Introduction

Capsule Endoscopy (CE) offers a minimally invasive method for comprehensive visualization of the gastrointestinal (GI) tract. Protruding lesions are relatively common findings in CE, with variable incidence and diverse pathological significance. Accurate detection of these lesions is crucial but remains challenging due to the time-consuming nature of CE interpretation and susceptibility to human error. While artificial intelligence (AI) presents a promising solution, real-world evidence evaluating its clinical performance is still scarce. To assess the diagnostic performance of a deep learning convolutional neural network (CNN) for the detection of protruding lesions in complete CE videos under real-world clinical conditions.

Aims & Methods

Our group conducted a prospective, multicenter validation study comparing AI-assisted CE reading to standard, conventional interpretation. A total of 211 CE videos, obtained using three different CE systems across seven centers in Portugal, Spain, Brazil, and the United States, were analyzed. Following initial standard readings, an independent expert conducted AI-assisted readings using a CNN specifically trained to detect small bowel protruding lesions. Discrepancies between conventional and AI-assisted reports were adjudicated by a third-party expert from an independent center to establish the reference standard. Diagnostic performance was assessed using sensitivity, specificity, accuracy, and the area under the receiver operating characteristic curve (AUC-ROC).

Results

AI-assisted reading detected 106 confirmed protruding lesions, compared to 42 identified through conventional reading. Sensitivity was significantly higher with AI-assisted reading (95.9% vs. 64.6%), although specificity was lower (78.7% vs. 96.1%). Overall accuracy was relatively lower with AI-assisted reading (81.2% vs. 91.5%). The AUC-ROC was 0.86 for AI-assisted and 0.80 for standard reading. Additionally, AI-assisted reading reduced the mean examination time to 316 seconds per video.

Conclusion

AI-assisted interpretation of complete CE videos significantly enhances the detection of protruding lesions compared to conventional reading, although at the expense of slightly reduced specificity. The inclusion of videos from multiple CE systems addresses interoperability challenges, while the participation of centers from four countries across two continents supports the model’s generalizability and real-world clinical applicability.

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), has emerged as one of the leading causes of chronic liver disease worldwide. MASLD is closely associated with components of metabolic syndrome, including obesity, insulin resistance, dyslipidemia, and hypertension. The role of gut microbiota dysbiosis in MASLD pathogenesis is increasingly recognized, with microbial imbalance contributing to systemic inflammation and metabolic disturbances.

Aims & Methods

The aim was to determine gut microbiota composition in patients with MASLD and evaluate the impact of probiotic therapy on metabolic, inflammatory, and lipid parameters. The study included 152 patients diagnosed with MASLD. Diagnosis was based on clinical, laboratory, and imaging findings, including ultrasound and steatometry, alongside cardiometabolic risk factors. Gut microbiota composition was evaluated using quantitative real-time PCR (qRT-PCR). Patients received a combined probiotic therapy containing Saccharomyces boulardii CNCM I-745, Lactobacillus acidophilus (LA-5), and Bifidobacterium lactis (BB-12). Changes in biochemical markers, lipid profiles, inflammatory parameters, and gut microbiota composition were assessed before and after therapy.

Results

At baseline, patients with MASLD demonstrated gut microbiota dysbiosis, characterized by an increased proportion of Firmicutes (50.3%) and Actinobacteria (15.34%), and an elevated Firmicutes/Bacteroides (F/B) index (5.02). Following probiotic therapy, significant improvements were observed: the proportions of Firmicutes and Actinobacteria decreased, the F/B index was reduced, and levels of ALT, AST, high-sensitivity C-reactive protein (hsCRP), total cholesterol, and triglycerides declined, while HDL-C levels increased. Positive correlations were identified between elevated Firmicutes and Actinobacteria and markers of cardiometabolic risk, such as hsCRP and triglycerides.

Conclusion

Gut microbiota dysbiosis is strongly associated with metabolic and inflammatory disturbances in MASLD. Combined probiotic therapy effectively corrected microbial imbalance, reduced systemic inflammation, and improved metabolic and lipid parameters. These findings support the role of microbiota-targeted interventions as an adjunctive approach in the comprehensive management of MASLD.

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease (NAFLD), is a leading cause of chronic liver pathology globally and is closely associated with metabolic syndrome components, including obesity, insulin resistance, dyslipidemia, and hypertension. Recent evidence emphasizes the significant role of gut microbiota dysbiosis in MASLD pathogenesis, with specific bacterial shifts contributing to metabolic disturbances and systemic inflammation.

Aims & Methods

The aim was to evaluate the gut microbiota composition in MASLD patients and assess the impact of probiotic therapy on metabolic, inflammatory, and lipid profile parameters. The study included 152 patients diagnosed with MASLD. Gut microbiota profiling was conducted using quantitative real-time PCR (qRT-PCR), and metabolic parameters were assessed via biochemical analyses. Patients received a combined probiotic regimen containing Saccharomyces boulardii CNCM I-745, Lactobacillus acidophilus (LA-5), and Bifidobacterium lactis (BB-12) for gut microbiota correction. Changes in biochemical markers, lipid profiles, and microbiota composition were evaluated before and after therapy.

Results

At baseline, MASLD patients showed a marked imbalance in gut microbiota, characterized by increased proportions of Firmicutes (50.3%) and Actinobacteria (15.34%), along with an elevated Firmicutes/Bacteroides (F/B) ratio (5.02). Probiotic intervention significantly reduced Firmicutes and Actinobacteria percentages and lowered the F/B ratio. Biochemically, there were significant decreases in ALT, AST, alkaline phosphatase, high-sensitivity C-reactive protein (hsCRP), total cholesterol, triglycerides, and increases in HDL-C levels. Positive correlations were found between elevated Firmicutes and Actinobacteria abundance and markers of cardiometabolic risk, such as hsCRP and triglycerides.

Conclusion

Gut microbiota dysbiosis plays a crucial role in the metabolic and inflammatory disturbances associated with MASLD. Combined probiotic therapy effectively improved gut microbial composition, reduced systemic inflammation, and positively influenced lipid metabolism, supporting its role as an adjunctive treatment strategy for MASLD.

Clinical Case Summary

Female patient, 53 years old, with personal history of autosomal dominant polycystic kidney disease (ADPKD) with polycystic liver disease that presented to the emergency department with jaundice and choluria. She denied other symptoms, such as fever, nausea or abdominal pain. The patient had started therapy with tolvaptan for ADPKD three months before, suspended after two months due to suspected liver toxicity. The patient denied taking other new medication, consumption of alcohol, herbal products or contact with animals. Laboratory tests revealed elevated C-reactive protein and markedly elevated liver enzymes (>10xULN) with bilirubin level of 6mg/dL. Abdominal ultrasound and CT scan showed an enlarged liver with multiple cysts, the largest measuring 12.5cm in diameter, with heterogeneous content and no mural enhancement and mild dilation of right intrahepatic bile ducts. A diagnosis of cholangitis was considered, empiric antibiotic therapy was initiated, and the patient was admitted. Abdominal MRI on day 7 demonstrated mild to moderate dilation of right biliary ducts, most likely caused by extrinsic compression from liver cysts. Due to this and to worsening cholestasis, with total bilirubin level reaching 11.7mg/dL, ultrasound-guided percutaneous drainage of the larger cyst was performed, without significant improvement in cholestatic parameters. Therefore, a percutaneous liver biopsy was obtained and revealed changes indicative of biliary outflow impairment but also histological evidence of mild resolving hepatitis, suggestive of possible concomitant drug toxicity. The patient improved over time, with normal bilirubin level two months after admission. Liver function was maintained throughout the course of disease. This case illustrates concurrent damage due to liver cysts biliary duct compression but also drug induced liver injury (DILI) caused by tolvaptan, a therapeutic agent with increasing use for slowing the progression of kidney function decline in ADPKD.

Clinical Case Summary

Introduction: Cholecystoduodenal fistula (CDF) is a rare gallstone complication causing abnormal communication between the gallbladder and duodenum. Surgical treatment carries significant risks in elderly patients due to frequent comorbidities. We present a minimally invasive strategy combining enteral nutrition support and endoscopic duodenal stenting for CDF management in a high-risk patient.
Case summary: An 84-year-old woman presented with intermittent right upper quadrant pain and fever for two months. Her medical history included hypertension, type 2 diabetes, and myocardial infarction. Examination revealed right upper quadrant tenderness without peritonitis. Laboratory findings indicated markedly elevated C-reactive protein and mild leukocytosis. Contrast-enhanced abdominal CT identified gallstones and duodenal wall thickening, suggesting CDF. Gastroscopy revealed gallstones within the duodenal bulb; following stone removal, a fistulous opening was visualised and confirmed by contrast imaging. Initial conservative therapy (antibiotics, acid suppression, nasojejunal nutrition) failed, with follow-up CT at 20 days showing persistent fistula patency. Considering advanced age and comorbidities, a multidisciplinary team opted for endoscopic duodenal stenting. Gastroscopy identified pinpoint stenosis in the duodenal bulb, which was endoscopically dilated, enabling successful placement of a fully covered metallic stent.Postoperatively, the patient resumed oral liquids and was discharged shortly thereafter. Follow-up confirmed stable stent position, resolution of biliary pneumatosis, and complete symptom relief.
Conclusion: This case highlights the effectiveness of combining enteral nutrition and endoscopic duodenal stenting as a safe, minimally invasive alternative for elderly, high-risk patients with CDF, meriting further investigation.

Disclosure

Nothing to disclose.

Introduction

The biliary tract cancers (BTC) are among the most frequent differential diagnosis of the obstructive cholestasis. Accurate diagnosis remains challenging, as conventional tools such as brush cytology and CA 19-9 lack sufficient sensitivity and histological confirmation is often difficult. The subsequent management of this condition involves the use of biliary tract stenting via endoscopic retrograde cholangiography to facilitate optimal bile flow. We have recently reported that biliary stents are a potential source of molecular biomarkers, including the microbiome.

Aims & Methods

The aim of this study was to investigate the potential of biliary stent microbiome patterns as a biomarker for BTC. Patients diagnosed with obstructive cholestasis of various aetiologies, including malignant disease, BTC and non-malignant disease (NM) including inflammatory and postoperative stenosis, were prospectively enrolled. The study was conducted in 3 steps including discovery, confirmation and validation cohorts to ensure reliability and reproducibility. The discovery cohort comprised a total of 123 patients (28 with BTC, 54 other malignancies and 69 NM). The confirmation cohort comprised 54 patients (16 with BTC) with the inclusion of stents from alternative time points or independent stents as part of the multi-stenting management from the same time point. The validation cohort included stents from 38 independent patients (11 with BTC). The DNA was extracted and subsequently analysed using 16S rRNA gene sequencing. The diagnostic performance was assessed using a receiver operating characteristic (ROC) curve, and the area under the curve (AUC) was calculated.

Results

There were significant differences in the stent-derived microbiome between BTC and patients with other conditions. BTC was associated with a higher abundance of following taxa Bacillales, Peptoniphilaceae, Erysipelotrichaceae and Actinomyces while Fusobacteriaceae, Klebsiella, Dialister and Anaeroglobus was increased in the non-malignant cohort. The calculation of the microbiome-based prediction score was performed by utilising the abundance of the significantly different taxa and applying logarithmic normalisation. ROC analysis on the testing cohort, revealed an AUC of 0.82 (95%-CI: 0.73 to 0.90, p < 0.0001) in prediction of BTC based on the microbial score. To confirm the data, independent analyses were performed using the confirmation cohort revealing comparable results with the AUC of 0.85 (95%-CI: 0.74 to 0.97, p < 0.0001). In the subsequent phase, an independent validation cohort was used to confirm the robustness of the findings. ROC analysis yielded an AUC of 0.83 (95% CI: 0.71–0.96, p = 0.0014), demonstrating promising reproducibility of the microbiome-based score as a diagnostic tool.

Conclusion

Patients with biliary stenosis exhibit distinct biliary microbial alterations. Using stent-derived microbiome data analysis, we developed a novel microbiome-based score to estimate the probability of BTC in patients with cholestasis. Results from both validation and confirmatory cohorts strongly support the utility of this tool for predicting BTC in patients with biliary stenosis.

Introduction

Metastasis is the leading cause of poor prognosis and high mortality in colorectal cancer (CRC). Chemokines play multifaceted roles in cancer immunity and progression. CCL7 is upregulated in CRC, but how CCL7 regulates CRC metastasis at the molecular level remains unclear.

Aims & Methods

In this study, we investigate the regulatory mechanisms and clinical significance of CCL7-mediated CRC metastasis.Immunohistochemistry (IHC) assay was performed to detect the expression of CCL7 and SOX4 in CRC tissue, moreover, the correlation between their expression and tumor distant metastasis, survival, and prognosis was analyzed. To explore their impact on CRC migration, invasion and metastasis, functional experiments and animal experiments were performed in vitro and in vivo, respectively. Gene expression changes were studied by real-time quantitative PCR (qRT‒PCR), Western Blot (WB) and RNA-seq analysis. Chromatin Immunoprecipitation sequencing (ChIP-seq), luciferase reporter assay and Electrophoretic Mobility Shift assay (EMSA) were implemented to explore the mechanisms.

Results

Two clinical cohorts showed that CCL7 and SOX4 were upregulated in CRC tissues and correlated with lymphatic metastasis, distant metastasis, and poor prognosis. Functionally, CCL7 and SOX4 promoted CRC cell proliferation, invasion and metastasis in vitro and in vivo, respectively. Rescue assays revealed SOX4 as a downstream molecule involved in CCL7-mediated CRC metastasis. Through binding to the promoter region of CD44 directly, SOX4 activated its transcription and promotes CRC metastasis, which we proved via promoter analysis assays and analysis of the results of ChIP-seq and RNA-Seq. The Wnt/β-catenin signaling pathway contributed to the regulation of these processes.

Conclusion

The chemokine CCL7 induces elevated expression of SOX4, which subsequently promotes CRC metastasis by transcriptionally upregulating CD44. The CCL7-SOX4-CD44 axis could be applied as a potential target and strategy for preventing and treating CRC metastasis in clinical settings.