期刊文献+

急性胰腺炎患者并发MODS的机制探讨 被引量:35

Mechanism of acute pancreatitis complicated with MODS
原文传递
导出
摘要 目的 探讨急性胰腺炎患者并发多器官功能不全综合征 (MODS)的机制 ,为防治MODS提供新的思路。方法 收集急性胰腺炎 (AP)患者 6 3例 ,以是否合并脏器功能障碍分为轻型 (n =39)重型(n =2 4 )两组 ,分别测定外周血内毒素、内毒素结合蛋白、内毒素抑制物、CD14以及PBMC中核因子 κB的活性 ,观察它们与MODS发生的关系。结果 ①本组患者MODS的发生率为 38 1%。②AP患者并发内毒素血症 ,其发生率为 74 6 % ,而且患者血浆内毒素结合蛋白、内毒素受体水平均升高 ,但血浆内毒素抑制物水平却明显降低 (P <0 0 5 )。③重型患者上述指标较轻型患者变化更为显著 (P <0 0 5 )。结论 持续内毒素血症、内毒素增敏系统水平增加、NF Objective To study the mechanism of acute pancreatitis complicated with MODS,and to provide a new way for preventing and treating MODS.Methods Sixty-three pancreatitis patients were divided into two groups:moderate group,patients without organ dysfunction;and severe group,patients with organ dysfunction.Plasma endotoxin,lipopolysaccaride binding protein(LBP),endotoxin inhibitor,sCD14,and nuclear factor-κB(NF-κB)activity in PBMC were determined.Results The incidence rate of MODS and endotoxemia in both groups were 38.1% and 75.64%,respectively.The levels of LBP and sCD14 was increased,but the level of cndotoxin inhibitor was reduced.The NF-κB activity in PBMC was increased,and was related to the severity.Conclusion Continuous endotoxemia,increasing LBP,sCD14,and NF-κB activation may be involved in the development of MODS in patients with acute pancreatitis.
出处 《中华急诊医学杂志》 CAS CSCD 2005年第3期222-224,共3页 Chinese Journal of Emergency Medicine
关键词 患者 MODS 急性胰腺炎 血浆内毒素 机制探讨 内毒素血症 发生率 并发 防治 收集 Acute pancreatitis Endotoxin Lipopolysaccaride binding protein sCD14 Nuclear factor-κB MODS
  • 相关文献

参考文献6

  • 1Kylanpaa A,Back ML, Takala A, et al. Cellular markers of systemic inflammation and immunesuppression in patients with organ failure due to severe acute pancreatitis. Scand J Gastroenterol,2001,36(10): 1100.
  • 2Arnalich F, Garcia-Palomero E, Lopez J, et al. Predictive value of nuclear factor κB activity and plasma cytokine levels in patients with sepsis.Infection And Immunity,2000,68(4):1942-1945.
  • 3Muller JM, Ziegler-Hettbrock HW, Baeuerle PA. Nuclear factor kappaB, a mediator of Lipopolysaccaride effects. Immunobiol,1993,187(3):233-256.
  • 4Rau B, Steinbach G, et al. Clinical value of lipopolysaccharide-binding protein (LBP)determinations in acute pancreatitis. Langenbecks Arch Surg,2003,388(3): 181-188.
  • 5Kitchens RL. Role of sCD14 in cellular recognition of bacterial lipopolysaccharides. Chem Immunol,2000,74(1):61-82.
  • 6吴丽颖,王兴鹏,Adler G.核因子-κB促使水肿型胰腺炎向坏死型胰腺炎转化[J].中华急诊医学杂志,2004,13(2):82-84. 被引量:15

二级参考文献4

  • 1Liu SF,Ye X,Malik AB,et al.Inhibition of NF-kappaB activation by pyrrolidine dithiocarbamate prevents in vivo expression of proinflammatory gene[].Circulation.1999
  • 2Fujihara SM,Cleaveland JA,Grosmaire LS,et al.A D- amino acid peptide inhibtor of NF- kappa B nuclear localization is effications in models of inflammatory disease[].J Immunol.2000
  • 3Hoshino K,Takeuchi O,Kawai T,et al.Cutting edge: Toll - like receptor 4 ( TLR4 ) - dificient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the LPS gene product[].J immunol.1999
  • 4Wig JD,Kochhar R,Ray JD,et al.Endotoxemia predicts outcome in acute pancreatitis[].Journal of Clinical Gastroenterology.1998

共引文献14

同被引文献309

引证文献35

二级引证文献205

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部