Published online May 14, 2020. doi: 10.3748/wjg.v26.i18.2187
Peer-review started: January 12, 2020
First decision: January 19, 2020
Revised: March 26, 2020
Accepted: April 15, 2020
Article in press: April 15, 2020
Published online: May 14, 2020
Processing time: 122 Days and 19.4 Hours
Acute pancreatitis (AP) is a common gastrointestinal disorder. Approximately 15%-20% of patients develop severe AP. Systemic inflammatory response syndrome and multiple organ dysfunction syndrome may be caused by the massive release of inflammatory cytokines in the early stage of severe AP, followed by intestinal dysfunction and pancreatic necrosis in the later stage. A study showed that 59% of AP patients had associated intestinal barrier injury, with increased intestinal mucosal permeability, leading to intestinal bacterial translocation, pancreatic tissue necrosis and infection, and the occurrence of multiple organ dysfunction syndrome. However, the real effect of the gut microbiota and its metabolites on intestinal barrier function in AP remains unclear. This review summarizes the alterations in the intestinal flora and its metabolites during AP development and progression to unveil the mechanism of gut failure in AP.
Core tip: Acute pancreatitis (AP) is a common clinical acute abdomen disease, and its incidence is increasing year by year. There are several reviews on the pathophysiology, therapeutic options and clinical trials of AP. However, the real effect of the gut microbiota and its metabolites on intestinal barrier function in AP remains unclear. This review summarizes the alterations in the intestinal flora and its metabolites during AP development and progression to unveil the mechanism of gut failure in AP.