Clinical Case Summary

Introduction: Syphilis is a sexually transmitted infection caused by the spirochete Treponema pallidum,Syphilitic hepatitis is a rare entity, and is under-diagnosed because of its non-specific clinical presentation, particularly in young adults. We present the case of a patient who was hospitalized with acute hepatitis and who tested positive for syphilis
Case report: This is the case of a 25 years-old patient,single,with the notion of unprotected sexual relations. The history of the disease goes back to 2 months with acholestatic jaundice associated a pruritus,a weight loss of 10 kg. The general examination found a frank cutaneous-mucous jaundice,lesions of scrapings.Abdominal examination showed a clinically normal liver, the examination of the lymph nodes revealed multiple lymph nodes.At abdominal and pelvic ultrasound showed hilar adenopathy. A thoraco-abdomino-pelvic scanner showed a adenopathies above and below the diaphragm.Biologically,there was acute cytolysis with ASATat 1211IU/L,ALAT at1191IU/L,icteric cholestasis with ALP at263IU/L,GGT at262IU/L,and total bilirubin at174mg/L,As part of the etiological work-up,the acute viral serologies were negative,The immunological work-up did not show signs of autoimmune hepatitis or primary biliary cholangitis,a syphilis serology was requested and was positive:a TPHA at 2560UI/L,a VDRL at 1/32UI/L,After eliminating all etiologies of cytolytic hepatitis,we retained the diagnosis of syphilitic hepatitis.A liver biopsy was performed which showed inflammatory infiltrate with the presence,on immunohistochemistry,of anti treponemal-pallidum antibodies,therapeutically,and considering the hepatic toxicity of penicillin G,we started a treatment based on rocephin 2g/d with spectacular biological improvement at H48 of the beginning of treatment.
Conclusion: Syphilitic hepatitis remains a rare cause of acute hepatitis and should be considered if there are risk factors and after all other causes of cytolytic hepatitis have been ruled out.

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.

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

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.

Clinical Case Summary

We present the case of a 37-year-old woman.No personal history or usual medication.Resorted to the emergency department due to diarrhea going on for 3 weeks, with around 3 nocturnal liquid stools, without blood or fever, associated with vomiting and the appearance of abdominal distension in the previous week.The abdomen was distended but depressible and painless.Analytically to highlight leukocytosis (18490/ul) with marked peripheral eosinophilia 7430/ul (40.7%) and slight changes in liver biochemistry.An abdominal CT showed “significant parietal thickening of the entire small intestine, gastric antrum and pylorus.Diffuse ascites".Diagnostic paracentesis and EDA were performed with evidence of a swollen and hyperemic pre-pyloric antrum, with slight pylorus resistance and duodenum with edematous mucosa.Biopsies of the body were performed, antrum and duodenum, the results of which showed a slight inflammatory infiltrate.From the study carried out, diagnostic paracentesis demonstrated 2220cells/mm3 with a predominance of eosinophils(80%).Other causes of tissue eosinophilia were excluded, namely systemic autoimmune diseases, vasculitis, celiac disease, and infections.Serum tryptase was normal and fecal calprotectin 158 mg/kg.The hypothesis of severe eosinophilic gastroenteritis was raised, affecting the serosa(presence of ascites),so prednisolone 40mg+pantoprazole 40mg was started, with improvement of symptoms and resolution of peripheral eosinophilia in the following day.The patient was discharged on the 3rd day, maintaining corticosteroid therapy and a subsequent progressive weaning regimen over approximately 8 weeks.Since then remains asymptomatic, analytically without peripheral eosinophilia and without thickening of the loops or free peritoneal effusion rated by MRI.Eosinophilic gastroenteritis is a rare benign entity that requires high clinical suspicion as well as exclusion of other causes.It is important to be alert to the possibility of this diagnosis.

References

Rached, A.A. and Hajj, W.E. (2016) ‘Eosinophilic gastroenteritis: Approach to diagnosis and management’, World Journal of Gastrointestinal Pharmacology and Therapeutics, 7(4), p. 513. doi:10.4292/wjgpt.v7.i4.513.
Sunkara, T. et al. (2019) ‘eosinophilic gastroenteritis: Diagnosis and clinical perspectives’, Clinical and Experimental Gastroenterology, Volume 12, pp. 239–253. doi:10.2147/ceg.s173130.

Disclosure

No conflict of interest

Introduction

​The gut microbiota is often altered in chronic liver diseases and hepatocellular carcinoma (HCC), and increasing evidence suggests that it may influence response to cancer immunotherapy. Strategies to modulate the gut microbiome (i.e., fecal microbiota transplant (FMT)) may help to improve efficacy of immune checkpoint inhibitors (ICIs) or even overcome resistance to ICIs.

Aims & Methods

​In this single-center phase II pilot study (ClinicalTrials.gov ID: NCT05750030), we plan to include 12 patients with advanced HCC who progressed on atezolizumab/bevacizumab. Patients will receive atezolizumab/bevacizumab every 3 weeks in combination with a single FMT via colonoscopy from donors with HCC who responded to PD-(L)1-based immunotherapy. The primary endpoint is safety, measured by incidence and severity of treatment-related adverse events (TRAEs). The main secondary endpoint is best overall response (BOR) according to RECISTv1.1 and mRECIST. Here, we report results of a preplanned interim analysis.

Results

Of 6 patients included so far, 5 were male, 5 had BCLC stage C, and 5 had Child-Pugh class A. All patients underwent successful FMT without any periinterventional complications. TRAEs related to FMT were all low-grade (grade 1-2) and included bloating (n=2), constipation (n=2), and diarrhea (n=1). TRAEs related to atezolizumab included one grade 2 pruritus, and TRAEs related to bevacizumab included arterial hypertension (one grade 3 and two grade 2) and proteinuria (one grade 3 and one grade 1). All patients had at least one follow-up imaging. Two patients had partial response, 3 patients had stable disease, and 1 patient had progressive disease as BOR according to both RECISTv1.1 and mRECIST, which corresponds to an objective response rate of 33% and a disease control rate of 83%.

Conclusion

Based on acceptable safety and promising efficacy results, the decision to continue recruitment in this trial was made. An update with longer follow-up will be presented at the meeting, including analyses of the gut microbiome.

Disclosure

AF received travel support from Takeda and Amgen, he received speaker honoraria from AbbVie
KP has nothing to disclose.
BS received travel support from AbbVie, AstraZeneca, Gilead and Ipsen, speaker honoraria from Eisai as well as grant support from AstraZeneca and Eisai.
BL received speaker honoraria from Chiesi and Gilead.
LP has nothing to disclose.
AK has nothing to disclose.
KR has nothing to disclose.
KZ has nothing to disclose.
MT received speaker honoraria from Albireo, BMS, Falk Foundation, Gilead, Intercept, Madrigal and MSD; he has advised for Abbvie, Albireo, BiomX, Boehringer Ingelheim, Falk Pharma GmbH, Genfit, Gilead, Hightde, Intercept, Ipsen, Jannsen, MSD, Novartis, Phenex, Pliant, Rectify Regulus, Siemens and Shire. He further received travel grants from Abbvie, Falk, Gilead Intercept and Jannsen and research grants from Albireo, Almylam, Cymabay, Falk, Gilead, Intercept, MSD, Takeda and Ultragenyx. He is also co-inventor of patents on the medical use of NorUDCA filed by the Medical Universities of Graz and Vienna.
DT served as a speaker and/or consultant and/or advisory board member for Siemens, Roche, Sanova, Bristol-Myers Squibb and received travel support from Bayer and Siemens.
CG nothing to disclose.
MP received speaker honoraria from Bayer, BMS, Eisai, Ipsen, Lilly, MSD, and Roche; he is a consultant/advisory board member for AstraZeneca, Bayer, BMS, Eisai, Ipsen, Lilly, MSD, and Roche; he received grants from AstraZeneca, Bayer, BMS, and Roche; he received travel support from Bayer, BMS, Ipsen, and Roche.