S Ono1, K Tokiwa, N Iwai. 1. Division of Surgery, Children's Research Hospital, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Abstract
BACKGROUND/ PURPOSE: Anomalous arrangement of the pancreaticobiliary duct (AAPBD) is closely related to congenital biliary dilatation and frequently associated with biliary tract malignancy. To examine the mechanism of biliary tract carcinogenesis in patients with AAPBD, we investigated histologically the early changes in cell proliferative kinetics of the gallbladder mucosa of children with AAPBD. METHODS: Twenty-three specimens of gallbladder were obtained from 23 children with AAPBD, and six control specimens were obtained from pediatric patients. All specimens were fixed routinely and paraffin embedded and examined histologically with H&E staining and immunohistochemically with monoclonal antibody Ki-67(MIB-1), which reacts with a human nuclear antigen associated with cell proliferation. Ki-67 labeling index (Ki-67 LI) was obtained by counting the numbers of Ki-67-positive cells per 1,000 gallbladder epithelial cells. RESULTS: Significant differences in Ki-67 LI were noted between children with and without AAPBD. Furthermore, Ki-67 LI and the incidence of epithelial hyperplasia of gallbladder were significantly higher in children with AAPBD in whom the major pancreatic duct joined the common bile duct (P-C type) than in those in whom the common bile duct joined the major pancreatic duct (C-P type). CONCLUSIONS: Cellular proliferative activity was increased in children with AAPBD, especially those with the P-C-type anomaly. These results suggest that the early mucosal changes of the gallbladder occurred in early childhood of patients with AAPBD and might be associated with gallbladder cancer. Early diagnosis and early surgical division of the biliary tract and pancreatic duct is recommended for children with AAPBD.
BACKGROUND/ PURPOSE:Anomalous arrangement of the pancreaticobiliary duct (AAPBD) is closely related to congenital biliary dilatation and frequently associated with biliary tract malignancy. To examine the mechanism of biliary tract carcinogenesis in patients with AAPBD, we investigated histologically the early changes in cell proliferative kinetics of the gallbladder mucosa of children with AAPBD. METHODS: Twenty-three specimens of gallbladder were obtained from 23 children with AAPBD, and six control specimens were obtained from pediatric patients. All specimens were fixed routinely and paraffin embedded and examined histologically with H&E staining and immunohistochemically with monoclonal antibody Ki-67(MIB-1), which reacts with a human nuclear antigen associated with cell proliferation. Ki-67 labeling index (Ki-67 LI) was obtained by counting the numbers of Ki-67-positive cells per 1,000 gallbladder epithelial cells. RESULTS: Significant differences in Ki-67 LI were noted between children with and without AAPBD. Furthermore, Ki-67 LI and the incidence of epithelial hyperplasia of gallbladder were significantly higher in children with AAPBD in whom the major pancreatic duct joined the common bile duct (P-C type) than in those in whom the common bile duct joined the major pancreatic duct (C-P type). CONCLUSIONS: Cellular proliferative activity was increased in children with AAPBD, especially those with the P-C-type anomaly. These results suggest that the early mucosal changes of the gallbladder occurred in early childhood of patients with AAPBD and might be associated with gallbladder cancer. Early diagnosis and early surgical division of the biliary tract and pancreatic duct is recommended for children with AAPBD.