Biliary pancreatic: reflux-induced acute pancreatitis - myth or possibility?

Citation
T. Arendt et al., Biliary pancreatic: reflux-induced acute pancreatitis - myth or possibility?, EUR J GASTR, 11(3), 1999, pp. 329-335
Citations number
21
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
ISSN journal
0954691X → ACNP
Volume
11
Issue
3
Year of publication
1999
Pages
329 - 335
Database
ISI
SICI code
0954-691X(199903)11:3<329:BPRAP->2.0.ZU;2-S
Abstract
Objective The mechanism whereby gallstone passage through the choledochoduo denal junction initiates acute pancreatitis is not known. We mimicked diffe rent patterns of stone impaction at the choledochoduodenal junction in a ra bbit model and studied whether these result in biliary pancreatic reflux an d the initiation of pancreatic inflammation. Methods In rabbits, catheters were introduced into the common bile duct (CB D) and the pancreatic duct. In five experiments, obstruction of these cathe ters at various time intervals mimicked different patterns of stone obstruc tion of both ducts prior to a stone impaction at the papilla of Vater: expe riment I - no obstruction of the pancreatic duct and the CBD; experiment II - separate obstruction of the CBD and the pancreatic duct; experiment III - selective obstruction of the CBD; experiment IV - separate obstruction of the CBD and the pancreatic duct and subsequent decompression of the pancre atic duct; experiment V - obstruction pattern as in experiment IV associate d with a bacterial infection of bile (10(8) E. coli/ml). Ductal pressures w ere recorded for 24 h. In order to study the effects of a subsequent impact ion of the stone at the papilla of Vater, the catheters in the CBD and in t he pancreatic duct were connected and mimicked a common channel behind a pa pillary stone. The flow direction of bile and pancreatic juice was directly observed. Pancreatic histology was analysed 24 h later. Results In experiments I-III, neither biliary pancreatic reflux nor acute p ancreatitis was observed. In experiments IV and V, obstruction of the CBD c aused an increase in the biliary pressure to 17 +/- 3 cm H2O, whereas the p ancreatic duct pressure dropped to subnormal levels following obstruction a nd selective decompression (2 +/- 0.5 cm H2O). After the creation of a 'com mon channel', biliary pancreatic reflux was observed for 118 +/- 21 min. Fl ow of sterile bile into the pancreas was not harmful to the gland. Infected biliary pancreatic reflux initiated acute pancreatitis. Conclusions 1. Bile flow into the pancreas may occur. 2. Biliary pancreatic reflux may initiate acute pancreatitis. 3. Bile reflux-induced acute pancr eatitis requires previous biliary hypertension, temporary pancreatic duct o bstruction, and the bacterial infection of choledochal secretions. Eur J Ga stroenterol Hepatol 11:329-335 (C) 1999 Lippincott Williams & Wilkins.