ArticleJournal of Indian Association of Pediatric Surgeons
Exploring the Correlation between Immunohistochemical Findings and Bile Constituents in Choledochal Malformation Specimens.
Article in Journal of Indian Association of Pediatric Surgeons. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Inflammation and malignancy studies in choledochal cystic malformations (CDC) are scarce. This research explores the role of inflammation, bile composition, and markers like cyclooxygenase-2 (COX-2), phosphorylated ribosomal protein S6 (PS6), matrix metallopeptidase-9 (MMP9), and mammalian target of rapamycin (mTOR) in CDC. Materials and Methods: This is a cross-sectional observational study. The study was conducted between January 2021 and December 2023. Bile samples from children being operated for CDC were collected and analyzed for biochemical and enzymatic constituents, while excised specimens underwent histopathological and immunohistochemistry (IHC) COX-2, mTOR, PS6, and MMP9. Statistical analysis evaluated data relationships, including descriptive statistics, Chi-square tests, and linear regression. Results aimed to enhance understanding of CDC pathogenesis and identify potential biomarkers and therapeutic targets, with Results: Bile and histopathology samples from 30 children (median age: 72 months; 13 males, 17 females) with type 1 choledochal malformation were analyzed. All underwent surgery with uneventful recoveries. Significant findings included bile composition differences by age and abnormal pancreaticobiliary junction (APBJ) length. Histopathology and IHC showed COX-2, MMP9, and PS6 positivity, correlating with bile components and APBJ length. Conclusion: This study highlights a potential association between APBJ length, inflammatory markers (COX-2 and MMP9), and cellular proliferation (PS6) in children with type I choledochal malformation. The significant expression of these markers suggests that pancreatic reflux might initiate chronic inflammation and epithelial injury.
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