Clinical Case Summary

We report the case of a 16-year-old boy followed since age 10 for pancolitis-type ulcerative colitis (UC), resistant to 5-ASA, corticosteroids, immunosuppressants, anti-TNFα, and recently deemed refractory to ustekinumab. The disease was complicated by primary sclerosing cholangitis (PSC), leading to decompensated cirrhosis.
The patient presented with a moderate flare during ustekinumab induction, including diarrhea, rectal syndrome, abdominal pain, intractable vomiting, inflammatory lower-back pain, and new-onset ascites.
Colonoscopy revealed multiple polyps from rectum to cecum, some with irregular, raspberry-like surfaces, arising on normal-appearing mucosa without erythema or ulceration. Upper endoscopy, performed due to vomiting and hematemesis, showed grade III esophageal varices, portal hypertensive gastropathy, and multiple gastric polyps, some with similar irregular surfaces. MR enterography, though limited by suboptimal bowel distension, showed no small bowel polyposis.
These unexpected endoscopic findings introduced new challenges. Management options included treatment of refractory UC, assessment and surveillance of colonic and gastric polyps—raising concern for an underlying polyposis syndrome—and liver transplant evaluation for cirrhosis. The patient was treated with IV corticosteroids, then transitioned to an oral taper after clinical improvement.
Due to the complexity, a combined therapeutic approach (colectomy, gastrectomy, and liver transplantation) was considered unfeasible. The patient and family were counseled and referred to a national transplant and surgical center for sequential management planning: liver transplantation, followed by colectomy and endoscopic resection of gastric polyps.
This rare case highlights the therapeutic and diagnostic complexity of managing refractory pediatric UC with PSC, cirrhosis, and gastrointestinal polyposis, necessitating a highly individualized, multidisciplinary approach.

References

Figure 1 showing endoscopic images of the gastric (1a) and colonic (1b) polyposis
Figure 2 showing histological findings of biopsies of some of the gastric (2a) and colonic (2b) polyps
Figure 3 MR enterography of the patient showing no signs of small bowel involvement

Introduction

Defining pancreatic steatosis (PS) and establishing its association with pancreatic cancer has been a discussed theme in the last decade. However, no consensus guidelines have yet been published on the clinical relevance and management of PS. In this systematic review and meta-analysis, we investigated the association between PS and pancreatic ductal adenocarcinoma (PDAC).

Aims & Methods

Medical literature between 2007 and 2023 was reviewed for eligible trials investigating the prevalence of PS in patients with PDAC. Eligible studies reporting on PS, assessed via imaging or histology, were included. Our primary objective was to determine the association between PDAC and PS by comparing the prevalence of PS in individuals with- and without PDAC. Subsequently, an evaluation was conducted to determine whether the method of assessment (CT, MRI, EUS or histology) and study country was correlated with the association between PS and PDAC. Measures of effect size were determined using odds ratios (ORs) and corresponding 95% confidence intervals (95% CI).

Results

The systematic review identified a total of 23 studies, of which seventeen studies examined PS prevalence among PDAC patients. Overall, the pooled prevalence of PS in patients with PDAC. was 53.6% (95% CI 40.9-66.2). No significant difference in PS prevalence was observed across various diagnostic methods or geographical regions (p= 0.71 and p= 0.50, respectively). Overall, the pooled OR for PS in in patients with PDAC compared to controls was 3.23 (95% CI 1.86-5.60, Figure 1). Subgroup analysis did not reveal any difference according to country (p= 0.52), but higher OR was observed in studies using EUS for the assessment of PS (pooled OR=6.26, 95% CI 1.23-31.8) compared to studies using CT (pooled OR=3.31, 95% CI 1.93-5.68), histology (pooled OR=1.76, 95% CI 1.22-2.54) or MRI (pooled OR=1.19, 95% CI 1.06-1.33).

Conclusion

Patients with PDAC have notable prevalence of pancreatic steatosis (53.6%). Furthermore, PDAC patients are significantly more likely to have PS (OR 3.23). These findings underscore the importance of prioritizing a standardized approach to the diagnosis, follow-up, and treatment of PS. Future studies should prioritize the identification of patients with PS who will benefit from PDAC surveillance programs.