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|Title:||Pathophysiology of acute pancreatitis|
|Authors:||Bhatia, M. |
Adult respiratory distress syndrome
Multiple organ dysfunction syndrome
|Source:||Bhatia, M., Fei, L.W., Cao, Y., Hon, Y.L., Huang, J., Puneet, P., Chevali, L. (2005). Pathophysiology of acute pancreatitis. Pancreatology 5 (2-3) : 132-144. ScholarBank@NUS Repository. https://doi.org/10.1159/000085265|
|Abstract:||Acute pancreatitis is a common clinical condition. It is a disease of variable severity in which some patients experience mild, self-limited attacks while others manifest a severe, highly morbid, and frequently lethal attack. The exact mechanisms by which diverse etiological factors induce an attack are still unclear. It is generally believed that the earliest events in acute pancreatitis occur within acinar cells. Acinar cell injury early in acute pancreatitis leads to a local inflammatory reaction. If this inflammatory reaction is marked, it leads to a systemic inflammatory response syndrome (SIRS). An excessive SIRS leads to distant organ damage and multiple organ dysfunction syndrome (MODS). MODS associated with acute pancreatitis is the primary cause of morbidity and mortality in this condition. Recent studies have established the role played by inflammatory mediators in the pathogenesis of acute pancreatitis and the resultant MODS. At the same time, recent research has demonstrated the importance of acinar cell death in the form of apoptosis and necrosis as a determinant of pancreatitis severity. In this review, we will discuss about our current understanding of the pathophysiology of acute pancreatitis. Copyright © 2005 S. Karger AG, and IAP.|
|Appears in Collections:||Staff Publications|
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