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Acute pancreatitis

机译：急性胰腺炎

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Acute pancreatitis is associated with significant morbidity and a mortality rate of approximately 8%. In severe pancreatitis, necrosis at the site of inflammation and remote organ failure develop in the course of disease. Pancreatic injury is initiated by molecular events in acinar cells. Premature activation of digestive enzymes, disturbances of intracellular calcium, and activation of transcription factors such as NF-KB characterize the initial phase of acute pancreatitis. The release of proinflammatory mediators and the recruitment of immune cells expand the local disturbances to a systemic inflammatory response associated with failure of distant organs such as lungs or kidney. The use of transgenic or knockout mice together with classic models of secretagogue-induced pancreatitis has provided considerable insight into the role of individual cellular or humoral factors in different stages of experimental pancreatitis. Transfer of these findings into clinical management or novel therapeutic strategies so far has had only very limited success. This may be due to the limitation of pancreatitis models to mimic completely the human disease. Therefore, a distinction between experimental models and clinical acute pancreatitis has to be maintained. The first part of this review will therefore concentrate on the initiation of acinar cell injury in experimental pancreatitis. Novel insights covering the mechanism by which local pancreatic involvement expands into systemic inflammation described in the second part. Progress in the clinical management and treatment of acute pancreatitis in humans is the focus of the third part of this review.
机译：急性胰腺炎的发病率很高，死亡率约为8％。在严重的胰腺炎中，在疾病过程中会发生炎症部位的坏死和远端器官衰竭。胰腺损伤是由腺泡细胞中的分子事件引起的。消化酶的过早激活，细胞内钙的紊乱以及诸如NF-KB等转录因子的激活是急性胰腺炎的初始阶段。促炎性介质的释放和免疫细胞的募集将局部障碍扩大到与远处器官如肺或肾衰竭相关的全身性炎症反应。转基因或基因敲除小鼠与促分泌素诱导的胰腺炎的经典模型一起使用，已为深入了解个体细胞或体液因子在实验性胰腺炎不同阶段的作用提供了重要依据。迄今为止，将这些发现转移到临床管理或新颖的治疗策略中仅获得了非常有限的成功。这可能是由于胰腺炎模型无法完全模仿人类疾病所致。因此，必须保持实验模型与临床急性胰腺炎之间的区别。因此，本综述的第一部分将集中于实验性胰腺炎中腺泡细胞损伤的开始。新颖的见解涵盖了局部胰腺受累扩展为全身性炎症的机制，如第二部分所述。在人类的急性胰腺炎的临床管理和治疗方面的进展是本综述第三部分的重点。

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