INFLAMMATORY RESPONSE ON THE PANCREATIC ACINAR CELL INJURY

INFLAMMATORY RESPONSE ON THE PANCREATIC ACINAR CELL INJURY
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DOI:
10.1177/145749690509400203
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发表时间:
2005-06-01
影响因子:
2.4
通讯作者:
Bhatia, M.
Bhatia, M.
中科院分区:
医学3区
文献类型:
--
作者:
Bhatia, M.

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急性胰腺炎是一种炎症性疾病,炎症不仅影响发病机制,而且影响疾病的进程。急性胰腺炎早期腺泡细胞损伤导致局部炎症反应;如果明显,则导致全身炎症反应综合征(SIRS)。过度的SIRS可导致远处器官损害和多器官功能障碍综合征(MODS)。与急性胰腺炎相关的多器官功能障碍综合征是这种疾病发病率和死亡率的主要原因。我们和其他研究人员最近的研究已经确定了炎症介质如TNF-α、IL-1 β、IL-6、IL-8、CINC/GRO-α、MCP-1、PAF、IL-10、CD 40 L、C5 a、ICAM-1、MIP 1-α、RANTES、P物质和硫化氢在急性胰腺炎和由此产生的MODS中所起的关键作用。本文就胰腺腺泡细胞损伤后的炎症反应作一综述。
Acute pancreatitis is an inflammatory disorder, and inflammation not only affects the pathogenesis but also the course of the disease. Acinar cell injury early in acute pancreatitis leads to a local inflammatory reaction; if marked this leads to a systemic inflammatory response syndrome (SIRS). An excessive SIRS leads to distant organ damage and multiple organ dysfunction syndrome (MODS). MODS associated with acute pancreatitis is the primary cause of morbidity and mortality in this condition. Recent studies by us and other investigators have established the critical role played by inflammatory mediators such as TNF-alpha, IL-1 beta, IL-6, IL-8, CINC/GRO-alpha, MCP-1, PAF, IL-10, CD40L, C5a, ICAM-1, MIP1-alpha, RANTES, substance P, and hydrogen sulfide in acute pancreatitis and the resultant MODS. This review intends to present an overview of the inflammatory response that takes place following pancreatic acinar cell injury.