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Effect

THOMAS R. KELLY, MD; EVERETT P. BRATCHER, MD; WILLIAM H. FALOR, MD

AMA Arch Surg. 1964;89(2):317-321.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Since the classical experiments on the pathogenesis of acute pancreatitis by Rich and Duff¹ and Archibald,² the etiologic factors of significance have been multiplied and diversified. Recently, activation of trypsinogen within the pancreas^3,4 or biliary tree⁵ has 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,⁶ Rush,⁷ and Geis⁸ gave 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 inhibitor^2,9-11 or ovomucoid inhibitor,¹² it appears that a specific trypsin inhibitor should be efficacious in . . . [Full Text PDF of this Article]

Author Affiliations
AKRON, OHIO

From the Surgical Research Department of the Akron City Hospital.

Footnotes
Read before the 21st Annual Meeting of the Central Surgical Association, Rochester, Minn, Feb 27-29, 1964.

Supported in part by research grant from the J. A. Hartford Foundation, Inc.

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