Bhatia M, Brady M, Shokuhi S, Christmas S, Neoptolemos J P, Slavin J
Department of Surgery, Royal Liverpool University Hospital, University of Liverpool, Liverpool, L69 3GA, UK.
J Pathol. 2000 Feb;190(2):117-25. doi: 10.1002/(SICI)1096-9896(200002)190:2<117::AID-PATH494>3.0.CO;2-K.
Inflammatory mediators play a key role in acute pancreatitis and the resultant multiple organ dysfunction syndrome, which is the primary cause of death in this condition. Recent studies have confirmed the critical role played by inflammatory mediators such as TNF-alpha, IL-1beta, IL-6, IL-8, PAF, IL-10, C5a, ICAM-1, and substance P. The systemic effects of acute pancreatitis have many similarities to those of other conditions such as septicaemia, severe burns, and trauma. The delay between the onset of inflammation in the pancreas and the development of the systemic response makes acute pancreatitis an ideal experimental and clinical model with which to study the role of inflammatory mediators and to test novel therapies. Elucidation of the key mediators involved in the pathogenesis of acute pancreatitis will facilitate the development of clinically effective anti-inflammatory therapy.
炎症介质在急性胰腺炎及由此引发的多器官功能障碍综合征中起关键作用,而多器官功能障碍综合征是这种病症死亡的主要原因。最近的研究证实了诸如肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6、白细胞介素-8、血小板活化因子、白细胞介素-10、C5a、细胞间黏附分子-1和P物质等炎症介质所起的关键作用。急性胰腺炎的全身效应与败血症、严重烧伤和创伤等其他病症有许多相似之处。胰腺炎症发作与全身反应发展之间的延迟,使急性胰腺炎成为研究炎症介质作用和测试新疗法的理想实验和临床模型。阐明参与急性胰腺炎发病机制的关键介质将有助于开发临床有效的抗炎疗法。