WORLD JOURNAL OF EMERGENCY SURGERY

Full list of author information is available at the end of the articleSevere acute pancreatitis (SAP) has high mortality, but multiple and timely interventions can improve survival [1]. In patients with SAP, SIRS-related gut hypoperfusion and mucosal damage may occur early, and may contribute to clinical worsening. It has been showed that in SAP early gut mucosal damage severity correlates with clinical severity, as well as with the development of secondary infections [2]. High-mobility group box chromosomal protein 1 (HMGB1), originally discovered as a nuclear DNA-binding protein, was recently identified as a potent proinflammatory and late-acting mediator of endotoxin lethality [3]. Experimental models of SAP identified HMGB1 as a key contributor to gut barrier dysfunction, and found a significant correlation between HMGB1 serum levels and the severity of intestinal mucosal injury [4]. In clinical studies of SAP, HMGB1 acts as an early marker of disease worsening, by reflecting pancreatic tissue injury and inflammation. Serum levels of HMGB1 of SAP patients on admission are significantly higher tha