P-101: Progressive pancreatic atrophy in pediatric type 1 diabetes: a cross-sectional ultrasonographic study
A Wołoszyn-Durkiewicz, D Swieton, A Jankowska, M Kujawa, E Szurowska, K Myszczyński, M MyśliwiecAbstract
Introduction
Type 1 diabetes (T1D) is an autoimmune disorder characterized by progressive β-cell destruction. While research has focused on endocrine dysfunction, structural changes in the exocrine pancreas are increasingly recognized.
Objectives
The aim of this study was to compare pancreatic dimensions in children with type 1 diabetes (T1D) and healthy controls, and to identify factors influencing pancreatic size, including disease duration and metabolic control parameters.
Methods
This cross-sectional study involved 152 children (92 T1D, 60 healthy age- and sex-matched controls). Pancreatic dimensions were assessed via ultrasound and normalized to body surface area (AP-BSA). Multivariable linear regression was used to identify predictors of pancreatic size.
Results
The median diabetes duration was 4.79 years (IQR: 3.50–7.59). The reduction in pancreatic size in the T1D group was statistically significant (p < 0.001). The mean antero-posterior diameter of the pancreas, adjusted for body surface area (AP-BSA), was 24.11 ± 7.21 mm/m2 in the T1D group and 34.90 ± 6.68 mm/m2 in the control group. In the multivariable regression model, adjusted for gender, and BMI z-score, diabetes duration (β = -1.948, p <0.001) and age of T1D onset (β = -1.126, p <0.001) were identified as predictors of decreased AP-BSA in patients with type 1 diabetes, whereas glycated hemoglobin level (HbA1c) and daily insulin dose (units per kg) were not statistically significant.
Conclusions
Our study confirms that patients with T1D exhibit significantly smaller pancreatic size compared to healthy controls. This reduction appears to be a progressive change linked to T1D duration. Furthermore, the lack of association between pancreatic atrophy and HbA1c or insulin dosage suggests that structural loss may be driven by underlying autoimmune mechanisms rather than current metabolic status. Our findings demonstrate that ultrasonographic assessment of AP-BSA may be a practical tool for monitoring these changes.