Pathogenesis of Acute Pancreatitis.
- Author:
Hong Sik LEE
1
Author Information
1. Department of Internal Medicine, Korea University College of Medicine, Korea. hslee60@korea.ac.kr
- Publication Type:Review
- Keywords:
Acute Pancreatitis;
Pathogenesis;
Cytokine;
Trypsin activation
- MeSH:
Chemokines;
Cytokines;
Enzyme Activation;
Gallstones;
Hypertriglyceridemia;
Inflammation;
Pancreas;
Pancreatitis*;
Substance P
- From:Hanyang Medical Reviews
2007;27(1):42-48
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Acute pancreatitis is an inflammatory disorder which is developed by multiple etiologies such as gallstone, alcohol, hypertriglyceridemia, etc. The pathogenesis of acute pancreatitis is not fully clarified yet. However, it is widely accepted that intracellular premature activation of pancreatic digestive enzyme is the earliest initiating event. Intracellular premature enzyme activation is associated with co-localization with lysosomal enzyme cathepasin B and zymogen granule. The autodigestive injured pancreas is subject to inflammatory injury. Over the past few years, significant evidence has been accumulated stating that synthesis and release of proinflammatory cytokines and chemokines are responsible for local pancreatic injury and systemic dispersion of inflammation. Recently, a neurogenic mechanism of inflammation such as substance P and NK-1R has been elucidated in the pathogenesis of acute pancreatitis.
