Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/108155
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dc.titleInflammatory response on the pancreatic acinar cell injury
dc.contributor.authorBhatia, M.
dc.date.accessioned2014-11-20T05:59:27Z
dc.date.available2014-11-20T05:59:27Z
dc.date.issued2005
dc.identifier.citationBhatia, M. (2005). Inflammatory response on the pancreatic acinar cell injury. Scandinavian Journal of Surgery 94 (2) : 97-102. ScholarBank@NUS Repository.
dc.identifier.issn14574969
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/108155
dc.description.abstractAcute pancreatitis is an inflammatory disorder, and inflammation not only affects the pathogenesis but also the course of the disease. Acinar cell injury early in acute pancreatitis leads to a local inflammatory reaction; if marked this leads to a systemic inflammatory response syndrome (SIRS). An excessive SIRS leads to distant organ damage and multiple organ dysfunction syndrome (MODS). MODS associated with acute pancreatitis is the primary cause of morbidity and mortality in this condition. Recent studies by us and other investigators have established the critical role played by inflammatory mediators such as TNF-α, IL-1β, IL-6, IL-8, CINC/GRO-α, MCP-1, PAF, IL-10, CD40L, C5a, ICAM-1, MIP1-α, RANTES, substance P, and hydrogen sulfide in acute pancreatitis and the resultant MODS. This review intends to present an overview of the inflammatory response that takes place following pancreatic acinar cell injury.
dc.sourceScopus
dc.subjectAdult respiratory distress syndrome
dc.subjectChemokines
dc.subjectCytokines
dc.subjectLeukocytes
dc.subjectMultiple organ dysfunction syndrome
dc.subjectNeurogenic inflammation
dc.subjectSubstance P
dc.typeReview
dc.contributor.departmentPHARMACOLOGY
dc.description.sourcetitleScandinavian Journal of Surgery
dc.description.volume94
dc.description.issue2
dc.description.page97-102
dc.description.codenSJSCB
dc.identifier.isiutNOT_IN_WOS
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