Document Detail


Cytokine storm in acute pancreatitis.
MedLine Citation:
PMID:  12483260     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Efforts to unravel the events in the evolution of tissue damage in acute pancreatitis have shown a number of inflammatory mediators to be involved. The pathways of damage are similar, whatever the etiology of pancreatitis, with three phases of progression: local acinar injury, systemic response, and generalized sepsis. The proinflammatory response is countered by an anti-inflammatory response, and an imbalance between these two systems leads to localized tissue destruction and distant organ damage. Cytokines lie at the heart of the problem and are involved in all aspects of the cascade leading to systemic inflammatory response syndrome and multiple organ dysfunction syndrome. This review discusses the present knowledge about the role of various mediators in this process, their genetic control, and the effects of their modulation. The major proinflammatory mediators are tumor necrosis factor, interleukins 1, 6, and 8, platelet activation factor, and the chemokines. The major anti-inflammatory factors include interleukin 10, and interleukin 1 receptor antagonist. Emerging knowledge of new mediators as well as future strategy of damage control is discussed.
Authors:
Rohit Makhija; Andrew N Kingsnorth
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Journal of hepato-biliary-pancreatic surgery     Volume:  9     ISSN:  0944-1166     ISO Abbreviation:  J Hepatobiliary Pancreat Surg     Publication Date:  2002  
Date Detail:
Created Date:  2002-12-16     Completed Date:  2003-05-15     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9431940     Medline TA:  J Hepatobiliary Pancreat Surg     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  401-10     Citation Subset:  IM    
Affiliation:
University of Plymouth, Level 07, Derriford Hospital, Derriford Road, Plymouth, PL6 8DH, UK.
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MeSH Terms
Descriptor/Qualifier:
Acute Disease
Animals
Antibody Formation / physiology
Apoptosis / physiology
Disease Progression
Humans
Immunity, Cellular / physiology
Interleukin-1 / physiology
Interleukin-10 / physiology
Interleukin-6 / physiology
Interleukins / physiology*
Pancreatitis / immunology,  physiopathology*
Platelet Activating Factor / physiology
Systemic Inflammatory Response Syndrome / physiopathology
Tumor Necrosis Factor-alpha / physiology*
Chemical
Reg. No./Substance:
0/Interleukin-1; 0/Interleukin-6; 0/Interleukins; 0/Platelet Activating Factor; 0/Tumor Necrosis Factor-alpha; 130068-27-8/Interleukin-10

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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