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Pathogenesis of pancreatic encephalopathy in severe acute pancreatitis
引用本文:Xi-Ping Zhang and Hua Tian Department of General Surgery,Hangzhou First People''''s Hospital,Hangzhou 310006,China,and Department of General Surgery,Second Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China. Pathogenesis of pancreatic encephalopathy in severe acute pancreatitis[J]. Hepatobiliary & Pancreatic Diseases International, 2007, 0(2)
作者姓名:Xi-Ping Zhang and Hua Tian Department of General Surgery  Hangzhou First People''''s Hospital  Hangzhou 310006  China  and Department of General Surgery  Second Affiliated Hospital  Zhejiang University School of Medicine  Hangzhou 310003  China
作者单位:Xi-Ping Zhang and Hua Tian Department of General Surgery,Hangzhou First People's Hospital,Hangzhou 310006,China,and Department of General Surgery,Second Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China
摘    要:BACKGROUND: Pancreatic encephalopathy (PE) is a serious complication of severe acute pancreatitis (SAP). In recent years, more and more PE cases have been reported worldwide, and the onset PE in the early stage was regarded as a poor prognosis sign of SAP, but the pathogenesis of PE in SAP still has not been clarified in the past decade. The purpose of this review is to elucidate the possible pathogenesis of PE in SAP. DATA SOURCES: The English-language literature concern- ing PE in this review came from the Database of MEDLINE (period of 1991-2005), and the keywords of severe acute pancreatitis and pancreatic encephalopathy were used in the searching. RESULTS: Many factors were involved in the pathogenesis of PE in SAP. Pancreatin activation, excessive release of cytokines and oxygen free radicals, microcirculation abnormalities of hemodynamic disturbance, ET-1/NO ratio, hypoxemia, bacterial infection, water and electrolyte imbalance, and vitamin B1 deficiency participated in the development of PE in SAP. CONCLUSIONS: The pathogenesis of PE in SAP has not yet been fully understood. The development of PE in SAP may be a multi-factor process. To find out the possible inducing factor is essential to the clinical management of PE in SAP.


Pathogenesis of pancreatic encephalopathy in severe acute pancreatitis
Xi-Ping Zhang and Hua Tian. Pathogenesis of pancreatic encephalopathy in severe acute pancreatitis[J]. 国际肝胆胰疾病杂志, 2007, 0(2)
Authors:Xi-Ping Zhang and Hua Tian
Affiliation:Xi-Ping Zhang and Hua Tian Department of General Surgery,Hangzhou First People's Hospital,Hangzhou 310006,China,and Department of General Surgery,Second Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China
Abstract:BACKGROUND: Pancreatic encephalopathy (PE) is a serious complication of severe acute pancreatitis (SAP). In recent years, more and more PE cases have been reported worldwide, and the onset PE in the early stage was regarded as a poor prognosis sign of SAP, but the pathogenesis of PE in SAP still has not been clarified in the past decade. The purpose of this review is to elucidate the possible pathogenesis of PE in SAP. DATA SOURCES: The English-language literature concern- ing PE in this review came from the Database of MEDLINE (period of 1991-2005), and the keywords of severe acute pancreatitis and pancreatic encephalopathy were used in the searching. RESULTS: Many factors were involved in the pathogenesis of PE in SAP. Pancreatin activation, excessive release of cytokines and oxygen free radicals, microcirculation abnormalities of hemodynamic disturbance, ET-1/NO ratio, hypoxemia, bacterial infection, water and electrolyte imbalance, and vitamin B1 deficiency participated in the development of PE in SAP. CONCLUSIONS: The pathogenesis of PE in SAP has not yet been fully understood. The development of PE in SAP may be a multi-factor process. To find out the possible inducing factor is essential to the clinical management of PE in SAP.
Keywords:severe acute pancreatitis  pancreatic encephalopathy  pathogenesis  microcirculation  cytokines  phospholipase A2  oxygen free radicals  vitamin B1 deficiency
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