title: Soluble receptors released during acute pancreatitis interfere with the detection of tumor necrosis factor-alpha.
abstract: OBJECTIVE
  To evaluate the interfering effect of tumor necrosis factor-alpha soluble receptor when measuring circulating concentrations of tumor necrosis factor-alpha in an experimental model of acute pancreatitis.
  
  
  METHODS
  Randomized, controlled trial.
  
  
  METHODS
  Experimental laboratory.
  
  
  METHODS
  Male Wistar rats.
  
  
  METHODS
  Acute pancreatitis was induced by intraductal administration of 5% sodium taurocholate. Saline was administered in a control group. Serums were overloaded with known amounts of tumor necrosis factor-alpha or macrophage inflammatory protein-2.
  
  
  RESULTS
  Three hours after induction, serum concentrations of free tumor necrosis factor-alpha, total tumor necrosis factor-alpha, and soluble receptor of tumor necrosis factor-alpha were measured. No detectable concentrations of free tumor necrosis factor-alpha were found in any experimental group. By contrast, significant increases in total tumor necrosis factor-alpha and soluble receptor of tumor necrosis factor-alpha were found after induction of pancreatitis. Overloading of serum with tumor necrosis factor-alpha resulted in detection of 50% of the expected concentrations of free tumor necrosis factor-alpha from control animals and only of 5% from the pancreatitis group. Overloading the serum with macrophage inflammatory protein-2 resulted in a detection of 100% of the expected concentrations in both control and treated animals.
  
  
  CONCLUSIONS
  Circulating soluble receptor of tumor necrosis factor-alpha could interfere with the detection of tumor necrosis factor-alpha in some pathologies, such as pancreatitis, that are associated with increases in soluble receptor of tumor necrosis factor-alpha.
authors.affiliation: Department of Medical Bioanalysis, Institut d'Investigacions Biomèdiques de Barcelona-Consejo Superior de Investigaciones Científicas-Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain.
authors.forename: E
authors.initials: E
authors.lastname: Folch
authors.forename: A
authors.initials: A
authors.lastname: Serrano
authors.forename: L
authors.initials: L
authors.lastname: Sabater
authors.forename: E
authors.initials: E
authors.lastname: Gelpí
authors.forename: J
authors.initials: J
authors.lastname: Roselló-Catafau
authors.forename: D
authors.initials: D
authors.lastname: Closa
mesh_terms: D000208:Acute Disease; D000818:Animals; D054426:Chemokine CXCL2; D018925:Chemokines / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D008049:Lipase / Q000378:metabolism; D008297:Male; D010195:Pancreatitis / Q000201:enzymology / Q000378:metabolism*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D054426:Chemokine CXCL2; D018925:Chemokines; C404915:Cxcl2 protein, mouse; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase; D008049:Lipase