Inflammatory mediators in human acute pancreatitis: clinical and pathophysiological implications

BACKGROUND The time course and relationship between circulating and local cytokine concentrations, pancreatic inflammation, and organ dysfunction in acute pancreatitis are largely unknown. PATIENTS AND METHODS In a prospective clinical study, we measured the proinflammatory cytokines interleukin (IL...

Full description

Saved in:
Bibliographic Details
Published inGut Vol. 47; no. 4; pp. 546 - 552
Main Authors Mayer, J, Rau, B, Gansauge, F, Beger, H G
Format Journal Article
LanguageEnglish
Published London BMJ Publishing Group Ltd and British Society of Gastroenterology 01.10.2000
BMJ
BMJ Publishing Group LTD
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:BACKGROUND The time course and relationship between circulating and local cytokine concentrations, pancreatic inflammation, and organ dysfunction in acute pancreatitis are largely unknown. PATIENTS AND METHODS In a prospective clinical study, we measured the proinflammatory cytokines interleukin (IL)-1β, IL-6 and IL-8, the anti-inflammatory cytokine IL-10, interleukin 1β receptor antagonist (IL-1RA), and the soluble IL-2 receptor (sIL-2R), and correlated our findings with organ and systemic complications in acute pancreatitis. In 51 patients with acute pancreatitis admitted within 72 hours after the onset of symptoms, these parameters were measured daily for seven days. In addition, 33 aspirates from ascites and the lesser sac were measured. RESULTS Sixteen patients had mild acute pancreatitis (AP) and 35 severe AP (Atlanta classification); 18 patients developed systemic complications requiring treatment. All mediators were increased in AP. sIL-2R, IL-10, and IL-6 were significantly elevated in patients with distant organ failure. An imbalance in IL-1β/IL-1RA was found in severe AP and pulmonary failure. Peak serum sIL-2R predicted lethal outcome and IL-1RA was an early marker of severity. IL-6 was the best prognostic parameter for pulmonary failure. CONCLUSION Our results suggest that local mediator release, with a probable IL-1β-IL-1RA imbalance in severe cases, is followed by the systemic appearance of pro- and anti-inflammatory mediators. The pattern of local and systemic mediators in complicated AP suggests a role for systemic lymphocyte activation (triggered by local release of mediators) in distant organ complications in severe AP.
Bibliography:ark:/67375/NVC-527TM17X-L
PMID:10986216
istex:98B9D7081F7C6F872292F4FA4D635DBD19D5481C
local:gutjnl;47/4/546
href:gutjnl-47-546.pdf
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0017-5749
1468-3288
1458-3288
DOI:10.1136/gut.47.4.546