title: A study of intestinal permeability in relation to the inflammatory response and plasma endocab IgM levels in patients with acute pancreatitis.
abstract: BACKGROUND
  There is scarce information regarding intestinal permeability (IP) in patients with acute pancreatitis (AP) and its relationship with systemic inflammatory response and bacterial translocation (BT).
  
  
  OBJECTIVE
  To study IP in patients with mild and severe forms of AP as compared with controls and the presumed correlations between IP, the inflammatory response, and endotoxin.
  
  
  METHODS
  Sixty-eight patients with AP and 13 healthy controls were included. IP was assessed by means of the lactulose/mannitol (L/M) test, at admission (LMR1), and at the 15th day (LMR2). The presence of endotoxin was assessed by means of endotoxin-core antibodies type IgM (EndoCab IgM), at admission and 15 days later in patients with severe AP. Plasma levels of interleukins 6, 8, 10, and tumor necrosis factor alpha were tested within the first 72 hours from the onset of pain.
  
  
  RESULTS
  Both LMR1 and LMR2 were significantly higher in patients than in controls, and in patients with severe versus mild forms of AP. Plasma levels of Endocab IgM increased significantly in patients with severe AP. Basal plasma levels of pro- and anti-inflammatory cytokines were significantly higher in patients with severe AP. A significant correlation was found between LMR2 and Endocab IgM levels in patients with severe AP (r = 0.73, P = 0.02).
  
  
  CONCLUSIONS
  Patients with AP show an increased IP when compared with controls, being more relevant and persistent in severe cases. This seems related to an increase of endotoxemia late in the course of the disease, but not with an exacerbation of the systemic immune response.
authors.affiliation: Department of Internal Medicine, Hospital General Universitario Alicante, Hospital General Elche, Alicante, Spain.
authors.forename: Juan C
authors.initials: JC
authors.lastname: Penalva
authors.forename: Juan
authors.initials: J
authors.lastname: Martínez
authors.forename: Raquel
authors.initials: R
authors.lastname: Laveda
authors.forename: Angel
authors.initials: A
authors.lastname: Esteban
authors.forename: Carlos
authors.initials: C
authors.lastname: Muñoz
authors.forename: Jesús
authors.initials: J
authors.lastname: Sáez
authors.forename: José
authors.initials: J
authors.lastname: Such
authors.forename: Salvador
authors.initials: S
authors.lastname: Navarro
authors.forename: Faust
authors.initials: F
authors.lastname: Feu
authors.forename: José
authors.initials: J
authors.lastname: Sánchez-Payá
authors.forename: M
authors.initials: M
authors.lastname: Pérez-Mateo
mesh_terms: D000208:Acute Disease; D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000032:analysis*; D016022:Case-Control Studies; D004731:Endotoxins / Q000378:metabolism*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007075:Immunoglobulin M / Q000032:analysis*; D018836:Inflammation Mediators / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000502:physiology; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000097:blood / Q000503:physiopathology*; D010539:Permeability; D011336:Probability; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric
chemical_list: D004731:Endotoxins; D007075:Immunoglobulin M; D018836:Inflammation Mediators; D002097:C-Reactive Protein