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Article
November 1992

How and Where Does Acute Pancreatitis Begin?

Author Affiliations

From the Department of Surgery, Beth Israel Hospital and Harvard Medical School, Boston, Mass.

Arch Surg. 1992;127(11):1350-1353. doi:10.1001/archsurg.1992.01420110098019
Abstract

• 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 dietinduced, 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 lyososomal 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.

(Arch Surg. 1992;127:1350-1353)

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