title: Endotoxin and antiendotoxin antibodies in patients with acute pancreatitis.
abstract: OBJECTIVE
  To elucidate the time course of endotoxaemia and antiendotoxin antibodies in patients with acute pancreatitis.
  
  
  METHODS
  Prospective clinical study.
  
  
  METHODS
  University hospital, Germany.
  
  
  METHODS
  25 patients with oedematous (n = 9) or necrotising (n = 16) pancreatitis, and 20 healthy controls.
  
  
  METHODS
  Concentrations of endotoxin and immunoglobulins (classes G, M, and A) directed at two lipid A molecules, four lipopolysaccharides, and alpha-haemolysin of Staphylococcus aureus measurements in plasma during a 12 day period.
  
  
  RESULTS
  There were no differences in the degree of endotoxaemia between patients with oedematous and necrotising pancreatitis on admission. However, from the day after admission and throughout the observation period patients with necrotising pancreatitis had significantly higher concentrations of endotoxin than those with oedematous pancreatitis. Concentrations of IgM specific for endotoxin peaked at day 4, and then decreased in patients with oedematous pancreatitis while remaining high for those with necrotising pancreatitis. There was only a slight increase in IgA specific for endotoxin, and IgG and immunoglobulins to gamma-haemolysin remained steady throughout the observation period. There was strong cross-reactivity (r > 0.7) between IgM specific for endotoxin (70%), but this was less with IgA (52%), and IgG (20%).
  
  
  CONCLUSIONS
  Necrotising pancreatitis is accompanied by persistent endotoxaemia with an extended rise in antiendotoxin antibodies. Patients with oedematous pancreatitis have a transient endotoxaemia with a temporary increase of Ig specific for endotoxin. Endotoxin stimulates the synthesis of specific antibodies (IgM) despite general immunosuppression.
authors.affiliation: Department of General Surgery, University of Ulm, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Buttenschoen
authors.forename: D
authors.initials: D
authors.lastname: Berger
authors.forename: N
authors.initials: N
authors.lastname: Hiki
authors.forename: D C
authors.initials: DC
authors.lastname: Buttenschoen
authors.forename: C
authors.initials: C
authors.lastname: Vasilescu
authors.forename: F
authors.initials: F
authors.lastname: Chikh-Torab
authors.forename: M
authors.initials: M
authors.lastname: Seidelmann
authors.forename: H G
authors.initials: HG
authors.lastname: Beger
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000906:Antibodies / Q000097:blood*; D018988:Bacterial Translocation; D004731:Endotoxins / Q000097:blood* / Q000276:immunology; D004926:Escherichia coli; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000097:blood / Q000276:immunology*; D019283:Pancreatitis, Acute Necrotizing / Q000097:blood / Q000276:immunology; D011446:Prospective Studies; D014734:Vibrio cholerae
chemical_list: D000906:Antibodies; D004731:Endotoxins; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D008070:Lipopolysaccharides