Recent insights into the cellular mechanisms of acute pancreatitisReportar como inadecuado

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Canadian Journal of Gastroenterology - Volume 21 2007, Issue 1, Pages 19-24

Invited Review Department of Medicine, University Health Network and University of Toronto, Toronto, Ontario, Canada

Received 24 March 2006; Revised 24 March 2006

Copyright © 2007 Hindawi Publishing Corporation. This open-access article is distributed under the terms of the Creative Commons Attribution Non-Commercial License CC BY-NC, which permits reuse, distribution and reproduction of the article, provided that the original work is properly cited and the reuse is restricted to noncommercial purposes.


In acute pancreatitis, initiating cellular events causing acinar cell injury includes co-localization of zymogens with lysosomal hydrolases, leading to premature enzyme activation and pathological exocytosis of zymogens into the interstitial space. This is followed by processes that accentuate cell injury; triggering acute inflammatory mediators, intensifying oxidative stress, compromising the microcirculation and activating a neurogenic feedback. Such localized events then progress to a systemic inflammatory response leading to multiorgan dysfunction syndrome with resulting high morbidity and mortality. The present review discusses some of the most recent insights into each of these cellular processes postulated to cause or propagate the process of acute pancreatitis, and also the role of alcohol and genetics.

Autor: Laura I Cosen-Binker and Herbert Y Gaisano



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