Inflammatory response in the initial phase of acute pancreatitis: relationship to the onset and severity of the disease.
Pathophysiological theories on acute pancreatitis and its complications have been always based on the harmful role played by the activated pancreatic digestive enzymes at local and systemic levels. However, acute pancreatitis is an inflammatory disease in which a complex systemic response is produced, which involves the interaction of cells (neutrophils, monocytes/macrophages, platelets, lymphocytes, endothelial cells and fibroblasts) and different proteolytic systems (coagulation, fibrinolysis, kallikrein and complement systems). The more or less severe evolution of the disease may depend on the intensity of this inflammatory response, according to the potential capacity of its mediators to cause significant damage at local and systemic levels. The initial mechanism of this response may be the release of oxygen free radicals by the damaged pancreatic cells, which are able to activate the cascade of digestive pancreatic enzymes and initiate chemotaxis and activation of inflammatory cells. Based on the actual knowledges, the present article aims to analyze the role of the inflammatory response on the severity of acute pancreatitis.
Domínguez-Muñoz
J E
JE
Department of Internal Medicine-Gastroenterology, University Hospital of Bonn, Germany.
Viedma
J A
JA
Pérez-Mateo
M
M
Carballo
F
F
García Fe
M
M
D000208:Acute Disease; D000818:Animals; D006801:Humans; D008264:Macrophages / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D010179:Pancreas / Q000201:enzymology; D010195:Pancreatitis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D010447:Peptide Hydrolases / Q000502:physiology
D010447:Peptide Hydrolases