急性重症胰腺炎肠黏膜屏障损伤机制与临床治疗进展

Intestinal mucosal barrier injury mechanism and clinical treatment progress of severe acute pancreatitis

急性重症胰腺炎(SAP)是一种常见的临床急腹症,发病急,死亡率高。它可通过机体缺血缺氧、缺血-再灌注(IR)损伤、微生物屏障破坏、炎症介质的过度释放和表达、细胞凋亡等因素导致肠黏膜屏障功能的破坏并引发细菌移位和内毒素血症,甚至诱发全身炎症反应综合征(SIRS)和多器官脏器功能衰竭(MODS)。因此肠黏膜屏障的损伤与修复在急性重症胰腺炎病程进展及临床预防和治疗中有着特殊地位。本文将对急性重症胰腺炎疾病发展过程中肠黏膜屏障损伤的机制以及临床治疗进展作一概述。

Severe acute pancreatitis （SAP） is a common acute abdomen in clinic with a rapid onset and dangerous pathogenetic condition. SAP can cause an injury of intestinal mucosa barrier by the factors of ischemia and hypoxia, is- chemia-reperfusion （IR） injury, microbial barrier damage, the excessive release and expression of inflammatory media- tors . Apoptosis and nutritional deficiencies, leading to translocation of bacteria and endotoxemia, even induce the de- velopment of systemic inflammatory response syndrome （SIRS） and multiple organ dysfunction syndrome （MODS）. Therefore, injury and repair with intestinal mucosa barrier has a special status in the progression and clinical treatment of severe acute pancreatitis. In this review, we summarize studies on mechanisms of injury with intestinal mucosa barrier and clinical progress in SAP.