Introduction

Cholestatic pruritus in patients with primary biliary cholangitis (PBC) is frequently debilitating and lacks effective treatments. In the Phase 3 RESPONSE trial (NCT04620733), seladelpar, a first-in-class delpar (selective PPAR-delta agonist), significantly decreased pruritus in PBC patients with moderate to severe pruritus (numerical rating scale [NRS] ≥4 at baseline) vs placebo. Here, we further evaluated pruritus patterns in RESPONSE.

Aims & Methods

Patients with PBC who received ursodeoxycholic acid (UDCA) for ≥12 months or were UDCA intolerant and had alkaline phosphatase ≥1.67 x upper-limit-of-normal (ULN) and total bilirubin ≤2 x ULN were randomised 2:1 to receive daily oral seladelpar 10 mg or placebo for 12 months. We assessed trends in mean NRS over time and change in pruritus using various thresholds of improvement (eg, ≥3- and ≥4-point reductions in NRS, near resolution of itch [NRS ≤1]) in patients with NRS ≥4 or NRS ≥7 (severe itch) at baseline. Development of pruritus in patients without itch (NRS=0) at baseline and safety by subgroup of baseline NRS (≥4 or <4) were also evaluated.

Results

72 of 193 enrolled patients had a baseline NRS ≥4, with 49 randomised to seladelpar and 23 to placebo; 16 seladelpar and 12 placebo patients had NRS ≥7. Among patients with NRS ≥4 at baseline, seladelpar reduced the mean itch intensity from moderate to mild from Month 3 through 12, whereas the mean itch intensity for placebo remained moderate. For patients with baseline NRS ≥4, 46.9% of patients on seladelpar had a ≥3-point NRS decrease vs 21.7% on placebo at Month 12; a ≥4-point NRS decrease was achieved by 30.6% of seladelpar patients vs 8.7% placebo. A higher proportion of patients with baseline NRS ≥4 (26.5%) and NRS ≥7 (18.8%) on seladelpar experienced near resolution of itch at Month 12 vs 0% of patients on placebo. In patients without itch at baseline, 26.7% (4/15) of placebo patients reported pruritus at Month 12 vs 0% (0/30) of seladelpar patients. Adverse events were reported in 88.9% and 84.3% of patients with baseline NRS ≥4 and NRS <4, respectively, with similar proportions across treatment arms.

Conclusion

Seladelpar reduced pruritus severity in PBC patients with a durable effect over time and even led to near resolution of itch in some patients, an effect not observed with placebo. Seladelpar mitigated new onset of itch in patients without pruritus and was overall safe and well tolerated regardless of baseline itch.

Disclosure

AEK reports receiving grants or contracts from Gilead Sciences, Inc., Intercept Pharmaceuticals and Roche; consulting fees from AbbVie; Advanz Pharma; Alentis Therapeutics; Alfasigma; Astellas; AstraZeneca; Attovia Therapeutics; Avior Bio; Bayer; Bristol Myers Squibb; Böhringer-Ingelheim; CymaBay Therapeutics; Escient Pharmaceuticals; Falk; Gilead Sciences, Inc.; GSK; Guidepoint; Intercept Pharmaceuticals; Ipsen; Merck Sharp & Dohme; Mirum Pharma; Novo Nordisk; Rectify Pharma; Roche; and Takeda; payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing, or educational events from AbbVie; Advanz Pharma; AOP Orphan Pharmaceuticals; Bayer; Bristol Myers Squibb; CymaBay Therapeutics; Falk; Gilead Sciences, Inc.; GSK; Intercept Pharmaceuticals; Ipsen; Johnson & Johnson; Medscape; Merck Sharp & Dohme; Mirum Pharma; NewBridge Pharmaceuticals; Novartis; Roche; Vertex Pharmaceuticals; and Viofor; support for attending meetings and/or travel from Gilead Sciences, Inc.; participation on a data safety monitoring board with AbbVie; Advanz Pharma; Alentis Therapeutics; Alfasigma; AstraZeneca; Avior Bio; Bayer; Bristol Myers Squibb; CymaBay Therapeutics; Escient Pharmaceuticals; Falk; Gilead Sciences, Inc.; GSK; Guidepoint; Intercept Pharmaceuticals; Ipsen; Merck Sharp & Dohme; Mirum Pharma; Novo Nordisk; Roche; and Takeda; and a leadership or fiduciary role in other board, society, committee, or advocacy groups (paid or unpaid) with PBC Foundation, Swiss Association for the Study of the Liver (SASL), Swiss Gastroenterology Society (SGG), Swiss Hepa, and Swiss Transplant Society (STS). CL reports receiving research grants paid to her institution from Calliditas Therapeutics; CymaBay Therapeutics; Escient Pharmaceuticals; EWR; Gilead Sciences, Inc.; GSK; Intercept Pharmaceuticals; Ipsen; Kowa; Mirum Pharma; Target; and Zydus Pharmaceuticals; consulting fees from Calliditas Therapeutics; CymaBay Therapeutics; Gilead Sciences, Inc.; GSK; Intercept Pharmaceuticals; Ipsen; Kowa; and Mirum Pharma; and participation on a data safety monitoring board with COUR Pharmaceuticals. MJM reports receiving grants or contracts from CymaBay Therapeutics; Genfit; Gilead Sciences, Inc.; GSK; Ipsen; and Mirum Pharma; consulting fees from CymaBay Therapeutics, GSK, Intra-Sana Laboratories, Ipsen, Ironwood Pharmaceuticals, Mallinckrodt Pharmaceuticals, and Mirum Pharma; and support for attending meetings and/or travel from CymaBay Therapeutics, GSK, Ipsen, and Mallinckrodt Pharmaceuticals. CLB reports receiving grants or contracts to his institution from Boston Scientific; Bristol Myers Squibb; Calliditas Therapeutics; Cara Therapeutics; Chemomab; COUR Pharmaceuticals; CymaBay Pharmaceuticals; Gilead Sciences, Inc.; GSK; and Hanmi Pharmaceuticals; and consulting fees from Alnylam Pharmaceuticals; Chemomab; CymaBay Therapeutics; Gilead Sciences, Inc.; GSK; Ipsen; and NGM Bio. KVK reports receiving grants or contracts from 89Bio; Boston Scientific; Corcept Therapeutics; CymaBay Therapeutics; Genfit; Gilead Sciences, Inc.; GSK; Hanmi Pharmaceuticals; Intercept Pharmaceuticals; Ipsen; Janssen; Madrigal Pharmaceuticals; Mirum Pharma; Novo Nordisk; NGM Bio; Pfizer; Pliant Therapeutics; Terns Pharmaceuticals; Viking Therapeutics; and Zydus Pharmaceuticals; royalties or licences from UpToDate; consulting fees from 89Bio; CymaBay Therapeutics; Genfit; Gilead Sciences, Inc.; GSK; HighTide Biopharma; Inipharm; Intercept Pharmaceuticals; Ipsen; Madrigal Pharmaceuticals; Mirum Pharma; NGM Bio; and Zydus Pharmaceuticals; payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing, or educational events from AbbVie; Gilead Sciences, Inc.; and Intercept Pharmaceuticals; participation on a data safety monitoring board or advisory board with CTI and Medpace; and stock or stock options with Inipharm. GMH reports having consulted for Advanz Pharma; CymaBay Therapeutics; Falk; Gilead Sciences, Inc.; GSK; Intercept Pharmaceuticals; Ipsen; Kowa; Mirum Pharma; and Pliant Therapeutics. CH, SC, KY, and DBC are employees of Gilead Sciences, Inc., and may own stock in Gilead Sciences, Inc. CAM reports former employment with CymaBay Therapeutics, a Gilead Sciences, Inc., company, from 2007 to 2024; receiving consulting fees from Gilead Sciences, Inc.; being listed as an inventor on seladelpar patents; and a leadership or fiduciary role (paid or unpaid) with 89Bio (independent director). DEJJ reports receiving consulting fees for CymaBay Therapeutics, Ipsen, Kowa, and Umecrine, grants from Intercept, and participation on a speakers’ bureau for Falk, GlaxoSmithKline, Intercept, and Ipsen.

Introduction

Metabolic Dysfunction–Associated Steatotic Liver Disease (MASLD) is currently the leading cause of chronic liver disease worldwide, affecting more than 65% of patients with Type 2 Diabetes Mellitus (T2DM). The aim of our study was to determine the prevalence of MASLD among T2DM patients, with or without coexisting significant fibrosis, to assess its association with diabetic complications, and to identify the factors linked to MASLD in our population.

Aims & Methods

We conducted a retrospective, descriptive, and analytical study including T2DM patients admitted to the Endocrinology Department in 2019. MASLD diagnosis was based on the presence of hepatic steatosis detected by abdominal ultrasound or a Hepatic Steatosis Index (HSI) >36. Fibrosis was assessed using the Fibrosis-4 (FIB-4) index (with a threshold of ≥1.3 or <1.3). Chronic Kidney Disease (CKD) associated with T2DM was defined by an estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m² and/or dipstick-positive proteinuria (>1+). Diabetic Peripheral Neuropathic Pain (DPNP) was assessed using the Douleur Neuropathique 4 (DN4) questionnaire, and Diabetic Retinopathy was diagnosed via dilated eye examination.

Results

Among the 202 patients included, the median age was 57 years (±12 years) with a marked female predominance (sex ratio = 2.6). Regarding comorbidities, 58.4% of patients had hypertension and 34.2% had dyslipidemia. The median Body Mass Index (BMI) was 27 kg/m² (±5.62), with overweight or obesity present in 61.4% of the cohort. The median duration of diabetes was 10 years (±7.8 years). Impaired renal function (eGFR <60 ml/min/1.73 m²) was found in 9.9% of patients, and proteinuria in 6.9%. Diabetic neuropathy (DN4 score ≥4) was present in 7.9% of patients, while diabetic retinopathy was diagnosed in 37.6% of cases.
The prevalence of MASLD in our cohort was 73.3%. The median FIB-4 score was 0.91 (±0.63), with 25.7% of patients presenting a FIB-4 >1.3. Statistical analysis identified several factors significantly associated with the presence of MASLD: female sex (p=0.004), dyslipidemia (p=0.004), BMI (p<0.001), alanine aminotransferase (ALT) levels (p<0.001), low-density lipoprotein cholesterol (LDL-C) levels (p=0.006), and triglyceride levels (p=0.013). In particular, higher BMI was strongly associated with MASLD (Odds Ratio [OR] = 1.970; 95% Confidence Interval [CI]: 1.580–2.460; p<0.001), as were elevated ALT levels (OR = 1.115; 95% CI: 1.053–1.18; p<0.001).
However, after adjustment, LDL-C levels (p=0.163), triglycerides (p=0.402), dyslipidemia (p=0.329), and sex (p=0.360) were no longer significantly associated with MASLD. Finally, a significantly higher proportion of CKD was observed in patients with MASLD (22.3%) compared to those without MASLD (9.2%, p=0.036), although this association was not maintained in the subgroup with advanced fibrosis (FIB-4 >1.3).

Conclusion

Our study confirmed the high prevalence of MASLD among patients with T2DM. Early screening is therefore essential, particularly in female patients and in those presenting with chronic kidney disease or other associated cardiometabolic risk factors such as obesity and dyslipidemia.

References

Younossi ZM, Golabi P, Price JK, Owrangi S, Gundu-Rao N, Satchi R, Paik JM. The Global Epidemiology of Nonalcoholic Fatty Liver Disease and Nonalcoholic Steatohepatitis Among Patients With Type 2 Diabetes. Clin Gastroenterol Hepatol. 2024 Oct;22(10):1999-2010.e8. doi: 10.1016/j.cgh.2024.03.006. Epub 2024 Mar 21. PMID: 38521116.

Introduction

Visceral artery pseudoaneurysms typically originate from the splanchnic circulation, often as a result of inflammation, trauma, or infection. If left untreated, these pseudoaneurysms carry a near 100% mortality rate. Endovascular intervention by interventional radiologists is currently the preferred treatment approach. The role of endoscopic ultrasonography (EUS)-assisted interventions in managing visceral pseudoaneurysms is an evolving area of clinical practice.

Aims & Methods

In this retrospective single-centre study conducted between January 2020 to December 2024, the technical and clinical success of EUS-guided embolisation of visceral arterial pseudoaneurysms was assessed. Technical success was defined as absence of blood flow on color doppler imaging after successful placement of coil or in combination with thrombin. Clinical success was defined as the absence of re-bleeding or pseudoaneurysm recurrence during a follow-up period of 12 weeks.

Results

A total of 26 patients (88.46% males) were included, selected based on computed tomography angiography (CTA). EUS could not visualize pseudoaneurysms in two patients, thus EUS-guided intervention could be performed successfully in 24/26 patients, yielding a technical success rate of 92.30%. The median age of the study population was 33 years (IQR 25-42). The most common underlying condition was pancreatitis, with chronic pancreatitis affecting 17/26 patients (65.38%) and acute pancreatitis affecting 7/26 patients (26.92%). The splenic artery was the most frequently involved (13/26 patients, 50%), followed by the gastroduodenal artery (9/26 patients, 34.61%). The median size of the pseudoaneurysms was 1.5 cm (IQR 1-2.6 cm). Clinical success was achieved in 20/24 patients (83.33%). Despite technical success, three patients experienced early re-bleeding. Two patients were managed with rescue procedures, while one patient succumbed to bleed despite rescue intervention. One patient had a recurrence of pseudoaneurysm.

Conclusion

EUS-guided embolization using coil, alone or in combination with thrombin, is a safe and effective method for managing visceral arterial pseudoaneurysms, even as a first-line intervention. This approach warrants further validation in larger cohorts and its direct comparison with the endovascular approach.

Disclosure

No Conflict of Interest

Introduction

Tryptophan metabolism is severely disrupted in IBD. Pro-inflammatory cytokines activate the first rate-limiting enzyme IDO1 leading to tryptophan degradation through the kynurenine pathway. Although Trp degradation typically support de novo NAD synthesis via KP activation, evidence suggests a metabolic block at the downstream enzyme QPRT in IBD. STING has been described as inducing the secretion of type I interferons and other inflammatory cytokines, suggesting its important role in regulating intestinal homeostasis. Several studies have reported an association between STING-mediated IDO1 activity and its role in promoting tumour immune evasion. However, the relationship between STING pathway and tryptophan metabolism in intestine has not be understood. This study aims to investigate the effect of STING signalling on tryptophan degradation and explore how the metabolic blockage in tryptophan-NAD axis may influence STING-mediated immune response.

Aims & Methods

To investigate the STING pathway's role in tryptophan metabolism within the intestinal microenvironment, we utilized human colonic fibroblast cell line CCD-18co. Quantitative RT-PCR and Western blot were employed to measure mRNA and protein expression. Tryptophan metabolism was quantified via LC-MS. QPRT knockdown was achieved using siRNA transfection. Transcriptomic changes were analysed by RNA sequencing. Intracellular NAD level were assessed by NAD-Glo assay. Seahorse assay was conducted to evaluate mitochondrial function.

Results

We screened a range of established IDO1-inducing cytokines (IFNγ, TNFα, etc.) and compared their effects on IDO1 expression with STING agonists diABZI, dsDNA and 2'3'cGAMP. STING agonists induced significantly higher IDO1 expression than any of the cytokines tested. While cultivation of in presence of Anifrolumab (type I IFN receptor antagonist) and Tofacitinib (pan-JAK inhibitor) strongly inhibited STING-induced IDO1 upregulation. LC-MS showed upregulation of IDO1 drive tryptophan into kynurenine pathway, which was again inhibited by Anifrolumab and Tofacitinib.
To mimic the reduced QPRT expression in IBD, we performed QPRT knockdown followed by RNA sequencing. Loss of QPRT resulted in spontaneous activation of type I interferon signature, which was further amplified upon stimulation with STING agonists, leading to a pronounced inflammatory transcriptional response. Mechanistically, QPRT-deficient cells exhibited reduced intracellular NAD levels and signs of mitochondrial dysfunction, including opening of the mitochondrial permeability transition pore (mPTP), release of mitochondrial DNA and RNA into the cytosol, and subsequent activation of the cGAS-STING and RIG-I/MAVS pathways, respectively. These events collectively led to a pronounced induction of type I interferons and pro-inflammatory cytokines. Notably, supplementation with nicotinamide riboside (NR) restored intracellular NAD levels and significantly attenuated the heightened inflammatory response induced by QPRT knockdown.

Conclusion

Our findings reveal a novel mechanism by which STING activation in intestinal fibroblasts promotes tryptophan metabolism via kynurenine pathway. Furthermore, QPRT deficiency-induced metabolic disruption amplifies STING-mediated pro-inflammatory responses via the release of mitochondrial nucleic acids, a process that can be effectively attenuated by supplementation with NAD precursors.

Introduction

Pain in chronic pancreatitis (CP) varies between patients in pattern, severity, and psychological impact. CP pain assessment has been focused on intensity, missing the complexity. To address the importance of multidimensional pain evaluations, we aimed to identify pain phenotypes based on multidimensional pain assessments and examine their association with clinical factors.

Aims & Methods

We studied 248 patients with painful CP from Asia, Europe, and the USA. A cluster analysis was performed on patients with painful CP, including five pain dimensions from the COMPAT-SF questionnaire (severity, fluctuation, provocative factors, spreading pain, and qualitative descriptors). The resulting clusters were compared based on demographics and clinical data, including patient-reported outcomes and quantitative sensory testing.

Results

		Cluster 1	Cluster 2	Cluster 3	p-value​
Questionnaires	Quality of life	66.3 (22.5)	64.8 (27.7)	51.1 (24.6)	<0.001
	Catastrophizing	10.7 (11.2)	19.1 (12.4)	24.3 (13.0)	<0.001
	Anxiety	5.3 (4.1)	6.2 (4.2)	8.7 (4.5)	<0.001
	Depression	4.3 (4.3)	5.5 (4.6)	7.3 (4.7)	<0.001
	Sleep	5.0 (3.5)	5.9 (3.8)	7.5 (4.5)	<0.001
QST	PPDT sum, kPa	2284 (997)	1811.5 (574.6)	1640.1 (600.4)	<0.001
	PPTT sum, kPa	2909.6 (1247.3)	2227.1 (691.3)	2184.9 (903.2)	<0.001
	Temporal summation, abdomen	1.7 (1.8)	1.9 (1.5)	1.4 (1.8)	0.178
	CPM (%)	2.3 (18.3)	5.1 (23.7)	7.2 (17.7)	0.135

Three distinct pain phenotypes were identified in the cluster analysis. Cluster 1 (n=73) included patients with low-severity pain; Cluster 2 (n=80) was characterized by severe, fluctuating pain; and Cluster 3 (n=95) comprised patients reporting constant, severe pain. Patients in Clusters 1 and 2 reported low scores across the remaining dimensions, whereas Cluster 3 consistently scored higher. Quality of life and sleep were best in Cluster 1, declined in Cluster 2, and were lowest in Cluster 3 (both p<0.001). Scores for anxiety, depression, and catastrophizing increased progressively across clusters (all p<0.001). Sensory testing revealed a pattern of increasing hyperalgesia, with Cluster 3 showing the most pronounced responses (p<0.001).

Conclusion

The COMPAT-SF questionnaire identifies three pain phenotypes in CP. Greater pain severity and persistence correlate with increased hyperalgesia, higher psychological distress, and worse overall well-being.

Introduction

Linked Color Imaging (LCI) is an endoscopic system that emphasizes the red mucosal color to identify subtle areas of inflammation. Endoscopic imaging, including LCI classification and LCI index, has been reported as a predictor of histological healing (HH) in ulcerative colitis (UC). Endoscopic changes (LCI classification, LCI index) in vedolizumab treatment have not been reported to date.

Aims & Methods

This study aimed to evaluate endoscopic remission and HH using LCI endoscopy at week 22 of vedolizumab treatment in patients with moderate to severe UC. This was a phase 4, multicenter, open-label, single-arm, prospective study involving 12 patients with moderately to severely active UC receiving vedolizumab. Vedolizumab was administered for 54 weeks. Endoscopy and mucosal sampling from most inflamed sites or the patient’s rectum when all sites had equal endoscopic severity were performed at weeks 0, 22, and 54 to assess the LCI index, LCI classification, Mayo endoscopic score (MES), Nancy score (If MES = 0, it was collected from the rectum). This study was also evaluated a variety of possible factors such as fecal calprotectin, serum vedolizumab concentration and mucosal gene expression associated with changes induced by vedolizumab. LCI index was numerically evaluated for the redness of a 40-pixel square area within the LCI image. LCI classification was defined by assigning one of the three categories (A, no redness; B, redness with visible vessels; C, intense redness without visible vessels). HH was defined as a Nancy score ≤1, and clinical outcomes were compared between HH and non-HH groups. Correlation coefficients between LCI endoscopy and other clinical markers (MES, Nancy score, fecal calprotectin and vedolizumab concentration) were analyzed at weeks 0, 22, and 54. Gene expression analysis was performed on 374 genes, comparing HH (n=8) vs. non-HH (n=3) and LCI classification A (n=5) vs. LCI classification B and C (n=6) at week 22. Biomarkers common to HH and LCI-A were identified as LCI-Deep remission (L-DR) markers.
The study was registered with the Japan Clinical Trial Registry (Identifier: UMIN000042855).

Results

At week 22, 66.7% (8/12) achieved histological healing (HH), while 50.0% (6/12) met LCI classification A criteria. The LCI index change from baseline showed a statistically significant difference between HH and non-HH (week 22: p=0.021; week 54: p=0.011).Correlation analysis demonstrated that LCI index was significantly associated with: MES (week 22: ρ=0.729, week 54: ρ=0.789), Nancy score (week 22: ρ=0.695, week 54: ρ=0.725), fecal calprotectin (week 22: ρ=0.555, week 54: ρ=0.783), vedolizumab concentration (week 22: ρ=0.758, week 54: ρ=-0.418). Gene expression analysis identified IL1B, CXCL11, CD38, CSF2RB, PTPN6, CD86, NFKB2, IFNAR2, STAT1, GNAI2, FES and IRF9 as L-DR markers, as they were commonly associated with both HH and LCI classification A. There are genes involved in NF-κB signaling pathway and JAK-STAT signaling pathway associated with UC. HH and LCI endoscopy have been found to correlate well but do not perfectly align.
In this study, we proposed a definition of L-DR, which encompasses both HH and LCI endoscopic remission.

Conclusion

This study introduces L-DR as a novel definition for combined endoscopic (LCI-A) and HH (Nancy score ≤1) in UC patients receiving vedolizumab. Additionally, we identified candidate L-DR biomarkers that may serve as potential indicators of deep remission.

Disclosure

Tomohisa Takagi, Male, (Kyoto Prefectural University of Medicine, Kyoto, Japan):
Scholarship funds from Mitsubishi Tanabe Pharma Corporation,
Collaborative research fund from PreMedica Inc.,
Lecture fees by Mochida Pharma. Co., Ltd., Yanssen Pharmaceutical K.K., EA Pharma. Co., Ltd., Mitsubishi Tanabe Pharma Corporation, Towa Pharmaceutical Co., Ltd., Takeda Pharmaceutical Co., Ltd., and Pfizer Japan Inc.
Kazuhiko Uchiyama, Male, ( Kyoto Prefectural University of Medicine, Kyoto, Japan):
Collaboration research fund from Janssen Pharma. K.K.
Lecture fee by Mitsubishi Tanabe Pharma. Co. Ltd. and Janssen Pharma. K.K.
Yuji Naito, Male, (Kyoto Prefectural University of Medicine, Kyoto, Japan):
Scholarship funds from Taiyo Kagaku Co. Ltd., Morinaga Co. Ltd., Miyarisan Pharma Co. Ltd, Morishita-Jintan Co. Ltd., Fujikko Co. Ltd., Mizkan Co. Ltd., Mykinso Co. Ltd.
Collaboration research fund from Takeda Pharma. Co. Ltd. and Taiyo Kagaku Co., Ltd.
Lecture fees by Takeda Pharma. Co. Ltd., Mochida Pharma. Co. Ltd., Biofermin. Co. Ltd., Otsuka Pharma. Co. Ltd., and Miyarisan Pharma. Co. Ltd.

Clinical Case Summary

A 37-year-old woman with a history of heavy alcohol use (3–4 bottles of wine weekly) presented with abdominal pain and haematemesis. She had experienced intermittent abdominal pain for two years. On assessment, she was stable apart from mild tachycardia and epigastric tenderness; melaena was confirmed on rectal exam. Blood tests revealed severe anaemia (Haemoglobin "Hb" 40 g/L from a baseline of 154 g/L). Gastroscopy showed severe oesophagitis without active bleeding. Abdominal CT showed a hyperdense focus in the neck of the pancreas, raising suspicion of a neuroendocrine tumour. After blood transfusion, she was discharged (Hb 73 g/L) with plans for outpatient colonoscopy and endoscopic ultrasound (EUS) to characterise the pancreatic neck lesion.
Two days later, she was readmitted with recurrent haematemesis and a Hb drop to 56 g/L. She was stabilized and discharged again. The day after her discharge, she underwent an EUS examination in our unit. The EUS revealed signs indicative of chronic pancreatitis, as well as a thick-walled vascular structure measuring 20 mm, adjacent to the head of the pancreas. This structure appeared to originate from a posterior branch of the gastroduodenal artery, and was consistent with a pseudo-aneurysm eroding into the wall of the duodenum. A subsequent triple phase CT scan showed an increase in the size of the hyperdense focus in the neck of the pancreas, raising concern for a pseudoaneurysm near the pancreaticoduodenal artery. Following these findings, the patient underwent successful coil embolization of the pseudoaneurysm.
Conclusion: In patients with chronic alcohol use, upper gastrointestinal bleeding (UGIB) may arise from complications of pancreatitis, such as pseudoaneurysm formation, rather than solely intraluminal causes. This case highlights the need for early identification and intervention in such rare but potentially life-threatening conditions.