Introduction

Acute pancreatitis (AP) is an acute disease of the pancreas with several serum indicators of the disease severity (C-reactive protein (CRP), procalcitonin (PCT)), but none of them are accurate. YKL-40 (chitinase-3-like-1 protein) is a glycoprotein that plays a mayor role in the inflammation and angiogenesis. Development of peripancreatic fluid collections (PFC) in the AP complicates the clinical course of the disease and often requires advanced endoscopic or surgical treatment. Early recognition of PFCs could lead to new therapeutic options and their improved management.

Aims & Methods

The aim of our study was to compare the diagnostic yield of YKL-40 and interleukin 6 (IL-6) versus routine laboratory markers in prediction of PFCs in AP. This prospective study recruited 57 patients (23 male, 34 female) with AP at the University Hospital Center Sestre Milosrdnice, Zagreb, from June 2020 until December 2021. After obtaining informed consent, patients had blood drawn for routine laboratory studies (including CRP and PCT) with additional 7 milliliters of blood for determining serum concentrations of YKL-40 and IL-6 on admission and 48 hours after admission. Presence of PFCs was determined with a computer tomography scan carried out 72-96 hours after admission. Analysis were performed using enzyme-linked immunosorbent assay (ELISA). Receiver operating characteristic curve was calculated, confidence intervals were obtained using bootstrap method with 1000 iterations, and areas under the curve (AUCs) were compared using Kruskal-Wallis, Dunn, and Mann-Whitney tests.

Results

The AUC values are presented in Table 1. Post-hoc Dunn test with Bonferroni correcton indicated that there is a statistical difference between all pairwise comparisons in AUC scores for PFC predicton of investigated biomarkers both on admission and 48 hours after admission (P <0.05). Both YKL-40 and IL-6 had an order of magnitude better AUC scores than CRP and PCT. At 48 hours after admission, CRP AUC scores improved drastically, reaching AUC scores comparable with YKL-40 and IL-6, with all of the biomarkers having AUC scores in range of moderately good predictors. IL-6 had the best AUC scores overall in both groups.

Table 1.

Conclusion

Results demonstrated that IL-6 on admission and YKL-40 (alongside CRP) 48 hours after admission may be good early predictors for PFCs and the need for future invasive treatments, but due to small sample size and low study power further measurements are needed to confirm these preliminary results.

References

1. Arvanitakis M, Dumonceau JM, Albert J, et al. Endoscopic management of acute necrotizing pancreatitis: European Society of Gastrointestinal Endoscopy (ESGE) evidence-based multidisciplinary guidelines. Endoscopy. 2018;50(5):524-546.
2. Lee DW, Cho CM. Predicting Severity of Acute Pancreatitis. Medicina (Kaunas). 2022;11;58(6):787.

Clinical Case Summary

For decompensated advanced chronic liver disease (dACLD) individuals, the onset of refractory ascites (RA) represents a dramatic event (6-month survival rate < 50%). In this setting, a relevant proportion of RA patients develop Hepatorenal Syndrome-Acute Kidney Injury (HRS-AKI) with limited therapeutic and survival chances.
An 81-year-old female dACLD RA patient was admitted to our department to receive large-volume paracentesis (LVP). Eradicated HCV infection, type II diabetes, and chronic obstructive pulmonary disease were her comorbidities.
The AKI onset imposed the intravenous (i.v.) human albumin (HA) (1 g/kg/die) administration, followed by the proper dosage of terlipressin (for HRS-AKI) within the first 72 hours (h), subsequently discontinued due to the persistence of anuria and the worsening of respiratory failure.
To simultaneously address uremic symptoms and facilitate ascites drainage, a Tenckhoff catheter was placed, and peritoneal dialysis (PD) started with a single icodextrin dwell, resulting in the removal of 14 L of ascites and an improvement in AKI within the subsequent 72h. After one week, she was discharged, receiving a specific PD schedule. After the readmission due to the difficulties in administering i.v. HA, we proposed administering HA via the intraperitoneal route, creating an HA-enriched PD (PD+HA) home-performable schedule by adding two vials of 100 ml of HA 20% to 800 ml of icodextrin solution (40 g in 1000 ml/die; lasting: 12 hours; frequency: every other day) (Figure 1).
The patient has been performing this PD schedule for 12 months (~0.5 L of ascites is discharged every other day before performing PD+HA dwell). During the follow-up, no PD-related complications (e.g., peritonitis) and liver-related events requiring hospitalization have been observed.
We report the first successful use of PD+HA, highlighting the cruciality of a multidisciplinary (hepatologists-nephrologists) approach in the management of dACLD-RA HRS-AKI patients.

References

1. Moreau, R.; Delègue, P.; Pessione, F.; Hillaire, S.; Durand, F.; Lebrec, D.; Valla, D.-C. Clinical Characteristics and Outcome of Patients with Cirrhosis and Refractory Ascites. Liver Int 2004, 24, 457–464, doi:10.1111/j.1478-3231.2004.0991.x.
2. Moore, K.P.; Wong, F.; Gines, P.; Bernardi, M.; Ochs, A.; Salerno, F.; Angeli, P.; Porayko, M.; Moreau, R.; Garcia-Tsao, G.; et al. The Management of Ascites in Cirrhosis: Report on the Consensus Conference of the International Ascites Club. Hepatology 2003, 38, 258–266, doi:10.1053/jhep.2003.50315.
3. Nadim, M.K.; Kellum, J.A.; Forni, L.; Francoz, C.; Asrani, S.K.; Ostermann, M.; Allegretti, A.S.; Neyra, J.A.; Olson, J.C.; Piano, S.; et al. Acute Kidney Injury in Patients with Cirrhosis: Acute Disease Quality Initiative (ADQI) and International Club of Ascites (ICA) Joint Multidisciplinary Consensus Meeting. J Hepatol 2024, 81, 163–183, doi:10.1016/j.jhep.2024.03.031
4. Brown, E.A.; Blake, P.G.; Boudville, N.; Davies, S.; de Arteaga, J.; Dong, J.; Finkelstein, F.; Foo, M.; Hurst, H.; Johnson, D.W.; et al. International Society for Peritoneal Dialysis Practice Recommendations: Prescribing High-Quality Goal-Directed Peritoneal Dialysis. Perit Dial Int 2020, 40, 244–253, doi:10.1177/0896860819895364.

Clinical Case Summary

In advanced chronic liver disease (ACLD) patients, the endoscopic evidence of esophageal and/or gastric varices denotes the presence of clinically significant portal hypertension (CPSH), representing the main clinical consequence of portal hypertension (PH).
In this setting, although infrequently, besides typical sites (i.e., esophagus and stomach), PH-related varices can manifest even in other atypical portosystemic-shunt districts, including the vagina. CSPH-related vaginal varices bleeding can occur as a rare complication documented by limited case reports.
A 62-year-old female patient with viral (eradicated Hepatitis C Virus infection)-related- decompensated (grade 2 ascites)-ACLD, complicated by CSPH (grade F2 esophageal varices), was admitted to our Department in February 2025 for microcitic anemia. Anamnesis revealed a previous gastric cancer managed with total gastrectomy resection in 2021.
On admission, abdominal imaging showed radiological signs of ACLD/PH (coarse pattern, splenomegaly, dilated splenic-portal axis). Esophagogastroduodenoscopy ruled out active sources of bleeding, whereas colonoscopy revealed anal congestive not-bleeding varices. During the hospitalization, an episode of metrorrhagia imposed gynecologic evaluation with vaginal speculum examination. This assessment documented vaginal varices with the relative rupture as the current cause of the bleeding, suggesting this site is the further district for (CS)PH manifestation consequently to potentially occurred total gastrectomy-determined changes in abdominal vascular anatomy.
In ACLD patients receiving surgery altering abdominal vascularization, variceal bleeding represents a possible CSPH-related complication occurring even in atypical sites, such as the vagina. This scenario imposes an adequate tailored management, monitoring unusual bleeding signs, and adopting appropriate preventive strategies by including gynecologic evaluation in follow-up.

References

1. McHugh PP, Jeon H, Gedaly R, Johnston TD, Depriest PD, Ranjan D. Vaginal varices with massive hemorrhage in a patient with nonalcoholic steatohepatitis and portal hypertension: Successful treatment with liver transplantation. Liver Transpl. 2008 Oct;14(10):1538-40. doi: 10.1002/lt.21506. PMID: 18825698.
2. Kreek MJ, Raziano JV, Hardy RE, Jeffries GH. Portal hypertension with bleeding vaginal varices. Ann Intern Med. 1967 Apr;66(4):756-9. doi: 10.7326/0003-4819-66-4-756. PMID: 6067181.
3. Chan G, Taqi A, Drage M, Quan D. A case report of massive vaginal variceal hemorrhage in a patient with cirrhosis secondary to nonalcoholic steatohepatitis unresolved even after successful liver transplantation. Transplant Proc. 2013 Mar;45(2):835-7. doi: 10.1016/j.transproceed.2012.04.033. Epub 2012 Sep 19. PMID: 23267803.
4. Lebrec D, Benhamou JP. Ectopic varices in portal hypertension. Clin Gastroenterol. 1985 Jan;14(1):105-21. PMID: 3872747.
5. Nagata J, et al. Vaginal bleeding in a patient with type C liver cirrhosis without a past history of laparotomy: successful treatment with partial splenic artery embolization. Clin J Gastroenterol. 2012 Aug;5(4):275-81. doi: 10.1007/s12328-012-0316-3. Epub 2012 Jun 30. PMID: 26182393.

Clinical Case Summary

Introduction: Cirrhosis complicated by portal hypertension often leads to gastrointestinal bleeding, predominantly from esophageal varices. However, the occurrence of lower GI bleeding from rectal varices and angiodysplasias represents a rarer and more complex clinical scenario. We report the case of a 62-year-old man with cirrhosis and multiple vascular anomalies requiring multidisciplinary management.
Patient observation: The patient, with a history of Type 2 diabetes, coronary artery disease, and prior cholecystectomy, was diagnosed with cirrhosis of presumed autoimmune origin, despite non-confirmatory liver biopsy. He experienced recurrent upper GI bleeding from esophageal varices, managed with beta-blocker therapy. More recently, a massive lower GI bleed led to endoscopic assessment revealing gigantic rectal varices and diffuse colonic angiodysplasias. Stabilisation was achieved by treating the angioddysplasias endoscopically with APC.
Figure 1&2: endoscopic images
Discussion: This case illustrates the difficulty of managing complex portal hypertension complications. While beta-blockers reduce bleeding risk from esophageal varices, rectal varices and angiodysplasias pose additional therapeutic challenges. Endoscopic sclerotherapy, band ligation, or embolization may be required, but their efficacy in diffuse vascular anomalies remains limited. The presence of multiple bleeding sources demands vigilant surveillance and individualized management strategies. Moreover, coexisting comorbidities like diabetes and cardiovascular disease complicate procedural risks and therapeutic decisions.
Conclusion: Managing cirrhosis complicated by giant rectal varices and angiodysplasias requires a multidisciplinary and tailored approach. This case highlights the importance of ongoing surveillance, optimized medical therapy, and readiness for endoscopic or interventional radiology techniques to prevent further decompensations and preserve quality of life.

Introduction

Even though numerous risk factors and methods for prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) have been identified, it persists as the most prevalent complication. Administration of 100mg diclofenac prior to ERCP represents the most frequently used prophylaxis. Diclofenac is predominantly metabolized by various cytochrome P450 enzymes. The potential presence of single nucleotide polymorphisms (SNP) in these enzymes could cause interindividual variability in metabolization rates, which could affect serum plasma levels of diclofenac. Given the limited available research on this subject, the aim of this study was to investigate whether differences in presence of SNPs in the CYP-enzymes involved in diclofenac metabolism were associated with PEP.

Aims & Methods

This multicentre cohort study included patients above 18 years who underwent ERCP between 2012 and 2022. Upon inclusion, patients were divided into the PEP or control group. Real-time polymerase chain reactions were performed on buccal smear samples to identify gene variants involved in the diclofenac metabolism (e.g. CYP2C8*3). Secondary endpoints were validation of known and possibly yet unknown risk factors for PEP.

Results

In total, 103 patients were included in the PEP group and 245 in the control group. DNA amplification was possible in 91.5% of the genetic variants and revealed that heterozygous carriers of CYP2C8*3 variant were associated with a lower frequency of PEP (OR 0.2; 95% CI 0.0-0.8). Pancreatic duct cannulation (OR 3.0; 95% CI 1.4-6.6) and precut sphincterotomy (OR 3.1; 95% CI 1.2-8.0) were both found as independent risk factors for PEP.

Conclusion

This study showed that heterozygous carriers of the CYP2C8*3 variant have a lower risk of developing PEP. To investigate gene variants affecting real-time diclofenac plasma levels, we have started a study in which we prospectively collect blood samples to enhance DNA quality and to analyze the existence of a correlation between PEP and reduced diclofenac levels. If this correlation is confirmed, further research is needed to investigate the optimal dosage of diclofenac in wild type CYP2C8 patients.

Introduction

Gastric cancer (GCA) is the 5^th most common cancer and 3^rd leading cause of cancer-related death. Helicobacter pylori (H. pylori) is the chief risk factor. The prevalence of H. pylori in Africa is between 60-90%, despite this GCA appears to be low, the so-called African enigma.

Aims & Methods

Aim: To document the epidemiological profile and risk factors of GCA in a South African cohort.
Methods: A retrospective folder review of patients with GCA from 2018-2022

Results

443 patients were included; median age= 63 (range 29-86), 65% male (61% ≥ 60 years old). HPT (38.2%) and diabetes (17.6%) were the main comorbidities. 46% and 8.4% had history of smoking and alcohol use respectively. NSAID and PPI use were reported in 8.8% and 7% respectively. The commonest symptom was loss of weight (38.6%) and epigastric pain (29%). 68% had a Hb<12g/dl with a median Hb=10 (range 3.8-17). Endoscopically, gastritis or duodenitis or ulcers were recorded in 63% of cases. The commonest site of GCA was non-cardia (82.2%); antral and corpus cancers in 40.9% and 53.2% respectively. Histologically, H. pylori was reported in 11.5%, while chronic atrophic gastritis (CAG) in 15.6%. H. pylori was not associated with either antral or corpus cancer, or CAG, however PPIs were associated with a reduced odd of antral cancer, OR=0.42, CI=0.18-0.97, p=0.04. None of the other demographic or clinical factors were associated with the location of GCA.

Conclusion

GCA is higher in males and those ≥60 years. Loss of weight and anaemia are key red flags. Non-cardia gastric cancers are the commonest in this cohort. The low prevalence of H. pylori suggests previous eradication, although CAG was high, thus maintaining the increased risk of non-cardia CGA. Interestingly, PPI use was significantly protective against developing antral cancer. This highlights the need to treat H. pylori before CAG occur.

Disclosure

​​​​​Nil