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Idiopathic Acute Pancreatitis in Paediatric Inflammatory Bowel Disease: Clinical Features and Outcomes in a
Giovanna Fernanda Vazzana1, Alessia Romano2, Claudio Romano1
1Pediatric Gastroenterology and Cystic Fibrosis Unit, Department of Human Pathology in Adulthood and Childhood "G. Barresi", University Hospital "G. Martino", Messina, Italy.
Insights
Idiopathic acute pancreatitis (AP) in children with inflammatory bowel disease (IBD) is typically mild but can recur. Pancreatic function remains normal despite recurrent episodes, suggesting a gut-pancreas connection.
Area of Science:
- Gastroenterology
- Pediatric Gastroenterology
- Pancreatology
Background:
- Inflammatory bowel disease (IBD) affects children and can have extraintestinal manifestations.
- Acute pancreatitis (AP) is a rare complication in pediatric IBD patients.
- Secondary causes of AP must be excluded to identify idiopathic cases.
Purpose of the Study:
- To characterize idiopathic AP in pediatric IBD patients.
- To describe clinical features, timing, and long-term outcomes.
- To investigate potential links to active intestinal inflammation.
Main Methods:
- Retrospective single-center cohort study (2018-2024).
- Inclusion of pediatric IBD patients diagnosed with AP after excluding secondary causes.
- Analysis of clinical, laboratory, imaging, and outcome data.
Main Results:
- 16/395 (4.1%) pediatric IBD patients developed AP; 12 (3%) met criteria for idiopathic AP.
- Idiopathic AP occurred during active disease (75%) or post-surgery (25%), predominantly in ulcerative colitis.
- All episodes were mild; 67% experienced acute recurrent pancreatitis (ARP) within 9 months, with preserved pancreatic function.
Conclusions:
- Idiopathic AP in pediatric IBD is mild but recurrent, linked to active colonic inflammation.
- Recurrence does not impair pancreatic function, suggesting an immune-mediated gut-pancreas axis.
- Further multicenter studies are needed to confirm findings and explore pathogenesis.
Aim:
To describe the clinical characteristics, timing, and long-term outcomes of idiopathic acute pancreatitis (AP) in paediatric inflammatory bowel disease (IBD) after systematic exclusion of secondary causes.
Methods:
We conducted a retrospective single-centre cohort study of paediatric IBD patients followed between January 2018 and December 2024. AP diagnosis and severity were classified according to the North American Society for Paediatric Gastroenterology, Hepatology and Nutrition (NASPGHAN) criteria. Patients with drug-induced, metabolic, infectious, genetic, or structural causes were excluded. Clinical, laboratory, imaging, and outcome data were analysed.
Results:
Among 395 paediatric IBD patients, 16 (4.1%) developed AP. After excluding four azathioprine-related cases, 12 patients (3%) were included (50% male; median age 10.6 years). Ulcerative colitis (UC) predominated (67%), with colonic involvement in all cases. Idiopathic AP occurred during active disease in 75% and after IBD-related surgery in 25%. All episodes were mild and resolved with supportive management without complications. Ultrasound showed focal pancreatic inflammatory changes in 58% of patients, predominantly involving the body and tail, while diffuse pancreatic enlargement was reported in 5 patients (42%). Over a median follow-up of 3.7 years, 8/12 patients (67%) developed acute recurrent pancreatitis (ARP), with a median time to recurrence of 9 months. No patients developed pancreatic insufficiency or diabetes. Serum IgG4 levels were negative in all patients. Among those who developed ARP, genetic testing revealed no pathogenic variants.
Conclusions:
Idiopathic AP in children with IBD appeared to be a mild but potentially relapsing condition associated with active intestinal inflammation and colonic disease. Pancreatic function remained preserved despite recurrence, which may be consistent with an immune-mediated gut-pancreas axis. Given the limited sample size, these findings should be considered hypothesis-generating, and prospective multicentre studies are required to confirm these observations and better characterise the underlying pathogenesis.
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