Review
Copyright ©2009 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Mar 28, 2009; 15(12): 1427-1430
Published online Mar 28, 2009. doi: 10.3748/wjg.15.1427
Acute pancreatitis: Etiology and common pathogenesis
Guo-Jun Wang, Chun-Fang Gao, Dong Wei, Cun Wang, Si-Qin Ding
Guo-Jun Wang, Chun-Fang Gao, Dong Wei, Cun Wang, Si-Qin Ding, Institute of Digestive Surgery and Department of General Surgery, 150 Hospital of Chinese PLA, Gaoxin District, Luoyang 471031, Henan Province, China
Author contributions: All the authors contributed equally to this review.
Correspondence to: Chun-Fang Gao, MD, PhD, Institute of Digestive Surgery and Department of General Surgery, 150 Hospital of Chinese PLA, Gaoxin District, Luoyang 471031, Henan Province, China. cchunfang@163.com
Telephone: +86-379-64169001
Fax: +86-379-64169112
Received: January 7, 2009
Revised: February 19, 2009
Accepted: February 26, 2009
Published online: March 28, 2009
Abstract

Acute pancreatitis is an inflammatory disease of the pancreas. The etiology and pathogenesis of acute pancreatitis have been intensively investigated for centuries worldwide. Many causes of acute pancreatitis have been discovered, but the pathogenetic theories are controversial. The most common cause of acute pancreatitis is gallstone impacting the distal common bile-pancreatic duct. The majority of investigators accept that the main factors for acute billiary pancreatitis are pancreatic hyperstimulation and bile-pancreatic duct obstruction which increase pancreatic duct pressure and active trypsin reflux. Acute pancreatitis occurs when intracellular protective mechanisms to prevent trypsinogen activation or reduce trypsin activity are overwhelmed. However, little is known about the other acute pancreatitis. We hypothesize that acute biliary pancreatitis and other causes of acute pancreatitis possess a common pathogenesis. Pancreatic hyperstimulation and pancreatic duct obstruction increase pancreatic duct pressure, active trypsin reflux, and subsequent unregulated activation of trypsin within pancreatic acinar cells. Enzyme activation within the pancreas leads to auto-digestion of the gland and local inflammation. Once the hypothesis is confirmed, traditional therapeutic strategies against acute pancreatitis may be improved. Decompression of pancreatic duct pressure should be advocated in the treatment of acute pancreatitits which may greatly improve its outcome.

Keywords: Acute pancreatitis, Pathogenesis, Etiology, Pancreatic duct obstruction, Pancreatic hyperstimulation, Pancreatic duct pressure