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.

Introduction

Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a growing global health concern. While lifestyle factors and metabolic dysfunction play a significant role in MASLD pathogenesis, emerging evidence highlights the contribution of genetic predispositions in modulating disease susceptibility and progression. Among these, variants in the cholesteryl ester transfer protein (CETP) gene have garnered attention due to their involvement in lipid metabolism and cholesterol homeostasis.

Aims & Methods

This study aims to investigate the role of CETP gene variants in MASLD, aiming to uncover genetic links to steatosis development. This study is a prospective case control study. The patients were all recruited from the outpatient clinic at the Internal Medicine Department, Minia University from January 2021 to December 2022. Of 2797 patients, 80 MASLD patients aged 20-65 years old with steatosis and one or more factors of metabolic syndrome were included. All patients with chronic liver, renal or cardiac disease and pregnancy are excluded. A group of 20 health patients was added as a case control.100 patients were categorized into 4 groups; obese diabetic group (n=25), obese nondiabetic (n=20), lean diabetic group (n=15), lean nondiabetic (n=20), control group (n=20). All medical history, demographic data, laboratory investigations, imaging data are collected.

Results

Of 100 subjects, 70 were females (70%), 28 patients had hypertension (28%). Lipid profile of 4 groups shows significant difference in total cholesterol and triglyceride (P<0.001). mutant genotype (AA) of CETP gene was significantly more in lean nondiabetic group while wild type (CC) was more prevalent among obese diabetic group (P<0.001).The wild type (CC) CETP correlated more with higher hepatic steatosis index (HIS) and higher values of fatty liver index (FLI) and hence with more steatosis, however the mutant genotype (AA) correlated with lesser HSI and significantly with lower values of FLI and hence correlated poorly with steatosis (P<0.001).

Conclusion

Understanding the genetic predispositions in MASLD pathogenesis as the interplay between CETP gene variants and metabolic factors may pave the way for personalized therapeutic strategies targeting lipid metabolism and cholesterol homeostasis in MASLD management. This study highlights the significant role of CETP gene variants in modulating hepatic steatosis in MASLD patients. The wild-type CETP genotype (CC) is associated with higher HSI, FLI values and greater steatosis severity particularly in obese diabetic individuals. Conversely, the mutant genotype (AA) correlates with lower steatosis indices, suggesting a protective effect against hepatic fat accumulation, especially in lean non-diabetic populations. This study underscores the potential role of CETP gene variations in influencing steatosis severity in MAFLD, offering insights into personalized risk stratification and accurate diagnosis of MAFLD.

Disclosure

Nothing to disclose

Clinical Case Summary

Introduction: Non-occlusive mesenteric ischemia (NOMI) is a rare but critical condition resulting from insufficient mesenteric blood flow without arterial occlusion. When complicated by portal venous thrombosis and small bowel obstruction, NOMI presents significant diagnostic and therapeutic challenges, requiring early recognition and multidisciplinary management to improve outcomes.
Methods: This study retrospectively analyzed a NOMI patient with portal venous thrombosis and small bowel obstruction, reviewing clinical history, imaging, treatment strategies, and outcomes. The effectiveness of catheter-directed thrombolysis with anticoagulation and surgical intervention for recurrent ischemia was assessed, including recurrence rates and treatment outcomes.
Results: A 60-year-old male with atrial fibrillation, presented with prolonged abdominal pain and bloating. Imaging showed mesenteric and portal venous thrombosis causing small bowel obstruction. He underwent catheter-directed thrombolysis with initial improvement. However, symptoms recurred one month later, necessitating small bowel resection due to chronic ischemia. Postoperatively, the patient recovered well with no further recurrence.
Conclusions: This study emphasizes the need for early diagnosis and multidisciplinary management in NOMI with portal venous thrombosis. Catheter-directed thrombolysis with anticoagulation effectively restores mesenteric blood flow, while surgical intervention is key for recurrent ischemia. Tailored, evidence-based approaches are crucial for optimizing outcomes.
The poster will include specimen images, immunohistochemical images, and abdominal CT images.

Clinical Case Summary

Celiac disease (CD), an autoimmune enteropathy triggered by gluten ingestion, commonly presents with gastrointestinal symptoms but can also manifest with various extra-intestinal symptoms, including cutaneous manifestations. Erythema nodosum (EN), a form of acute hypodermitis, is a rare extra-intestinal manifestation of CD and is often associated with other conditions such as infections and inflammatory enteropathies. We report the case of an 11-year-old girl who presented with erythema nodosum and was subsequently diagnosed with celiac disease. The patient exhibited deep, painful red nodules on the anterior surface of both legs and the dorsal surface of the feet, which persisted for a month prior to her referral. Laboratory testing revealed markers of celiac disease, and endoscopic evaluation revealed mosaic antritis and duodenitis with a characteristic fish-scale appearance. Duodenal biopsy confirmed a diagnosis of celiac disease (Marsh stage 3c class), with a significant intraepithelial lymphocytosis of 47%. After initiating a strict gluten-free diet, the patient showed complete resolution of the skin lesions within six weeks. This case underscores the importance of considering celiac disease in the differential diagnosis of erythema nodosum, particularly in patients with unexplained cutaneous manifestations. It also highlights the potential benefits of early screening for celiac disease in patients with EN, as a strict gluten-free diet can lead to both dermatological and gastrointestinal improvement. Further research is needed to establish a clear causal relationship between celiac disease and erythema nodosum.

Clinical Case Summary

Melioidosis, caused by Burkholderia pseudomallei, is an infectious disease endemic to tropical and subtropical regions. It poses a particular risk to immunocompromised individuals. This case report describes a 48-year-old male with Crohn's disease on biologic therapy who developed pulmonary melioidosis—a condition rarely reported among patients receiving biologics for inflammatory bowel disease.
A 48-year-old male, working as a plaster renderer in rural Queensland, presented with a productive cough, sore throat, fever, and night sweats. He had a background of Crohn’s disease and ankylosing spondylitis, managed with Adalimumab, mesalazine, and intermittent corticosteroids. He denied recent travel or gardening exposure.
Melioidosis was confirmed by positive cultures for Burkholderia pseudomallei from sputum and bronchial washings. Imaging demonstrated bilateral lower zone airspace opacities, a right-sided pleural effusion, and mediastinal lymphadenopathy, with CT features suggestive of a mass-like lesion in the right middle lobe bronchus. The overall picture was consistent with pulmonary melioidosis complicated by lymphadenopathy.
The patient received intravenous ceftazidime for four weeks, followed by oral trimethoprim-sulfamethoxazole for three months. Adalimumab was withheld during the acute infection, and he was managed with mesalazine (4.8 g daily) and prednisolone (20 mg daily) for his IBD.
Conclusion: In melioidosis-endemic areas, inflammatory bowel disease patients receiving biologic therapy can be safely managed if there is early recognition and prompt initiation of appropriate antimicrobial treatment. This case underscores the importance of maintaining a high index of suspicion for melioidosis in immunosuppressed patients presenting with respiratory symptoms in endemic regions.

References

1. Image of CT cross sectional image of right middle lobe mass