Digestion最新文献

Background: Artificial intelligence (AI) applications in endoscopy, particularly computer-aided detection (CADe), have shown consistent benefit in randomized controlled trials (RCTs), with improvements in adenoma detection rate (ADR) and reductions in adenoma miss rate (AMR). Despite these findings, adoption of CADe in routine colonoscopy remains controversial, with international guidelines issuing divergent recommendations.

Summary: Evidence from RCTs demonstrates that CADe increases ADR, predominantly through detection of diminutive adenomas, while its effect on advanced adenomas is limited. Real-world implementation studies show comparatively diminished benefits, likely explained by factors which are difficult to measure, such as the absence of Hawthorne effect in real-world practice, the quality of mucosal exposure and decision-making regarding diminutive polyps. Cost-effectiveness analyses generally favour CADe even with varying assumptions across healthcare systems, although these are based on the high degree of improvement in ADR seen in RCTs with CADe. Potential harms include increased polypectomy of non-neoplastic lesions, higher lifetime colonoscopy burden, and the risk of deskilling among endoscopists. Concerns remain about bridging the gap between trial efficacy and real-world effectiveness, optimizing surveillance intervals, and mitigating deskilling and human-AI interaction issues.

Key messages: (1) CADe improves ADR in RCTs, but real-world effectiveness is inconsistent and often lacklustre. (2) Gains in ADR are largely derived from diminutive adenomas, and less with advanced adenomas, with uncertain impact on clinically significant outcomes such as colorectal cancer incidence and mortality. (3) Cost-effectiveness analyses are generally favourable, but dependent on assumptions about ADR improvement, CADe cost, and surveillance policies. (4) Deskilling and altered endoscopist behaviour represent important considerations that require further study. (5) Future integration of CADe with computer-aided diagnosis (CADx) and quality-assurance (CAQ) tools may maximize clinical benefit and cost-effectiveness, but evidence gaps must be addressed before widespread implementation.

Introduction: Esophageal achalasia is a rare motility disorder, and esophagogastroduodenoscopy (EGD) alone has limited diagnostic accuracy, often leading to delayed diagnosis. High-resolution manometry (HRM) remains the diagnostic gold standard, but its availability in primary care is limited. Therefore, more accessible diagnostic methods are needed. Given the widespread use of chest X-ray, we investigated whether it reveals distinctive features in achalasia patients.

Methods: In this retrospective cohort study, 215 patients with esophageal achalasia treated between 2015 and 2024 were analyzed. Diagnostic yields of EGD, esophagography, and computed tomography (CT) were evaluated among patients who underwent these examinations in primary care facilities. Chest X-rays were systematically reviewed for paratracheal radiolucency, and a novel radiographic sign-the Paratracheal Air Stripe Sign (PASS)-was defined as a paratracheal radiolucent area with a minimum width of ≥5 mm and length of ≥20 mm. To assess specificity, an additional analysis was performed in 210 patients with esophageal cancer as a non-achalasia control cohort.

Results: Diagnostic yields in primary care were 41.4% for EGD, 88.4% for esophagography, and 34.8% for CT. PASS was present in 67.0% of achalasia cases and more frequent in patients with type I achalasia, sigmoid-type morphology, and advanced esophageal dilation. Among patients undiagnosed by EGD, 63.9% exhibited PASS. In the non-achalasia control cohort, PASS was observed in 18.0% of cases, predominantly in patients with structural esophageal changes such as tortuosity or dilatation.

Conclusion: PASS represents a novel and clinically useful chest X-ray feature associated with esophageal achalasia. Its relatively high prevalence, even among cases missed by EGD, and low occurrence in non-achalasia patients suggest that routine assessment of PASS in chest X-rays may aid early detection and timely referral for definitive diagnosis, particularly in primary care settings.

Background and aim: The efficacy of electroacupuncture (EA) treatment in alleviating visceral hypersensitivity with irritable bowel syndrome (IBS) has been established. Abnormal bile acid metabolism and farnesoid X receptor (FXR) expression are recognized as potential contributors to visceral hypersensitivity in IBS. This study as a preclinical study of the IBS visceral hypersensitivity, explored the potential of EA to reduce visceral hypersensitivity in rats with IBS by improving bile acid metabolism and FXR expression. Methods：Heterotypic intermittent stress (HIS) for 9 days was used to induce visceral hypersensitivity in constipation-predominant irritable bowel syndrome (IBS-C). EA/Sham EA bilateral ST36 and LR3 acupoints began on the 5th day of HIS. Electromyography of the abdominal external oblique muscle and calcitonin gene-related peptide were used to assess colonic hypersensitivity. Colonoscopy and histopathological examination were used to evaluate pathological changes in the colon. Bile acid composition was analyzed using high performance liquid chromatography-mass spectrometry (HPLC-MS/MS), while FXR expression in colon tissue was quantified through immunofluorescence and Western blot.

Results: HIS induced visceral hypersensitivity in IBS-C rats. EA not only regulated bile acid levels in the feces of IBS-C rats, but it also had a downregulatory effect on the overexpression of FXR in the colon tissue of rats with IBS-C. The therapeutic effects were better than those of the sham EA. EA treatment alleviated visceral hypersensitivity in the colon of IBS-C rats.

Conclusion: Our data suggested that EA normalised colonic bile-acid signaling and FXR protein expression in an IBS-C rat model, offering a mechanistic hypothesis for future clinical evaluation.

Background: Emerging evidence highlights the gut microbiota as a key contributor to the pathophysiology of irritable bowel syndrome (IBS), acting through complex interactions with intestinal motility, immune function, epithelial barrier integrity, and the gut-brain axis. This narrative review summarizes current knowledge regarding the roles of the gut microbiota and their metabolites in IBS.

Summary: We discuss alterations in the gut microbiota in IBS, with particular emphasis on changes in short-chain fatty acid production, bile acid metabolism, serotonin signaling, and gas handling. Special attention is given to microbial metabolites as mediators of visceral hypersensitivity, intestinal permeability, and neuromodulation within the microbiota-gut-brain axis. Major alterations in the gut microbiota of IBS are characterized by a reduction in Bacteroidetes, Bifidobacteria, and Faecalibacterium, accompanied by an increase in Firmicutes. We explain the importance of butyrate metabolism in colonic epithelial cells for maintaining the anaerobic environment of the gut. In addition, we review the impact of diet-microbiota interactions, including FODMAP restriction, resistant starch intake, and protein fermentation, on symptom generation and microbial stability.

Key message: Although accumulating evidence supports a link between gut dysbiosis and IBS, establishing causal relationships remains challenging due to disease heterogeneity and dietary influences. Future large-scale, well-phenotyped, multi-omics studies integrating microbiota, metabolomic, and host factors are required to elucidate underlying mechanisms and to guide personalized therapeutic strategies for IBS.

Background: For intermediate-sized (10-20 mm) superficial non-ampullary duodenal epithelial tumors (SNADETs), various endoscopic resection (ER) techniques are available, including conventional endoscopic mucosal resection (EMR), underwater EMR (UEMR), and endoscopic submucosal dissection (ESD). However, the optimal method remains uncertain.

Summary: We conducted a systematic review of studies published from January 2013 to August 2023 using PubMed and the Japan Medical Abstracts Society database. Eligible studies reported ER outcomes for SNADETs of ≤20 mm. Data were extracted from 14 cohort studies (3 multicenter of lesions 10-20 mm in size and 11 single-center of lesions less than 20 mm), including en bloc and R0 resection rates, delayed bleeding, intraoperative and delayed perforation, and recurrence. In the multicenter studies, the pooled en bloc resection rates for EMR, UEMR, and ESD of intermediate-sized SNADETs were 82.7%, 74.8%, and 94.6%, respectively. The corresponding R0 resection rates were 54.2%, 50.6%, and 80.9%. Delayed bleeding rates were similar across methods (3.3% for EMR, 3.2% for UEMR, and 5.4% for ESD). However, intraoperative and delayed perforation were more frequent with ESD (7.9% and 3.0%) than with EMR (1.1% and 0.3%) and UEMR (0.0% and 0.0%). Single-center studies showed consistent trends, with ESD achieving higher resection rates but also showing greater variability in adverse events. Recurrence rates were about 5% for EMR and UEMR, with no recurrences reported after ESD.

Key messages: While ESD provides superior resection quality, EMR and UEMR offer favorable outcomes with fewer adverse events. Given their safety and efficacy profiles, EMR and UEMR should be considered appropriate first-line treatment options for intermediate-sized SNADETs.

Introduction: A new, minimally invasive method is needed to evaluate both esophageal muscle contraction and esophageal wall distensibility under physiological conditions. The primary objective of this study was to establish a novel examination method for evaluating esophageal wall motion using a transnasal endoscope with an endoscopic ultrasonography (EUS) probe. The secondary objective was to apply this method to gain new pathophysiological insights into the clinical subtypes of achalasia diagnosed by high resolution manometry.

Methods: The study included 20 patients with dysphagia. Patients were instructed to swallow 20 ml of oral rehydration solution while a transnasal endoscope and a 20 MHz EUS probe were used to record the swallowing motion. The esophageal lumen area and muscle layer thickness were measured on still images from recorded videos. The reproducibility of the method was evaluated for both internal and external consistency. The study also analyzed differences in esophageal wall motion among achalasia subtypes using two new parameters: the muscle layer contraction rate and the esophageal wall distension rate.

Results: The new transnasal EUS method was safely performed in all 20 patients without complications, and the images were sufficient for analysis. The reproducibility evaluation showed significant positive correlations for both internal and external reproducibility. The esophageal wall distensibility and muscle layer contraction rates differed between esophageal achalasia subtypes.

Conclusions: This pilot study successfully established a new, safe, and reproducible method for evaluating esophageal wall motion using transnasal EUS. This method will lead to a deeper understanding of the pathophysiology of esophageal motility disorders and potentially to the development of new treatment strategies.

Background: High-risk chronic atrophic gastritis (CAG; OLGA/OLGIM III-IV) carries significant gastric cancer (GC) risk, yet lacks reliable gastric stem cell (GSC)-based biomarkers. We evaluated GSC markers LGR5 (proliferative) and TFF2 (protective) for risk stratification and their Wnt/β-catenin-mediated mechanisms.

Methods: TCGA/GEO bioinformatics analysis preceded immunohistochemical validation in 60 clinical samples. Protein co-expression (Wnt/β-catenin, Ki67, Bax) was assessed. Diagnostic/prognostic power was tested via ROC and Kaplan-Meier analyses. Functional networks were deciphered through GO/KEGG enrichment.

Results: High-risk CAG and GC tissues showed LGR5 upregulation and TFF2 downregulation (P<0.001). IHC confirmed these patterns, with concurrent Wnt activation (β-catenin↑, Cyclin D1↑) and proliferation-apoptosis imbalance (Ki67↑, Bax↓). TFF2 outperformed LGR5 in diagnosing high-risk CAG (AUC: 0.89 vs. 0.76). Poor GC prognosis correlated with high LGR5/low TFF2 (P<0.05). Co-expression networks linked LGR5 to metabolic genes (CPS1, ADH6) and TFF2 to mucosal defense (GKN1, PGC).

Conclusion: LGR5 and TFF2 are promising biomarkers for high-risk CAG identification. Their inverse expression reflects GSC dysregulation via Wnt/β-catenin signaling, offering mechanistic insights for early intervention.

With the increasing proportion of the Helicobacter pylori (Hp)-naïve population in Japan, conventional Hp-infected gastric neoplasms (HpIGNs) have decreased, whereas Hp-naïve gastric neoplasms (HpNGNs) are being detected more frequently. Hp infection remodels the gastric mucosa and promotes tumorigenesis through a high mutational burden and epigenetic dysregulation, contributing to the histologically diverse and aggressive nature of HpIGNs. In contrast, HpNGNs arise with few genetic and epigenetic alterations, resulting in limited morphological diversity determined by the type of their background mucosa. Most HpNGNs arise in the fundic gland mucosa and exhibit a gastric phenotype, whereas those arising from the pyloric gland mucosa or gastric cardia show a variable phenotype. Regardless of histologic subtype, HpNGNs are generally biologically indolent, except for a subset arising in the gastric cardia. The histological classification of HpNGNs does not always fit conventional diagnostic frameworks for gastric neoplasms. In particular, foveolar-type adenomas (FGAs) need to be subclassified into flat and raspberry types, which represent distinct molecular entities. Furthermore, HpNGNs with a MUC6-dominant gastric phenotype, including gastric adenocarcinomas of fundic gland or fundic gland mucosa type (GA-FG/GA-FGM) and some flat-type FGAs with partial MUC6-dominant components, and pyloric gland adenomas (PGAs) form a morphological and molecular continuum, occasionally making histological distinction difficult. A comprehensive disease concept integrating these lesions may help resolve this diagnostic issue. As the prevalence of Hp infection continues to decline worldwide, HpNGNs are expected to emerge as a distinct disease entity, highlighting the need for refined diagnostic frameworks and risk-based surveillance strategies in the post-Hp era.

Background: The Fecal Immunochemical Test (FIT) is a wide available fecal biomarker that could evaluate the disease activity in IBD. The aim is to assess the correlation between the FIT and fecal calprotectin (FC) for evaluating IBD activity.

Methods: Unicentric, transversal cohort study. Consecutive patients with IBD were included and FIT and FC were determined. The clinical activity was assessed with Truelove-Witts and Yamamoto-Furusho index for UC patients while Harvey-Bradshaw and CDAI for CD patients. Spearman's rank correlation test was used to assess the correlation between FIT and FC. Sensitivity, specificity, and positive and negative predictive values for FIT and FC were calculated. Receiver operator curves were constructed.

Results: A total of 206 patients were included. One hundred forty-eight (72%) patients had diagnosis of UC and 58 (28%) with CD. The median of FIT was 2.8 g/g (range, 2.6 - 2394 g/g) and the median for FC level was 265.5 g/g (range, 22 - 6285 g/g). There was a very good correlation between FIT with and FC in UC patients (rs= 0.745, P < 0.01) and moderate in CD patients (rs = 0.574, P < 0.01). A FIT cutoff of 2.6 g/g identified endoscopic activity in UC patients with a sensitivity of 78%, specificity of 86%, PPV of 91% and NPV of 67% with an AUC of 0.852 (95% IC 0.758-0.946).

Conclusion: FIT can be an alternative fecal biomarker to assess the disease activity in UC patients.

Introduction European and national Celiac Disease (CeD) guidelines offer an easy pathway to diagnose CeD. The German CeD Registry aimed to assess symptoms and clinical findings before diagnosis, diagnostic delay, care during the diagnostic process, and factors associated with persistence of symptoms. Methods Individuals with CeD provided demographic, clinical and healthcare-related information. Participants were divided into four subgroups according to age at diagnosis (>18 or <18 years) and year of diagnosis (before and since 2012). Factors associated with symptoms after at least 1-year on a gluten free diet (GFD) were assessed using multivariate logistic regression. Results From 11/2019 to 10/2021, 2333 participants were enrolled. After exclusion of 169 (7.2%), 2164 remained for analysis, thereof 796 (36.8%) were diagnosed <18 years, and 1283 (59.3%) since 2012. Most common symptoms before diagnosis included abdominal pain (83%), bloating (82%), fatigue (78%), and diarrhoea (71%). Diagnostic delay after 2012 was longer in adults than children (median 4.4 years [IQR 1.2-13.0] versus 1.1 [IQR 0.5 - 2.2], respectively) (p<0.001). Guideline-conform diagnoses increased over time. After diagnosis, only 60% received professional dietary counselling. Factors associated with symptoms despite GFD included female gender (OR 1.79 [95%CI 1.34; 2.40], p<0.001), same symptom before diagnosis (OR 3.45 [2.45; 4.96], p<0.001), insufficient information provided at diagnosis (OR 1.25 [1.00; 1.57], p=0.046), and age at diagnosis (per decade) (OR 1.11 [1.04;1.18], p<0.001), but not time since diagnosis. Conclusions Our findings revealed deficits in awareness, the diagnostic process, and post-diagnostic care that are linked to decreased clinical improvement over time.