Factors That Worsen Disease Severity in Acute Pancreatitis: Implications for More Innovative Nutrition Therapy

摘要

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.