA-induced lipid accumulation, alleviated insulin resistance, and stimulated FA β-oxidation. Additionally, vitamin D further enhanced the therapeutic effects of AITC on MASLD.

Conclusion: AITC provides a robust molecular basis for improving MASLD by activating hepatic VDR and driving the downstream HNF-4α/MTTP/ApoB signaling pathway. This pathway reduces hepatic lipid accumulation, promotes FA β-oxidation, and improves insulin resistance, establishing AITC as a promising treatment for MASLD.

Background: One of the main aims of colonoscopy is to detect and remove precancerous polyps. Multiple studies have shown that computer-aided detection (CADe) technology enhances key metrics, including adenoma detection rate (ADR), among endoscopists with low baseline detection rates. However, these findings largely come from controlled prospective studies where CADe is systematically used and endoscopists are aware they are being monitored for such metrics, bringing inherent biases. In Australia, CADe implementation is not yet standard practice, and its availability varies across endoscopy centers. We hypothesized that greater endoscopist use of CADe would be associated with higher ADR in real-world clinical settings.

Aim: To evaluate how varying levels of endoscopist use of CADe affect adenoma detection and other colonoscopy quality metrics in a tertiary Australian center, where CADe was available for all elective procedures from 2023.

Methods: A single-center retrospective cohort study was conducted at a tertiary Australian center after introduction of the Olympus Endo-AID^® CADe module in July 2023, available for all elective procedures. Colonoscopy reports from six months before and after implementation were reviewed. Endoscopists were grouped by observed CADe usage. The primary outcome was change in ADR by group. Secondary outcomes included sessile serrated lesion detection rate (SSL-DR), adenomas per patient (APP), and sessile serrated lesions per patient (SPP).

Results: Seven endoscopists performed 636 pre-CADe and 386 post-CADe colonoscopies. Two endoscopists used CADe 100% of the time, four used it 50%-99%, and one did not use CADe. No endoscopists used CADe 1%-50% of the time. ADR significantly improved from 29% to 41.9% in the 50%-99% group (odds ratio 1.77, 95%CI: 1.13-2.75, P = 0.01). No ADR change was observed in the 100% group, which had a baseline ADR above 60%, although APP increased from 0.90 to 2.08 (relative risk 2.31, 95%CI: 1.97-2.73, P < 0.0001). SSL-DR and SPP were not significantly affected by CADe.

Conclusion: In this real-world study, the availability of CADe was associated with an uptake by the majority of the endoscopists and led to significant improvement in ADR even when not being used in all procedures. Similarly to previous studies, no such benefit was observed for endoscopists who had a high baseline ADR. However, endoscopists with high baseline ADR did improve their APP after introduction of CADe. In addition, CADe availability did not improve SSL-DR across the cohort. This real-world significant increase from moderate baseline ADR reinforces its benefit when adopted in routine clinical practice.