胆胰合流异常发病机制的研究进展  

Advances in the pathogenesis of pancreaticobiliary maljunction

作　　者：程里礼 周义 刘辉 陈怡发 Cheng Lili;Zhou Yi;Liu Hui;Chen Yifa(Department of General Surgery SectionⅠ,Ezhou Center Hospital,Ezhou 436000,China)

机构地区：[1]鄂州市中心医院普外一科,鄂州436000

出　　处：《中华肝胆外科杂志》2022年第2期154-157,共4页Chinese Journal of Hepatobiliary Surgery

摘　　要：胆胰合流异常是胆总管和主胰管末端在十二指肠壁外汇合,或形成较长的共同通道导致胆汁和胰液混合返流,从而引起一系列的胆胰疾病,甚至导致胆道恶性肿瘤的发生。胆胰合流异常的发病机制较为复杂,涉及到胆道流体动力学、磷脂酶A2激活、蛋白酶激活、氨基酸脂肪代谢、基因突变等。本文总结了关于胆胰合流异常发病机制的研究进展,以期为临床医师提供参考。Pancreaticobiliary maljunction means the common bile duct and the main pancreatic duct in the duodenal wall,or is the formation of a long common channel leading to biliopancreatic reflux,resulting a series of biliopancreatic diseases,and even the occurrence of biliary malignancy.The pathogenesis of pancreaticobiliary maljunction is complex,involving biliary fluid dynamics,the activation of phospholipase A2,protease activation,amino acids,fat metabolism,gene mutation.This paper summarized the latest study of the pathogenesis of the pancreaticobiliary maljunction to let clinicians understand pancreaticobiliary maljunction diseases,and provide new treatment ideas.

关 键 词：胆总管 胰腺 磷脂酶类A2 奥狄括约肌 

分 类 号：R575.6[医药卫生—消化系统]