Enteral nutrition prevents bacterial translocation but does not improve survival during acute pancreatitis.

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Abstract
INFECTIOUS COMPLICATIONS account for more than 80% of mortality in human acute pancreatitis (AP).1,2 Although the pathogenesis of infection in AP is unclear, it is known that the microorganisms that cause pancreatic infection and sepsis in patients with AP are generally common enteric bacteria.2,3 This suggests that these bacteria may originate from the gastrointestinal tract. In fact, recent work on animals in AP has demonstrated that there is a loss of gut mucosal integrity with subsequent bacterial and/or endotoxin translocation (BET) from the gut lumen to other organs.4,5 However, few reports have demonstrated that BET per se has deleterious consequences for the host in experimental models of AP.