title: Intramucosal acidosis and the inflammatory response in acute pancreatitis.
abstract: OBJECTIVE
  The aim of this study was to assess the host response and diminished bowel perfusion during acute pancreatitis.
  
  
  METHODS
  A total of 19 patients admitted with established diagnoses of acute pancreatitis on the basis of clinical findings, elevated serum amylase to more than four times the upper limit or by contrast radiology. Patients were stratified into mild and severe pancreatitis using the Atlanta criteria. Blood samples were obtained from in-dwelling lines or direct venipuncture within 12 h of admission and 24 hourly thereafter for measurements of plasma endotoxin, EndoCab immunoglobulin (Ig)G and IgM antibodies, tumor necrosis factor (TNF), p55 TNF receptor, and IL-6. A gastric tonometer was inserted in place of a nasogastric tube for intramucosal pH evaluation.
  
  
  RESULTS
  Episodes of endotoxaemia were more common and endotoxin concentration significantly higher at presentation in the severe group compared to the mild group of patients. A greater consumption of IgM antibody was found in those with severe disease. The decrease in IgM antibody concentration was shown to be a specific host response, as a fall in concentration of antibodies to a neutral antigen, tetanus toxoid, was not observed. Significantly greater elevations were found in p55 TNF receptor and IL-6 concentrations in the severe group in comparison to those suffering mild pancreatitis. Significant correlations were found between gastric intramucosal pH and EndoCab IgM antibody, p55 TNF receptor, and IL-6.
  
  
  CONCLUSIONS
  These results suggest that endotoxemia, an acute inflammatory response, and a reduction in bowel perfusion may occur in severe acute pancreatitis. The endotoxemia and inflammatory response may be due to the permeation of bacteria and their breakdown products across a disrupted bowel mucosal barrier.
authors.affiliation: Department of Surgery, The Queen's University of Belfast, Institute of Clinical Science, Northern Ireland, United Kingdom.
authors.forename: C V
authors.initials: CV
authors.lastname: Soong
authors.forename: H G
authors.initials: HG
authors.lastname: Lewis
authors.forename: M I
authors.initials: MI
authors.lastname: Halliday
authors.forename: B J
authors.initials: BJ
authors.lastname: Rowlands
mesh_terms: D000208:Acute Disease; D004731:Endotoxins / Q000097:blood; D005753:Gastric Mucosa / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D010195:Pancreatitis / Q000097:blood / Q000150:complications* / Q000378:metabolism*; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology*
chemical_list: D004731:Endotoxins