How and where does acute pancreatitis begin?
M. L. Steer
Department of Surgery, Beth Israel Hospital, Boston, Mass. 02215.
Circumstantial evidence suggests that gallstone-induced pancreatitis is
triggered by obstruction of the pancreatic duct. In this report I will
review the results of studies conducted during the last decade that have
employed the diet-induced, secretagogue-induced, and duct
obstruction-induced models of experimental pancreatitis to investigate the
early events that lead to the development of acute pancreatitis. In each of
these models, digestive enzyme zymogens and the lysosomal hydrolase
cathepsin B were found to become colocalized. These observations have led
to the hypothesis that intra-acinar cell activation of digestive enzyme
zymogens by lysosomal hydrolases may be an important critical event in the
development of acute pancreatitis. Recent morphologic studies evaluating
the initial 24 hours after ligation of the opossum pancreatic duct indicate
that the earliest lesions in this model of hemorrhagic pancreatitis occur
in acinar cells.
