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ERCP and ES have been shown, in a worldwide review of prospectively reported series, to cause AP in 5.1 and 4.1% of patients, respectively.1 ' Although the incidence of severe disease and death were not particularly high in this review, ERCP-induced AP has been linked to more severe pancreatitis when compared with other causes. Attempts to minimize the incidence of AP after ERCP and ES have focused on the elimination of procedure-related techniques that predispose to AP and on pharmacologic intervention to reduce the risk of this complication. Comparisons of high- and low-osmolality contrast agents have not shown a difference in the incidence of postprocedure pancreatitis. The avoidance of multiple attempts to cannulate the major papilla, use of high-pressure, or rapid injection of contrast medium into the pancreatic duct decreases the risk of postprocedure AP. Patient-related factors such as young age and ERCP for the evaluation of suspected sphincter of Oddi dysfunction have also been shown to be associated with an increased incidence of AP. Pharmacologic attempts to prevent ERCP- and ES-induced AP have included antibiotics, antiproteases (aprotinin and gabexate mesylate), pancreatic secretory inhibitors (glucagon,

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