Clinical Case Summary

Eosinophilic gastroenteritis is a rare digestive inflammation that can affect one or more layers of gastrointestinal wall
The subserosal form is the most common variety.
We report here a case of eosinophilic ascites diagnosed in the hepato-gastro-enterology department
Here we report a case of a 45-year-old man, admitted to our department for generalized abdominal pain evolving for 2 years. On physical examination, he presented a minimal ascites. Laboratory examinations revealed hypereosinophilia at 2480/mm³ with a normal blood smear, total IgE elevated at 125 U/ml, C reactive protein, albumin, liver and kidney functions were normal. The standard stool test showed no parasites but contained 35% of eosinophils.
Prick test was positive to mites, cats, shrimps, almonds, and peanuts.
Abdominal CT revealed a minimal ascites with infiltration of mesenteric fat and diffuse thickening bowel wall.
The gastroscopy and colonoscopy showed erythema in duodenum and recto-colic mucosa, an eosinophilic infiltration at 20 per HPF was found only at the colonic wall.
The laparoscopy found an inflammation of the bowel and peritoneum without visualization of nodules, the ascites was exudative and rich in eosinophils, the peritoneal biopsy didn’t show any specific fibro-inflammatory remodeling.
An Albendazole trial was instituted for 5 days at a dose of 400mg per day. The evolution was marked by the regression of abdominal pain and blood eosinophilic polynuclear cells decreased to 21/ mm³.
An ultrasound is planned after 3 months to affirm the ascites draying up.

Introduction

There has been a shift from percutaneous drainage towards endoscopic ultrasound (EUS)-guided drainage for management of post-operative pancreatic fluid collections (POPFC). However, available series have been limited by sample size and little is known about the factors that may influence clinical success.

Aims & Methods

Our aim was to evaluate the outcomes of EUS-guided drainage of POPFC following pancreatic surgery and identify predictors of clinical success.
We performed a retrospective review of patients who underwent EUS-guided drainage of POPFC between 2014 and August 2024 at three academic centers. Primary outcome was clinical success, defined as the complete radiological regression of the collection and resolution of symptoms without the need for additional drainage procedures.

Results

In total, 265 cases were included (mean age 64 [SD±13.9] years, 37% pylorus-resecting pancreatoduodenectomy). Early drainage (≤14 days) was performed in 52% of cases (n=138) and DPPS were used in 209 cases (79%).
Clinical success with a single EUS drainage procedure was achieved in 160 cases (60.4%). Step-up interventions were required in 67 patients (25.3%), 37 of which required endoscopic revision only. Technical success was achieved in 90% (n=238) and adverse events occurred in 43 cases (16%).
Stent type, drainage timing, splenectomy and drainage route did not seem to significantly influence clinical success. Multivariate analysis including stent type and surgical history, showed that distal pancreatectomy was an independent risk factor for clinical failure.

Conclusion

EUS-guided drainage of POPFC was effective in the majority of cases with a single procedure, although distal pancreatectomy was suggested as an independent risk factor for clinical failure. These results further support the use of EUS-guided drainage for the management of postoperative collections.

Disclosure

HH declares no competing interests. MB received trial support from Boston Scientific and holds consultancy agreements with Dekra, Ovesco and Prion Medical. GV received lecture fees from Boston Scientific and travel grants from Pentax Medical and Euromedical. RVW holds a consultancy agreement with Boston Scientific. Schalk van der Merwe holds the Cook chair in Interventional endoscopy, has consultancy agreements with Cook, Pentax and Olympus and co-chairs the Boston-Scientific Chair in Therapeutic Biliopancreatic Endoscopy.

Introduction

Inflammatory Bowel Disease (IBD) is characterized by chronic inflammation and metabolic dysregulation in the intestinal epithelium. Serine, a non-essential amino acid synthesized via the rate-limiting enzyme phosphoglycerate dehydrogenase (PHGDH), maintains cellular redox balance. Serine metabolism is upregulated in cancer and immune cells, supporting survival and growth. Our previous study showed ER stress-mediated rewiring of serine metabolism was a key molecular feature in IBD. However, the mechanism of how PHGDH-related serine metabolism influences the IBD process remains unclear.

Aims & Methods

We hypothesized that serine metabolism provided a novel metabolic switch to maintain immunological homeostasis in the intestinal epithelium of IBD patients.
Clinical analysis of PHGDH was assessed in the public database of IBD cohorts, correlating PHGDH expression with endoscopic or clinical disease activity. To explore the molecular regulation of de novo serine synthesis via PHGDH, we used murine intestinal epithelial cells (Mode-K cells) and murine intestinal organoids. WB and IHC were performed to analyze in vitro ER stress and PHGDH expression in the DSS colitis model. Mode-K cells were subjected to serine starvation and co-treated with LPS. Proinflammatory cytokines were evaluated by qPCR and ELISA. Metabolic supplements formate and hypoxanthine were tested to mitigate the overactivation of inflammation. Total starvation was assessed by using serine deprivation medium and the PHGDH inhibitor BI-4916. RNA sequencing and proteomic analyses were performed to investigate molecular mechanisms.

Results

Clinically, we observed upregulated PHGDH expression in IBD patients, showing a strong association between serine metabolism and IBD severity. Using the DSS-induced colitis model, we showed elevated ER stress and serine synthesis under inflammation. When the serine pathway was completely blocked, we observed a dramatically enhanced inflammatory signature upon LPS treatment. Total starvation led to impaired mitochondrial function as assessed by the Seahorse assay. Combining RNAseq and proteomic analysis, we identified C/EBPβ as the critical regulator in mediating cellular inflammation under total serine starvation via the NF-κB pathway.

Conclusion

In this study, we demonstrated the critical roles of PHGDH and serine metabolism in regulating cellular inflammatory responses under ER stress. Notably, we revealed that disruption of serine metabolism accelerated intestinal inflammation via the C/EBPβ-NF-κB axis, which provided new insights into the pathophysiology of IBD.