Abstract
Severe acute pancreatitis is a disease process distinguished by increasing oxidative stress and potential destruction of the pancreatic gland. An initial injury to the acinar cell initiates a sentinel event, which leads to a vicious cycle of inflammation and cell death by either apoptosis or necrosis. Whether the acute inflammation resolves or goes on to a pattern of chronicity may be related to genetic predisposition, failure to remove injurious agents, and innate systems for antioxidant defense. The degree to which nutrition therapy can modulate oxidative stress, maintain intestinal function, and preserve the structure of the acinar cell is truly amazing. Understanding the mechanisms involved in this complex disease process and the manner in which these mechanisms are influenced by dietary agents affords new and exciting therapeutic options for the future.
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