Recent advances in pancreaticobiliary maljunction View Full Text


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Article Info

DATE

2002-02

AUTHORS

Yoshiro Matsumoto, Hideki Fujii, Jun Itakura, Masanori Matsuda, Bunsei Nobukawa, Kohichi Suda

ABSTRACT

. The purpose of this review is to evaluate our current knowledge of the embryologic etiology of pancreaticobiliary maljunction (PBM), its diagnosis, clinical aspects, and treatment, and to clarify the mechanisms of PBM involvement in carcinogenesis. Although the embryologic etiology of PBM still awaits clarification, an arrest of the migration of the common duct of the biliary and pancreatic ducts inwards in the duodenal wall has hitherto been speculated to result in a long common channel in PBM. However, we propose the hypothesis that the etiology of PBM is caused by a disturbance in the embryonic connections (misarrangement) of the choledochopancreatic duct system in the extremely early embryo. That is, PBM is an anomaly caused by a misarrangement whereby the terminal bile duct joins with a branch of the ventral pancreatic duct system, including the main pancreatic duct. PBM is frequently associated with congenital bile duct cyst (CCBD). However, these two anomalies are thought to have different embryonic etiologies. The diagnostic criteria for PBM are the radiological and anatomical detection of the extramural location of the junction of the pancreatic and biliary ducts in the duodenal wall. However, in PBM patients with a short common duct (less than 1 cm in length), detection of the extramural location is difficult. The clinical features of PBM are intermittent abdominal pain, with or without elevation of pancreatic enzyme levels; and obstructive jaundice, with or without acute pancreatitis, while the clinical features of PBM patients with CCBD are primary bile duct stone and acute cholangitis. The optimum approach for the treatment of PBM is the prevention of the reciprocal reflux of bile and pancreatic juice in the pancreas and the bile duct system. To achieve these aims, the surgical approach is most effective, and complete biliary diversion procedures with bile duct resection (for example, choledochoduodenostomy or choledochojejunostomy of the Roux-en-Y type) are most useful. Recently, it has been recognized that the development of biliary ductal carcinoma is associated with PBM. That is, the development of gallbladder cancer occurs frequently in PBM patients without CCBD, and bile duct cancer originating from the cyst wall also occurs in PBM patients with CCBD. It is speculated that the pathogenesis of the bile duct or gallbladder cancer in PBM patients involves the reciprocal reflux of bile and pancreatic juice. Investigations of epithelial cell proliferation in the gallbladder of PBM patients, and of K-ras mutations and p53 suppressor gene mutations, loss of heterozygosity of p53, and overexpression of the p53 gene product in gallbladder cancer and noncancerous lesions in PBM patients have been carried out in various laboratories around the world. The results support the conclusion that PBM is a high risk factor for the development of bile duct carcinoma. More... »

PAGES

45-54

References to SciGraph publications

  • 1996-08. An analysis of mutagens in the contents of the biliary tract in pancreaticobiliary maljunction in SURGERY TODAY
  • 1999-09. Mucosal cell proliferation activity of the gallbladder in children with anomalous arrangement of the pancreaticobiliary duct in JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
  • 1997-12. Biliary carcinogenesis in pancreaticobiliary maljunction in JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
  • 1997-03-01. End‐to‐side choledochoduodenostomy: A widely applicable procedure for biliary reconstruction in JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
  • 1997-11. Carcinoma of the gallbladder and anomalous arrangement of the pancreaticobiliary ductal system: Cell kinetic studies of gallbladder epithelial cells in JOURNAL OF GASTROENTEROLOGY
  • 1991-04. Bile flow analysis by hepatobiliary scintigraphy in the terminal bile duct in patients with congenital malformations of the pancreatico-biliary ductal system in JOURNAL OF GASTROENTEROLOGY
  • 1999-09. p53 Gene mutations and overexpression of p53 product in cancerous and noncancerous biliary epithelium in patients with pancreaticobiliary maljunction in JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
  • 1999-09. Genetic abnormalities involved in the pathogenesis of gallbladder carcinoma in JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
  • 1999-09. Epithelial cell proliferation and gene mutation in the mucosa of gallbladder with pancreaticobiliary malunion and cancer in JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
  • 1999-09. Cellular kinetics and gene mutations in gallbladder mucosa with an anomalous junction of pancreaticobiliary duct in JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
  • 1999-09. Carcinogenesis in the biliary system associated with APDJ in JOURNAL OF HEPATO-BILIARY-PANCREATIC SCIENCES
  • Identifiers

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    http://scigraph.springernature.com/pub.10.1007/s005340200004

    DOI

    http://dx.doi.org/10.1007/s005340200004

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1019638890

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/12021897


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    25 schema:description Abstract. The purpose of this review is to evaluate our current knowledge of the embryologic etiology of pancreaticobiliary maljunction (PBM), its diagnosis, clinical aspects, and treatment, and to clarify the mechanisms of PBM involvement in carcinogenesis. Although the embryologic etiology of PBM still awaits clarification, an arrest of the migration of the common duct of the biliary and pancreatic ducts inwards in the duodenal wall has hitherto been speculated to result in a long common channel in PBM. However, we propose the hypothesis that the etiology of PBM is caused by a disturbance in the embryonic connections (misarrangement) of the choledochopancreatic duct system in the extremely early embryo. That is, PBM is an anomaly caused by a misarrangement whereby the terminal bile duct joins with a branch of the ventral pancreatic duct system, including the main pancreatic duct. PBM is frequently associated with congenital bile duct cyst (CCBD). However, these two anomalies are thought to have different embryonic etiologies. The diagnostic criteria for PBM are the radiological and anatomical detection of the extramural location of the junction of the pancreatic and biliary ducts in the duodenal wall. However, in PBM patients with a short common duct (less than 1 cm in length), detection of the extramural location is difficult. The clinical features of PBM are intermittent abdominal pain, with or without elevation of pancreatic enzyme levels; and obstructive jaundice, with or without acute pancreatitis, while the clinical features of PBM patients with CCBD are primary bile duct stone and acute cholangitis. The optimum approach for the treatment of PBM is the prevention of the reciprocal reflux of bile and pancreatic juice in the pancreas and the bile duct system. To achieve these aims, the surgical approach is most effective, and complete biliary diversion procedures with bile duct resection (for example, choledochoduodenostomy or choledochojejunostomy of the Roux-en-Y type) are most useful. Recently, it has been recognized that the development of biliary ductal carcinoma is associated with PBM. That is, the development of gallbladder cancer occurs frequently in PBM patients without CCBD, and bile duct cancer originating from the cyst wall also occurs in PBM patients with CCBD. It is speculated that the pathogenesis of the bile duct or gallbladder cancer in PBM patients involves the reciprocal reflux of bile and pancreatic juice. Investigations of epithelial cell proliferation in the gallbladder of PBM patients, and of K-ras mutations and p53 suppressor gene mutations, loss of heterozygosity of p53, and overexpression of the p53 gene product in gallbladder cancer and noncancerous lesions in PBM patients have been carried out in various laboratories around the world. The results support the conclusion that PBM is a high risk factor for the development of bile duct carcinoma.
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    37 advances
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    43 aspects
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