Observational studyClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association2024
The Role of Pancreatitis Risk Genes in Endocrine Insufficiency Development After Acute Pancreatitis in Children.
Observational study in Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Role of genetic risk on progression to diabetes in children with acute pancreatitis.medRxiv : the preprint server for health sciences · 2026Article
- A recurrence prediction model based on serological indicators in children with acute pancreatitis without pancreaticobiliary anatomical abnormalities.Frontiers in pediatrics · 2026Article
- Acute pancreatitis gut dysbiosis persists at 1-year follow-up and is associated with clinical outcomes.Journal of pediatric gastroenterology and nutrition · 2025Article
- Acute Pancreatitis in Children: It's Not Just a Simple Attack.Gastroenterology · 2025Review
- Genetics of diabetes and its complications: a comprehensive review.Diabetology & metabolic syndrome · 2025Review
- Islet Autoantibodies and Their Association With β-Cell Function and Diabetes Measures in Children With Acute Recurrent and Chronic Pancreatitis.Diabetes care · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
BACKGROUND &
aimsAcute pancreatitis (AP) is increasingly recognized as a risk factor for diabetes mellitus (DM). We aimed to study the association of pancreatitis genes with pancreatic endocrine insufficiency (pre-DM and DM) development post-AP in children.
methodsThis was an observational cohort study that enrolled subjects ≤21 years with their first episode of AP and followed them for 12 months for the development of pancreatic endocrine insufficiency. Pancreatitis risk genes (CASR, CEL, CFTR, CLDN2, CPA1, CTRC, PRSS1, SBDS, SPINK1, and UBR1) were sequenced. A genetic risk score was derived from all genes with univariable P < .15.
resultsA total 120 subjects with AP were genotyped. Sixty-three subjects (52.5%) had at least 1 reportable variant identified. For modeling the development of pancreatic endocrine insufficiency at 1 year, 6 were excluded (2 with DM at baseline, 3 with total pancreatectomy, and 1 death). From this group of 114, 95 remained normoglycemic and 19 (17%) developed endocrine insufficiency (4 DM, 15 pre-DM). Severe AP (58% vs 20%; P = .001) and at least 1 gene affected (79% vs 47%; P = .01) were enriched among the endocrine-insufficient group. Those with versus without endocrine insufficiency were similar in age, sex, race, ethnicity, body mass index, and AP recurrence. A model for pre-DM/DM development included AP severity (odds ratio, 5.17 [1.66-16.15]; P = .005) and genetic risk score (odds ratio, 4.89 [1.83-13.08]; P = .002) and had an area under the curve of 0.74.
conclusionsIn this cohort of children with AP, pancreatitis risk genes and AP disease severity were associated with pre-DM or DM development post-AP.
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