Nutrition in Acute Pancreatitis: From the Old Paradigm to the New Evidence

Abstract

The nutritional management of acute pancreatitis (AP) patients has widely changed over time. The "pancreatic rest" was the cornerstone of the old paradigm, and nutritional support was not even included in AP management. Traditional management of AP was based on intestinal rest, with or without complete parenteral feeding. Recently, evidence-based data underlined the superiority of early oral or enteral feeding with significantly decreased multiple-organ failure, systemic infections, surgery need, and mortality rate. Despite the current recommendations, experts still debate the best route for enteral nutritional support and the best enteral formula. The aim of this work is to collect and analyze evidence over the nutritional aspects of AP management to investigate its impact. Moreover, the role of immunonutrition and probiotics in modulating inflammatory response and gut dysbiosis during AP was extensively studied. However, we have no significant data for their use in clinical practice. This is the first work to move beyond the mere opposition between the old and the new paradigm, including an analysis of several topics still under debate in order to provide a comprehensive overview of nutritional management of AP.

Keywords: acute pancreatitis; immunonutrition; nutrition; probiotic.

Figure 1

Gut–pancreas axis during AP. (a) During AP, we observe a reduction in AMPs production by the pancreas. This facilitates bacterial overgrowth and the release of inflammatory cytokines such as TNF-α, IL-1, IL-6, IL-8, and IFN-γ. At the same time, intestinal dysbiosis is associated with a reduction in the production of SCFAs, resulting in increased intestinal permeability and worsening pancreatic damage. (b) Immunonutrients modify the inflammatory response that occurs during AP, and act on the damaged intestinal barrier. SCFAs: short-chain fatty acids; AMPs: antimicrobial peptides; TNF-α: tumor necrosis factor-α; IL-1: interleukin-1; IL-6: interleukin-6; IL-8: interleukin-8; IFN-γ; Interferon-gamma; Arg: arginine; Gln: glutamine; PUFAs: omega-3-unsatured fat acids. Created with BioRender.com.