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急性胰腺炎后胰腺损伤机制的研究进展 被引量:7

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摘要 急性胰腺炎(acute pancreatitis,AP)是临床上常见的一种危重疾病,其病情进展快,病死率高,尤其是重症急性胰腺炎(severe acute pancreatitis,SAP),病程早期即可出现全身炎性反应综合征(systemic inflammatory response syndrome,SIRS),进而引发多系统和器官衰竭(muhisystem and organ failure,MSOF),目前尚无理想的临床治疗应对措施。毫无疑问,胰腺是胰腺炎发病的初始部位,因此,弄清胰腺炎后胰腺损伤的机制,对了解胰腺炎的起病进而控制其病情的进展尤为重要。本文拟对AP后胰腺损伤机制的研究进展作一概述。
出处 《西南国防医药》 CAS 2013年第2期217-219,共3页 Medical Journal of National Defending Forces in Southwest China
基金 四川省科学事业计划基金资助项目(2011JTD0010)
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参考文献24

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同被引文献79

  • 1杨智勇,王春友,熊炯炘,陶京,许逸卿,刘涛.重症急性胰腺炎大鼠血清高迁移率族蛋白-1水平的时相变化及意义[J].华中科技大学学报(医学版),2004,33(4):466-468. 被引量:23
  • 2王敏,许志伟,雷若庆,毛恩强,陈胜,王建承,吴卫泽,韩天权,汤耀卿,张圣道.重症急性胰腺炎临床特征及治疗方案的选择[J].中华外科杂志,2007,45(11):746-749. 被引量:21
  • 3周丽杰.抗凝血酶Ⅲ、蛋白C在血栓形成性疾病、妊高征、糖尿病中的变化及意义[J].医药前沿,2013,(14):170-171.
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  • 10张安,董晓静.乌司他丁与奥曲肽联合治疗重症急性胰腺炎的临床试验[J].中国临床药理学杂志,2008,24(2):104-106. 被引量:32

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