Abstract
Since the classical experiments on the pathogenesis of acute pancreatitis by Rich and Duff1and Archibald,2the etiologic factors of significance have been multiplied and diversified. Recently, activation of trypsinogen within the pancreas3,4or biliary tree5has been indicated as the cause of pancreatitis. Although the mechanisms by which trypsinogen is first activated and then extravasated are not agreed upon it is generally conceded that the manifestations of acute hemorrhagic pancreatitis may all be attributed to the release of activated trypsin from the pancreas. Coffey,6Rush,7and Geis8gave support to the trypsinogen-activation etiology of hemorrhagic pancreatitis by demonstrating during the acute phase an increase in serum proteolytic activity synchronous with a decrease in antiproteolytic activity. Despite the equivocal results following the use of soybean trypsin inhibitor2,9-11or ovomucoid inhibitor,12it appears that a specific trypsin inhibitor should be efficacious in
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