Foitzik T
Chirurgische Klinik I, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin.
Zentralbl Chir. 2001 Jan;126(1):4-9. doi: 10.1055/s-2001-11716.
Septic complications are an important factor for the morbidity and mortality of acute pancreatitis. The gut has been identified as a source of infection early in the course of the disease allowing intestinal bacteria to translocate into pancreatic necrosis and other organs. Bacterial translocation is promoted by an impaired intestinal mucosal barrier which can be attributed to the reduced oxygen and substrate supply of the intestine during the early systemic response to the pancreatic injury. A rat model of severe acute pancreatitis has been used to confirm the hypothesis that an impaired mucosal barrier can be stabilized by supplying certain nutritients, vitamins and trace elements. Following a discussion of the many aspects of bacterial translocation and gut derived sepsis, the role of the gut and nutrition for the development of septic complications in acute pancreatitis is summarized as follows: Early in the course of acute pancreatitis the gut is a target organ of the primary systemic inflammatory response (SIRS) to pancreatic injury. SIRS-induced gut barrier dysfunction promoting bacterial translocation makes the gut the motor for secondary (septic) complications. As a septic focus the gut becomes a target for therapeutic measures aimed at stabilizing the impaired gut barrier. Nutritive factors demonstrated to improve impaired gut barrier function include early enteral feeding and specific factors like glutamine which are essential for enterocytes and colonocytes in stress. Experimental data are presented to underline the significance of these nutritive factors and subsequent randomized multicenter trials performed to verify the positive experimental results are introduced. The effect of other nutritive factors (e.g. omega-3-fatty acids) has not yet been systemically investigated. Thus, experimental and clinical studies need to be performed for evaluating their effect on bacterial translocation and the disease course in acute pancreatitis.
感染性并发症是急性胰腺炎发病和死亡的重要因素。肠道已被确定为疾病早期的感染源，使得肠道细菌易位至胰腺坏死组织及其他器官。肠道黏膜屏障受损会促进细菌易位，这可归因于胰腺损伤早期全身反应期间肠道氧供和底物供应减少。一种重症急性胰腺炎大鼠模型已被用于证实如下假说：通过提供某些营养素、维生素和微量元素可稳定受损的黏膜屏障。在讨论了细菌易位和肠源性脓毒症的诸多方面后，肠道和营养在急性胰腺炎感染性并发症发生发展中的作用总结如下：在急性胰腺炎病程早期，肠道是对胰腺损伤的原发性全身炎症反应（SIRS）的靶器官。SIRS诱导的肠道屏障功能障碍促进细菌易位，使肠道成为继发性（感染性）并发症的驱动因素。作为一个感染灶，肠道成为旨在稳定受损肠道屏障的治疗措施的靶点。已证明可改善受损肠道屏障功能的营养因素包括早期肠内营养以及谷氨酰胺等应激状态下对肠上皮细胞和结肠上皮细胞至关重要的特定因素。文中给出了实验数据以强调这些营养因素的重要性，并介绍了随后进行的旨在验证阳性实验结果的随机多中心试验。其他营养因素（如ω-3脂肪酸）的作用尚未得到系统研究。因此，需要开展实验和临床研究以评估它们对急性胰腺炎细菌易位和病程的影响。
