title: Proinflammatory cytokines in alcohol or gallstone induced acute pancreatitis. A prospective study.
abstract: OBJECTIVE
  If differences of inflammatory pathways in acute pancreatitis exist for various etiologies, selective and specific antiinflammatory and other modulatory treatment regimens might be indicated. Circulating levels of prominent proinflammatory cytokines IL-6, 8, 18, and TNF-alpha were measured in patients having their first attack of either alcohol- or gallstone-induced acute pancreatitis.
  
  
  METHODS
  Seventy-five consecutive patients were prospectively included over a 15-month period, sixty of them being either alcohol- or gallstone-induced. All patients were treated according to a standardized algorithm. Blood samples were obtained immediately on admission and, again, at days 1, 2, and 14.
  
  
  RESULTS
  A significant effect of the etiology on the levels of IL-8 in the alcohol group as compared to the gallstone group (P=0.003) was found. No etiologic differences were observed for IL-6, IL-18, TNF-alpha, or CRP. Furthermore, no significant differences, either regarding the need for treatment at the intensive care unit or of 30-day mortality, were found.
  
  
  CONCLUSIONS
  The present study confirms previous findings and supports the hypothesis that, except for IL-8, the biochemical profile and clinical outcome is independent of the underlying etiology. Revealing the complex spatial and temporal profile of proinflammatory cytokine expression in acute pancreatitis is necessary and important for the development of a more targeted rational therapy.
authors.affiliation: Department of Surgery K, Bispebjerg Hospital, Copenhagen, Denmark. srdan.novovic@rh.regionh.dk
authors.forename: Srdan
authors.initials: S
authors.lastname: Novovic
authors.forename: Anders Møller
authors.initials: AM
authors.lastname: Andersen
authors.forename: Annette Kjaer
authors.initials: AK
authors.lastname: Ersbøll
authors.forename: Ole Haagen
authors.initials: OH
authors.lastname: Nielsen
authors.forename: Lars Nannestad
authors.initials: LN
authors.lastname: Jorgensen
authors.forename: Mark Berner
authors.initials: MB
authors.lastname: Hansen
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000097:blood* / Q000276:immunology*; D005260:Female; D042882:Gallstones / Q000097:blood / Q000150:complications* / Q000276:immunology*; D006801:Humans; D020382:Interleukin-18 / Q000097:blood / Q000276:immunology; D015850:Interleukin-6 / Q000097:blood / Q000276:immunology; D016209:Interleukin-8 / Q000097:blood / Q000276:immunology; D008297:Male; D008875:Middle Aged; D010195:Pancreatitis / Q000097:blood / Q000209:etiology* / Q000276:immunology*; D019512:Pancreatitis, Alcoholic / Q000097:blood / Q000276:immunology; D011446:Prospective Studies; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000276:immunology; D055815:Young Adult
chemical_list: D015415:Biomarkers; D016207:Cytokines; C508600:IL6 protein, human; D020382:Interleukin-18; D015850:Interleukin-6; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein