Scandinavian Journal of Gastroenterology最新文献

Background/aim: Endoscopic submucosal dissection (ESD) for early gastric cardiac cancer (EGCC) faces anatomical challenges. This study aims to develop and validate a predictive model for ESD difficulty in EGCC, providing a basis for matching difficulty levels with endoscopists' experience.

Methods: This multicenter retrospective study included 514 EGCC patients from five tertiary hospitals (2017-2025). Patients from the 900th Hospital were randomized to training (n = 206) and internal validation (n = 164) cohorts; four other hospitals formed an external cohort (n = 144). Predictors with high collinearity (VIF ≥ 5) were excluded. Predictor selection was performed using LASSO regression, followed by multivariable logistic regression. Model performance was assessed using ROC curves, calibration plots, and decision curve analysis (DCA).

Results: The clinical scoring model incorporated four factors: Paris type III lesion (3 points), maximum diameter ≥3 cm (1 point), submucosal invasion (5 points), and lesion located on the anterior wall of the cardia (3 points). Model performance demonstrated an AUC of 0.784 (95% CI, 0.695-0.876) in the training cohort, 0.762 (95% CI, 0.653-0.884) in internal validation, and 0.740 (95% CI, 0.636-0.845) in external validation. Difficulty stratification was defined as: easy (0, 1, or 3 points), intermediate (4, 5, or 6 points), and difficult (8 or 11 points).

Conclusion: This validated system optimizes endoscopist matching, reducing costs and recurrence in EGCC ESD.

Background: Coeliac disease (CeD) affects 1-2% of the western population. Diagnosis is based on serology and duodenal biopsy, but serology-based diagnosis in adults has been approved in Europe.

Objective: To evaluate the diagnostic performance of IgA anti-transglutaminase 2 (IgA-TG2) and IgG anti-deamidated gliadin peptides (IgG-DGP), and their combinations, compared with biopsy in a real-world secondary care setting.

Methods: Adult patients referred to secondary care endoscopy service at Oslo University Hospital for suspected CeD were invited to participate. CeD diagnosis followed European and Norwegian guidelines, requiring positive serology and mucosal damage.

Results: Among 312 evaluable patients, 215 were diagnosed with CeD between 2018 and 2024. Analysis of IgA-TG2 above threshold (>4 U/ml) showed 93% specificity and 94% sensitivity, while IgG-DGP (>20 U/ml) showed 88% specificity and 83% sensitivity. In ROC analyses, the AUC values were 0.98 and 0.95, respectively. Higher threshold (2x, 3x, 5x and 10x ULN) of IgA-TG2 increased specificity (99% to 100%) but lowered sensitivity (82% to 49%). Using IgG-DGP did not increase specificity but detected six missed CeD cases by IgA-TG2. Forty-two percent (n = 92) of cases could be diagnosed with a no-biopsy approach with 10x ULN IgA-TG2 at referral with 100% specificity.

Conclusion: Serology correlates strongly with histological changes, supporting diagnosis without gastroscopy. A 10x ULN threshold shows excellent specificity at the expense of sensitivity, thus lower thresholds may be preferable due to diminishing gains in specificity. IgG-DGP serves as a valuable complementary marker, that improves sensitivity and helps identify patients with weak IgA-TG2 responses.

Introduction: This systematic review and meta-analysis aimed to assess the safety and efficacy of oral microbiome therapy (OMT) for the treatment of recurrent Clostridioides difficile infection (CDI).

Methods: A comprehensive search was performed in PubMed, Cochrane library, Scopus and Embase. All randomized controlled trials (RCTs) meeting predefined inclusion criteria were included. Statistical analysis was performed using R software.

Results: Three RCTs comprising 469 patients were analyzed, of whom 250 (53%) received OMT and 219 (47%) received placebo. OMT significantly reduced CDI recurrence at week 8 compared to placebo (risk ratio [RR] 0.57; 95% confidence interval [CI] 0.33-0.99; p = 0.04). In exploratory efficacy analyses, no significant differences in recurrence were observed between groups when stratified by prior fidaxomicin use (RR 0.36; 95% CI 0.03-4.01; p = 0.40) or vancomycin use (RR 0.68; 95% CI 0.30-1.55; p = 0.35). Similarly, Firmicutes engraftment at week 1 (mean difference [MD] 41.78; 95% CI -10.55 to 94.11; p = 0.12) and week 8 (MD 34.06; 95% CI -2.49 to 70.61; p = 0.07) did not show statistically significant between-group differences. Safety outcomes and adverse events were comparable between OMT and placebo.

Conclusion: OMT seems to reduce CDI recurrence at week 8 compared with placebo while demonstrating a comparable safety profile, supporting its role as an effective, well-tolerated therapy for recurrent CDI. New studies are necessary to confirm these findings.

Registration: The study protocol was registered in the International Prospective Register of Systematic Reviews (PROSPERO) under registration number CRD420251022230.

Aim: Gastroesophageal reflux disease (GERD) is closely linked to esophageal motility dysfunction. While high-resolution manometry (HRM) remains the gold standard for evaluating esophageal motility, the conventional single water swallow (SWS) protocol may not fully capture motility abnormalities. This study investigates esophageal motility characteristics in GERD patients using solid food swallows (SFS) to better assess clinically relevant dysfunction.

Methods: Esophageal motility parameters were compared between GERD and non-GERD groups during both SWS and SFS. Correlations between SFS findings and dysphagia symptoms, endoscopic findings and reflux metrics were analyzed, followed by multivariate regression to identify independent GERD risk factors.

Results: Among 151 participants, 54 were diagnosed with GERD. Impaired SFS esophageal body motility was more prevalent in GERD versus non-GERD patients (p < 0.01). Moreover, the GERD group exhibited significantly higher rate of esophageal hypomotility during SFS compared to SWS (p < 0.001). With SFS testing, 35.2% (19/54) of GERD with normal SWS esophageal motility demonstrated Impaired SFS esophageal body motility. Multivariate analysis identified SFS esophageal body hypomotility (OR: 5.158, 95%CI: 2.439-10.909, p < 0.001) as independent GERD predictors. The prevalence of dysphagia symptom and esophagitis were higher in patients with esophageal hypomotility of SFS. Distal contractile integral of SFS positively correlated with mean nocturnal baseline impedance (r = 0.393), while inversely correlating with supine bolus clearance time (r=-0.326) and acid exposure (r=-0.403).

Conclusions: SFS unmask clinically significant esophageal dysmotility in GERD patients that SWS miss, revealing pathophysiology linked to prolonged acid exposure and mucosal injury. SFS-enhanced HRM protocols may improve GERD evaluation and risk stratification.

Introduction: Risk factors for gastric cancer in the long-term post-Helicobacter pylori (H. pylori) eradication cohort remain unclear. This study aimed to identify risk factors for gastric cancer in the long-term post-eradication cohort.

Methods: We conducted a retrospective case-control study. Patients who underwent endoscopic submucosal dissection for gastric cancer diagnosed more than 10 years after eradication therapy were defined as the Gastric Cancer (GC) group. Patients who remained free of gastric cancer for more than 10 years after eradication therapy were defined as the No Gastric Cancer (NGC) group. We compared clinical and endoscopic findings between the two groups after propensity score matching for age, sex, and post-eradication period.

Results: A total of 105 patients in the GC group and 127 patients in the NGC group were included. After matching, 95 pairs were created. In the GC group, open-type atrophy (p < 0.001), severe intestinal metaplasia (p < 0.001), map-like redness (p = 0.002), and xanthomas (p = 0.005) were significantly more frequent, whereas history of gastric ulcer (p = 0.022), history of duodenal ulcer (p = 0.015), and fundic gland polyps (p = 0.006) were significantly less frequent. Multivariate analysis identified open-type atrophy (odds ratio [OR], 10.40; 95% confidence interval [CI], 4.57-23.80) and severe intestinal metaplasia (OR, 5.15; 95% CI, 2.06-12.90) as independent risk factors.

Conclusion: We demonstrated that open-type atrophy and severe intestinal metaplasia were independent risk factors for gastric cancer in patients more than 10 years after eradication therapy of H. pylori.

Background: Inflammatory bowel disease (IBD) is often diagnosed during reproductive age, requiring adequate management during pregnancy. Physiological changes during pregnancy affect liver enzymes, complicating interpretation in a population prone to liver test abnormalities. This study aims to investigate liver enzyme trends throughout pregnancy in women with IBD.

Methods: A retrospective cohort study was conducted in three Dutch university hospitals. Pregnant women with IBD were included; liver enzyme levels were analyzed throughout pregnancy using Bayesian modeling. The association between liver enzymes and IBD disease activity, medication, pregnancy and adverse pregnancy outcomes was assessed, with estimated marginal means (EMMs) reported across trimesters and clinical subgroups.

Results: Liver enzyme levels exhibited significant trimester-specific variations in pregnant individuals with IBD. Levels of aminotransferases, γ-glutamyl transferase (γGT) and bilirubin generally declined, particularly in the second trimester, whereas alkaline phosphatase (ALP) levels increased markedly in the third trimester, mirroring physiological changes observed in healthy pregnancies. Adverse pregnancy outcomes were not associated with differences in liver enzyme levels. Several medications - particularly ustekinumab, vedolizumab, thiopurines, corticosteroids and amino salicylates - were associated with liver enzyme values or interacted with pregnancy, modulating the direction or magnitude of change. However, these effects were generally modest and remained within reference values.

Conclusions: In pregnant women with IBD, changes in liver enzyme levels reflect physiological gestational adaptations rather than pharmacologic effects. Although medication-specific interactions were detected, their clinical significance appears limited. Marked elevations in liver enzymes during pregnancy cannot routinely be attributed to IBD activity or medication and warrant urgent analysis.

Background: This meta-analysis aimed to evaluate the association between distinct KRAS mutations and overall survival (OS) in pancreatic ductal adenocarcinoma (PDAC) patients.

Methods: A comprehensive literature search was conducted across major databases to identify studies reporting hazard ratios (HRs) and 95% confidence intervals (CIs) for OS associated with key KRAS mutations (G12D, G12R, and G12V) in PDAC patients, from inception until January 2025. Subgroup analyses were carried out based on disease stage (resectable and borderline resectable as early-stage disease and locally advanced and metastatic as late-stage disease) and treatment approaches (operation, chemotherapy, or combination of both).

Results: KRAS G12D mutation was significantly associated with poor OS (HR = 1.64, 95% CI: 1.28-1.99, p < 0.05). In subgroup analysis, G12D mutation was significantly associated with poor OS in those receiving chemotherapy (HR = 1.29, 95%CI: 1.18-1.39, p < 0.05) and in those with late-stage disease (HR = 1.29, 95%CI: 1.18-1.39, p < 0.05). G12R was significantly associated with improved OS in patients receiving chemotherapy (HR = 0.74, 95% CI: 0.56-0.99, p = 0.042). G12V had a significant association with improved OS in patients with early-stage disease (HR = 0.67, 95% CI: 0.52-0.86, p = 0.002).

Conclusions: The study highlights the heterogeneous prognostic impact of KRAS mutations in PDAC. These findings suggest that the prognostic relevance of KRAS mutations in PDAC may depend on clinical factors such as treatment modality and disease stage.

Purpose: The sucrase-isomaltase (SI) gene encodes sucrase-isomaltase enzyme found on the intestinal brush-border that has a major function in the hydrolysis of sucrose, oligosaccharides, and starch. Mutations disrupting its function cause genetic sucrase-isomaltase deficiency (GSID). Variants leading to mild to moderate reductions in enzyme activity may mimic disorders of gut-brain interaction (DGBI), and differentiating the etiology is crucial for initiating appropriate treatment. In this study, we aim to determine the rate of GSID in individuals who underwent whole exome or clinical exome sequencing (WES/CES) for indications other than chronic gastrointestinal symptoms in a single-center cohort. We also focused on a second group, the pediatric DGBI patients, who underwent SI gene analysis, to evaluate the rate of GSID in pediatric DGBI patients and assess the clinical utility of SI gene testing in GSID diagnosis.

Methods: We retrospectively reviewed 980 patients who underwent WES/CES between 2017-2022, and 148 pediatric patients with DGBI evaluated between May 2021 and August 2022 who received SI gene analysis.

Results: The frequency of symptomatic GSID was found to be 0.3% among patients who underwent WES/CES, whereas it was 10% among pediatric DGBI patients. In DGBI patients carrying SI gene mutations, clinical improvement with a sucrose- and starch-free diet in combination with a sacrosidase response proved effective for establishing a diagnosis in all cases.

Conclusion: GSID has been frequently detected among pediatric DGBI patients. SI gene analysis combined with a sucrose-restricted diet and a sacrosidase challenge provides a reliable, non-invasive approach for definitive diagnosis.