title: Epithelial hyperplasia of the gallbladder in children with anomalous pancreaticobiliary ductal union.
abstract: OBJECTIVE
  Few data are available on the fate and incidence of epithelial hyperplasia throughout the life of anomalous pancreaticobiliary ductal union (APBD) patients. The pathological study in pediatric APBD patients is less recognized.
  
  
  METHODS
  Ten resected gallbladders obtained from children with APBD and control patients without APBD were examined histologically, and immunohistochemically for the detection of Ki-67 (as a proliferative marker) and p53. K-ras mutations in codon 12 were also examined. Epithelial hyperplasia was classified into high-grade and low-grade hyperplasia.
  
  
  RESULTS
  Six (60%) of 10 patients with APBD had epithelial hyperplasia of the gallbladder, whereas no patients without APBD exhibited this lesion. Diffuse epithelial hyperplasia was observed in 1 (50%) of 2 undilated-type APBD and 5 (63%) of 8 dilated-type. Two (33%) of 6 patients with epithelial hyperplasia exhibited high-grade hyperplasia. Ki-67 labeling index (LI) was significantly higher in hyperplastic mucosa than in control gallbladder mucosa. K-ras mutations and p53 overexpression were not detected in hyperplastic and normal mucosa.
  
  
  CONCLUSIONS
  Epithelial hyperplasia of the gallbladder accompanied by increased proliferative activity exists at birth or is acquired in childhood with APBD patients and may be an important factor predisposing to the development of gallbladder carcinoma.
authors.affiliation: Third Department of Internal Medicine, Asahikawa Medical College, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Tanno
authors.forename: T
authors.initials: T
authors.lastname: Obara
authors.forename: T
authors.initials: T
authors.lastname: Fujii
authors.forename: Y
authors.initials: Y
authors.lastname: Mizukami
authors.forename: N
authors.initials: N
authors.lastname: Yanagawa
authors.forename: T
authors.initials: T
authors.lastname: Izawa
authors.forename: H
authors.initials: H
authors.lastname: Ura
authors.forename: Y
authors.initials: Y
authors.lastname: Kohgo
mesh_terms: D002455:Cell Division; D002648:Child; D002675:Child, Preschool; D003135:Common Bile Duct / Q000002:abnormalities*; D004247:DNA / Q000032:analysis; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005704:Gallbladder / Q000378:metabolism / Q000473:pathology*; D005705:Gallbladder Diseases / Q000209:etiology / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D006965:Hyperplasia; D007124:Immunoenzyme Techniques; D007223:Infant; D007231:Infant, Newborn; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D009154:Mutation; D010183:Pancreatic Ducts / Q000002:abnormalities*; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D016283:Proto-Oncogene Proteins p21(ras) / Q000235:genetics / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D019394:Ki-67 Antigen; D016159:Tumor Suppressor Protein p53; D004247:DNA; C501009:HRAS protein, human; D016283:Proto-Oncogene Proteins p21(ras)