title: Role of the gut in the course of severe acute pancreatitis.
abstract: BACKGROUND
  The pathogenesis of acute pancreatitis remains elusive. Sepsis and multiple organ failure continue to cause death (overall mortality rate, approximately 10%) despite immense improvements in supportive, radiologic, and surgical therapy. The gut appears to play a key role in the development of these complications.
  
  
  OBJECTIVE
  To critically review the evidence implicating the gut in the pathogenesis of acute pancreatitis.
  
  
  METHODS
  Relevant English-language literature or abstracts cited in the MEDLINE database were reviewed.
  
  
  CONCLUSIONS
  Gram-negative enteric organisms account for most infections of pancreatic necrosis and subsequent sepsis, which suggests the gut as a source. Intestinal permeability is increased early in patients with severe acute pancreatitis and correlates with endotoxemia, which suggests translocation as a possible mechanism. The pathogenesis of the deranged function of the gut mucosal barrier and the possible sites of increase in intestinal permeability are discussed. The gut also plays a role in priming neutrophils and the release of inflammatory cytokines, which initiate and propagate nearly all the detrimental consequences of severe inflammation and sepsis. Future research avenues and potential therapeutic measures that may restore and preserve gut barrier function are explored.
authors.affiliation: Division of Surgery, The University of Leeds, and the Center for Digestive Diseases, The General Infirmary, Leeds, United Kingdom. Bammori@aol.com
authors.forename: Basil J
authors.initials: BJ
authors.lastname: Ammori
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D001419:Bacteria / Q000187:drug effects / Q000302:isolation & purification; D001424:Bacterial Infections / Q000150:complications*; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000382:microbiology* / Q000503:physiopathology; D009504:Neutrophils / Q000378:metabolism; D019283:Pancreatitis, Acute Necrotizing / Q000209:etiology* / Q000378:metabolism; D010539:Permeability
chemical_list: D000900:Anti-Bacterial Agents; D016207:Cytokines