Morphological changes in the biliary mucosa in pediatric patients with congenital biliary dilatation are more influenced by the duration of amylase exposure than by amylase levels in the gallbladder
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In brief
In brief
This retrospective study of 43 pediatric patients with congenital biliary dilatation demonstrates that cumulative amylase exposure over time, rather than amylase concentration alone, predicts biliary epithelial dysplasia risk. Findings suggest duration of pancreatic enzyme reflux is the critical factor in mucosal changes, with implications for surgical timing in children with pancreaticobiliary maljunction.
- Duration of amylase exposure (AMY level × patient age) predicts biliary dysplasia risk better than AMY concentration alone in PBM patients.
- Bile AMY exposure ≥662,400 IU/L×months is an independent risk factor for dysplasia in children with congenital biliary dilatation.
- All 43 pediatric CBD patients showed biliary epithelial hyperplasia; 30% had dysplasia, but none progressed to carcinoma at surgery.
- Early surgical intervention may reduce cumulative pancreatic enzyme exposure and lower dysplasia risk in pancreaticobiliary maljunction.
- Todani type Ia, Ic, and IVa CBD cases uniformly exhibit epithelial changes, emphasizing need for timely resection to prevent malignancy.
Written by the GCMD Library team from the article.
Abstract
Purpose
We investigated the relationship between bile amylase (AMY) levels and biliary epithelial changes in pancreaticobiliary maljunction (PBM), a congenital anomaly characterized by pancreaticobiliary reflux due to duct fusion outside the duodenal wall.
Methods
We enrolled 43 children with congenital biliary dilatation (CBD) of Todani types Ia, Ic, and IVa who underwent surgery at the Hokkaido Medical Center for Child Health and Rehabilitation between November 2007 and June 2023. We defined total AMY exposure in bile as bile AMY levels multiplied by the patient’s age (months), representing amount of estimated AMY exposure until surgery. We retrospectively investigated the relationships between bile AMY levels and clinicopathological findings.
Results
All patients exhibited hyperplasia in the gallbladder and bile duct epithelium, with dysplasia observed in 13 cases, but no carcinoma. Exposure to bile AMY ≥ 662,400 IU/L × months was an independent risk factor for dysplasia.
Conclusion
The amount of estimated AMY exposure in bile rather than AMY levels in the bile is an independent risk factor for dysplasia in the biliary mucosa.