Inflammatory mediators as therapeutic targets in acute pancreatitis.
Multi-organ dysfunction syndrome (MODS) is the primary cause of morbidity and mortality in acute pancreatitis. Recent studies have established the critical role played by inflammatory mediators such as TNFalpha, IL-1beta, IL-6, IL-8, CINC/GROalpha, PAF, IL-10, C5a, ICAM-1 and substance P in acute pancreatitis and the resultant MODS. Potentially, there is a therapeutic window between symptom onset and the development of distant organ damage, when anti-inflammatory therapy may be of use. Elucidation of the key mediators in acute pancreatitis coupled with the discovery of specific inhibitors may make it possible to develop clinically effective anti-inflammatory therapy.
Bhatia
M
M
Department of Surgery, University of Liverpool, Royal Liverpool University Hospital, UK. mbhatia@liverpool.ac.uk
Neoptolemos
J P
JP
Slavin
J
J
D000208:Acute Disease; D018925:Chemokines / Q000037:antagonists & inhibitors; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors*; D018799:Intercellular Adhesion Molecule-1 / Q000187:drug effects; D016753:Interleukin-10 / Q000037:antagonists & inhibitors; D010195:Pancreatitis / Q000188:drug therapy* / Q000209:etiology; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors; D013373:Substance P / Q000037:antagonists & inhibitors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D018925:Chemokines; D018836:Inflammation Mediators; D010972:Platelet Activating Factor; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D016753:Interleukin-10; D013373:Substance P