Evidence map›Paper›PMID 42245056›Full record

ArticlemedRxiv : the preprint server for health sciences2026

Role of genetic risk on progression to diabetes in children with acute pancreatitis.

Lu Zhang, Faizan Ahmed, Seth A Sharp, Han Sun, Swaraj Thaman, Clive H Wasserfall, Anna L Gloyn, Maisam Abu-El-Haija

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

8 authors.

Lu ZhangDepartment of Pediatrics, Stanford School of Medicine, Stanford University, CA, USA.
Faizan AhmedDivision of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Seth A SharpDepartment of Pediatrics, Stanford School of Medicine, Stanford University, CA, USA.
Han SunDepartment of Pediatrics, Stanford School of Medicine, Stanford University, CA, USA.
Swaraj ThamanDepartment of Pediatrics, Stanford School of Medicine, Stanford University, CA, USA.
Clive H WasserfallDepartment of Pathology, Immunology, and Laboratory, Medicine, University of Florida, FL, USA.
Anna L GloynDepartment of Pediatrics, Stanford School of Medicine, Stanford University, CA, USA.ORCID 0000-0003-1205-1844
Maisam Abu-El-HaijaDivision of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI Seung K Kim · 2017 to 2026
$19.5M
Diabetes Timing and Types and the Effect on Beta Cell Function Post-Acute Pancreatitis in ChildrenR03DK131156 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI ABU-EL-HAIJA, MAISAM · 2022 to 2023
$227k
NIDDK NIH HHS P30 DK116074NIDDK NIH HHS R03 DK131156
6 · The paper itself

Abstract

Background: Acute pancreatitis (AP) is an established risk factor for diabetes, with approximately 20% of children developing either prediabetes or diabetes within one year of their first episode. Little is known about the diabetes pathophysiology or which individuals are at highest risk. We aimed to evaluate whether genetic risk scores (GRS) for type 1 (T1D) and polygenic risk scores (PRS) type 2 diabetes (T2D) are associated with progression to dysglycemia following AP. Methods: Clinical data were available for 123 children (mean age (IQR), 12 (8-15) years; mean body mass index (BMI), 21.8) with AP who were followed for >1 year. Array genotyping coupled with imputation using the TOPMed reference panel was performed. Genetic ancestry was predicted using a random forest classifier. GRS for T1D and T2D were calculated using either an ancestry-appropriate (T1D-GRS) or a multi-ancestry (T2D-PRS) weighted framework. To evaluate risk compared to the population we used predefined GRS thresholds from UK Biobank. Results: Among the 123 subjects, 24 developed dysglycemia (5 with diabetes and 19 with prediabetes). The majority (75.6%, n=93) of children were of European ancestry. Comparison of the T1D-GRS burden with the UK BioBank showed numerically higher proportions for any given threshold. At the top 5% threshold, 9.7% of our cohort were classified as high-risk compared to 5% in UK Biobank (p<0.05). The elevated T1D-GRS could be primarily attributed to non-HLA variants and was more enriched in those testing positive for ≥1 islet-autoantibody. The T2D-PRS was also elevated in the dysglycemic group but only reached statistical significance in those who were obese. Conclusion: These findings highlight the potential role of both T1D-GRS and T2D-PRS in investigating diabetes susceptibility following AP.

Indexed as

Acute pancreatitisChildrenGenetic risk scoresType 1 DiabetesType 2 Diabetes

Identifiers

PMID42245056
PMCPMC13232395

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.