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Front Biosci. 2001 Oct 1;6:E66-76.

Pathophysiology of gallstone pancreatitis.

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  • 1University of California, San Francisco, 533 Parnassus Ave., Rm. U-372, San Francisco, CA 94143, USA.


Gallstone pancreatitis was first recognized as an entity by Opie in 1901 (1), and since then has generated volumes of literature which have attempted to explain its pathophysiology. Multiple animal experiments and human clinical studies in the past thirty years have led to a better understanding of both macro- and microscopic events which lead to pancreatic inflammation in the setting of a passing or impacted gallstone. Evidence suggests that pancreatic duct outflow obstruction is the initial event. Several possible sequelae of duct obstruction, including refluxed biliary-pancreatic secretions, pancreatic duct hypertension, and/or aberrant acinar cell secretion may result in pancreatic duct injury and release of pancreatic enzymes into the glandular interstitium, thus triggering a bout of acute pancreatitis. The details of many events related to gallstone pancreatitis remain unclear; this chapter attempts to present the pathophysiology of this disease as it is known today. Additionally, clinical presentation and treatment of gallstone pancreatitis will be reviewed briefly.

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