Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky, USA.
Nutr Clin Pract. 2019 Oct;34 Suppl 1:S43-S48. doi: 10.1002/ncp.10371. Epub 2019 Jul 22.
The pathophysiologic process of severe acute pancreatitis involves a vicious cycle of inflammation and increasing oxidative stress. Secretory defects trap activated pancreatic enzymes within the gland leading to autodigestion while circulatory abnormalities add the insult of ischemia/reperfusion injury. What may have the greatest impact in amplifying the systemic inflammatory response, though, is intestinal failure with breakdown of gut barrier defenses, subversion of submucosal immune responses, and emergence of a virulent pathobiome. Understanding the intricacies of these changes has broad-reaching implications for nutrition therapy, which should no longer be limited to the provision of early enteral feeding alone. Emerging strategies should attempt to maintain commensalism, bind potential pathogens, refaunate the microbiome, actively turn off inflammation, reset cross-talk signaling with epithelial receptors, and deliver nutrients further down the gastrointestinal tract to the level of greatest microbial burden. Innovative nutrition therapy for the patient with severe acute pancreatitis should be designed to address and include all of these strategies in order to shift the course of clinical outcome toward a pattern of recovery and homeostasis.
严重急性胰腺炎的病理生理过程涉及炎症和氧化应激增加的恶性循环。分泌缺陷使激活的胰腺酶在腺体内滞留,导致自身消化,而循环异常则增加缺血/再灌注损伤的损害。然而,可能对放大全身炎症反应产生最大影响的是肠道衰竭,肠道屏障防御功能崩溃,黏膜下免疫反应颠覆,以及毒性病理生物群落的出现。了解这些变化的复杂性对营养治疗具有广泛的意义,营养治疗不应仅限于早期肠内喂养。新兴策略应试图维持共生关系,结合潜在的病原体,重新定殖微生物组,积极抑制炎症,重新设定上皮受体的串扰信号,并将营养素输送到胃肠道的最大微生物负荷水平。严重急性胰腺炎患者的创新性营养治疗应旨在解决和包括所有这些策略,以改变临床结果的进程,朝着恢复和内稳态的模式发展。