Introduction

The evolution of inflammatory bowel disease (IBD) occurs across four epidemiological stages: emergence, acceleration in incidence, compounding prevalence and prevalence equilibrium; as put forward by Kaplan et al.¹ Newly industrialized countries are in the acceleration in incidence stage, which is associated with rapidly rising incidence and low prevalence, while the western world is in the compounding prevalence stage: stable incidence and rapidly increasing prevalence.
The Veszprém IBD cohort is one of the very few well-established prospective, population based inception cohorts worldwide, capable of delivering reliable epidemiological data.

Aims & Methods

Our aim was to analyze total, age and gender specific incidence and prevalence rates of ulcerative colitis (UC) patients over the past four decades (1977-2018).
Data of 1,370 UC patients were analyzed. Patient inclusion was between January 1, 1977 and December 31, 2018. All patients in Veszprem county, a well-defined administrational area of Hungary, was included. Both in-hospital and outpatient records were collected and comprehensively reviewed at diagnosis and during clinical follow-up. The source of age- and gender-specific demographic data for statistical analysis was derived from the results of a national population census in 1980, 1990, 2001 and 2011 (source: Hungarian Central Statistical Office). Prevalence rates were calculated in 1991, 2001, 2011 and 2015.

Results

Adjusted mean incidence rate of UC increased from 4.06 (CI95%: 2.47-6.66) /10⁵ person-years in 1977-1991 to 13.31 (CI95%: 10.71-17.50) /10⁵ in 1997-2001. The following years show a plateau/ slight decrease in incidence: 11.16 (CI95%: 8.18-15.23) /10⁵ in 2007-2011 and 10.92 (CI95%: 7.98-14.96) /10⁵ in 2012-2018. see Figure 1. Age specific mean incidence rates in the total cohort show a peak of disease onset at the age of 20-29 years (16.54 /10⁵ person-years), however incidence is only slightly lower at the age of 30-39 years (15.82 /10⁵ person-years).
The total prevalence of UC patients show a steady increase from 60.05 (CI95%: 52.07-68.42) /10⁵ persons in 1991 to 317.62 (CI95%: 299.62-336.70) /10⁵ in 2015. Age specific prevalence rates show similarly high prevalence rates among elderly patients (60-69y) compared to adult patients, meaning a saturation of age specific curves in the elderly. see Table 1. Age specific prevalence of UC among the 60-69 years old is as high as 506.42 (CI95%: 443.23-578.56) /10⁵ persons in 2015.

Conclusion

Incidence rates of UC patients plateaued around the 2000s and show slight decrease afterwards. Prevalence rates of UC show a steady increase, thus Hungary is well into the 3^rd epidemiological phase of compounding prevalence. As we already see a saturation of prevalence rates among elderly UC patients, a transition to the 4^th stage of prevalence equilibrium may began.

References

1. Kaplan GG, Windsor JW. The four epidemiological stages in the global evolution of inflammatory bowel disease. Nat Rev Gastroenterol Hepatol. 2021 Jan;18(1):56-66.

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

Clinical Case Summary

Introduction: Loeys-Dietz syndrome (LDS) is an autosomal dominant connective tissue disorder with multisystem involvement, predominantly affecting the cardiovascular system. Aortic aneurysms and dissections are common complications. LDS shares features with other connective tissue disorders, such as Marfan and Ehlers-Danlos syndromes (1).
Case report: A 44-year-old male with a marfanoid habitus, history of thyroid carcinoma treated with radioactive iodine, appendectomy complicated by hematoma and dehiscence, and Loeys-Dietz syndrome type 3 (SMAD3 variant), diagnosed after a Stanford type A aortic dissection in 2022. In 2023, he underwent left carotid-subclavian bypass and ascending aortic aneurysm repair with hybrid graft. Family history included aortic dissection and hiatal hernia. He was on levothyroxine, dicoumarol, and omeprazole. Referred to the motility unit for preoperative evaluation of a large hiatal hernia seen on CT (Figure 1A).
He reported diet-related occasional nocturnal heartburn and regurgitation, well-controlled with PPIs. No dysphagia or alarm symptoms. Gastroscopy showed an 8–10 cm partially volvulated hernia sac without mechanical or vascular compromise. Esophagogram (1B) confirmed a mixed hiatal hernia with severe reflux and delayed esophageal clearance. High-resolution manometry with impedance (HRIM) showed a short esophagus (21 cm), ineffective motility, incomplete bolus transit and early post-swallow reflux (1C). Due to high risk of postoperative dysphagia, partial fundoplication was advised, but conservative management was chosen given prior surgical dehiscence and good symptom control.
Discussion: Gastrointestinal manifestations of LDS are rare and understudied. Large hiatal and abdominal wall hernias are among the most frequent findings, due to altered structural support at the esophagogastric junction (4,5). GERD symptoms are common and may require multidisciplinary care. HRIM is essential for preoperative planning in these patients.

References

1. Gouda, P., Kay, R., Habib, M., Aziz, A., Aziza, E., & Welsh, R. (2022). Clinical features and complications of Loeys-Dietz syndrome: A systematic review. International journal of cardiology, 362, 158–167. https://doi.org/10.1016/j.ijcard.2022.05.065
2. Wang, X. J., Babameto, M., Babovic-Vuksanovic, D., Bowen, J. M., & Camilleri, M. (2021). Audit of Gastrointestinal Manifestations in Patients with Loeys-Dietz Syndrome and Vascular Ehlers-Danlos Syndrome. Digestive diseases and sciences, 66(4), 1142–1152. https://doi.org/10.1007/s10620-020-06265-8
3. Honrubia Lopez, R., Burgos García, A., & Palacios Lázaro, E. (2017). Multiple perforation of small-intestine diverticula in a patient with Ehlers-Danlos syndrome. Revista espanola de enfermedades digestivas, 109(1), 83. https://doi.org/10.17235/reed.2016.4452/2016
4. Castori, M., Morlino, S., Pascolini, G., Blundo, C., & Grammatico, P. (2015). Gastrointestinal and nutritional issues in joint hypermobility syndrome/Ehlers-Danlos syndrome, hypermobility type. American journal of medical genetics. Part C, Seminars in medical genetics, 169C(1), 54–75. https://doi.org/10.1002/ajmg.c.31431
5. Thwaites, P. A., Gibson, P. R., & Burgell, R. E. (2022). Hypermobile Ehlers-Danlos syndrome and disorders of the gastrointestinal tract: What the gastroenterologist needs to know. Journal of gastroenterology and hepatology, 37(9), 1693–1709. https://doi.org/10.1111/jgh.15927