Chinese General Practice ›› 2018, Vol. 21 ›› Issue (20): 2400-2403.DOI: 10.3969/j.issn.1007-9572.2018.00.076

Special Issue: 胰腺炎最新文章合集

• Monographic Research • Previous Articles     Next Articles

Novel Developments in the Pathogenesis of Acute Pancreatitis

  

  1. Department of Gastroenterology,Suzhou Municipal Hospital,Suzhou 234000,China
    *Corresponding author:GUO Zhi-guo,Associate chief physician;E-mail:gzglgyy@163.com
  • Published:2018-07-15 Online:2018-07-15

急性胰腺炎发病机制研究新观点

  

  1. 234000安徽省宿州市立医院消化内科
    *通信作者:郭志国,副主任医师;E-mail:gzglgyy@163.com

Abstract: Acute pancreatitis is a inflammatory disease of the pancreas manifested by inappropriate activation of trypsinogen,infiltration of inflammatory cells and destruction of pancreatic secretory cells.It can be life-threatening if the progression reaches an advanced stage.Because the pathogenesis is unclear yet,and there is few efficient clinical treatment for severe acute pancreatitis.Trypsin activation is mostly considered to be the factor associated with the pathogenesis of pancreatitis.During the process,pro-trypsinogen activation is associated with imbalance of trypsin-antitrypsin and genetic heterogeneity.In recent years,many studies revealed that pancreatitis is a multifactorial disease:alcohol and tobacco can injure small pancreatic duct and acinar cells,but the incidence of acute pancreatitis in drinkers is not increased significantly;pancreatic duct secretion can reduce pancreatic injury;some of animal models without trypsinogen activation still get acute pancreatitis;cytokines play an increasingly important role in the prediction of acute pancreatitis;cystic fibrosis transmembrane conductance regulator expression is closely related to the occurrence of severe acute pancreatitis;autophagy also plays an important role in the inflammatory reaction of the pancreas.

Key words: Pancreatitis, Cystic fibrosis transmembrane conductance regulator, Trypsin, Pancreatic duct cells, Autophagy

摘要: 急性胰腺炎是胰腺的炎症性疾病,表现为胰蛋白酶原不适当的活化、炎性细胞浸润及胰腺分泌细胞的破坏,若进展为重症急性胰腺炎可危及生命。由于发病机制不清,临床对重症急性胰腺炎的治疗缺乏有效方法。胰蛋白酶学说在胰腺炎发病机制中处于主导地位,其中前体胰蛋白酶原激活与胰蛋白酶-抗胰蛋白酶的失衡、遗传异质性相关。近年来多项研究揭示胰腺炎是多因素参与的疾病,乙醇与烟草可损伤小胰管及腺泡细胞,但饮酒者急性胰腺炎发病率升高并不显著。胰管分泌物可减轻胰腺损伤,缺乏胰蛋白酶原激活的动物模型仍有胰腺炎发生,细胞因子在预测急性胰腺炎的发生中发挥越来越重要作用,囊性纤维化跨膜传导调节因子表达与重症急性胰腺炎的发生密切相关,自噬在胰腺炎性反应中也扮演重要角色。

关键词: 胰腺炎, 囊性纤维化跨膜传导调节因子, 胰蛋白酶, 胰管细胞, 自噬