Abstract

One hundred years ago E. L. Opie proposed two distinct hypotheses to address the pathogenesis of gallstone-induced pancreatitis. These hypotheses appear mutually exclusive. The first predicts that impediment to the flow of pancreatic juice causes pancreatitis (the pancreatic duct obstruction hypothesis), whereas the second predicts that bile flow into the pancreatic duct behind an impacted gallstone would trigger the onset of acute pancreatitis (the common-channel hypothesis). One of the more convincing arguments against the latter hypothesis is the observation that bile, when experimentally perfused through the pancreatic duct of dogs, does not induce pancreatitis. This experimental situation had spontaneously developed in the patient we describe here: a biliopancreatic fistula had permitted the continuous flow of bile through a large portion of the pancreas, which was associated with cholangitis but had apparently never led to pancreatitis. This patient's case would suggest that in humans, just as in experimental animals, bile flow through the pancreatic duct is not necessarily involved in the onset of gallstone-induced pancreatitis and lends further support to Opie's pancreatic duct obstruction hypothesis.