Please use this identifier to cite or link to this item:
|Title:||Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome||Authors:||Bhatia, M.
|Keywords:||Acute respiratory distress syndrome
Multiple organ dysfunction syndrome
Systemic inflammatory response syndrome
|Issue Date:||Feb-2004||Citation:||Bhatia, M., Moochhala, S. (2004-02). Role of inflammatory mediators in the pathophysiology of acute respiratory distress syndrome. Journal of Pathology 202 (2) : 145-156. ScholarBank@NUS Repository. https://doi.org/10.1002/path.1491||Abstract:||Inflammatory response leading to organ dysfunction and failure continues to be the major problem after injury in many clinical conditions such as sepsis, severe burns, acute pancreatitis, haemorrhagic shock, and trauma. In general terms, systemic inflammatory response syndrome (SIRS) is an entirely normal response to injury. Systemic leukocyte activation, however, is a direct consequence of a SIRS and if excessive, can lead to distant organ damage and multiple organ dysfunction syndrome (MODS). When SIRS leads to MODS and organ failure, the mortality becomes high and can be more than 50%. Acute lung injury that clinically manifests as acute respiratory distress syndrome (ARDS) is a major component of MODS of various aetiologies. Inflammatory mediators play a key role in the pathogenesis of ARDS, which is the primary cause of death in these conditions. This review summarizes recent studies that demonstrate the critical role played by inflammatory mediators such as tumour necrosis factor (TNF)-α, interleukin (IL -1β, IL-6, platelet activating factor (PAF), IL-10, granulocyte macrophage-colony stimulating factor (GM-CSF), C5a, intercellular adhesion molecule (ICAM)-1, substance P, chemokines, VEGF, IGF-I, KGF, reactive oxygen species (ROS), and reactive nitrogen species (RNS) in the pathogenesis of ARDS. It is reasonable to speculate that elucidation of the key mediators in ARDS coupled with the discovery of specific inhibitors would make it possible to develop clinically effective anti-inflammatory therapy. Copyright © 2004 John Wiley & Sons, Ltd.||Source Title:||Journal of Pathology||URI:||http://scholarbank.nus.edu.sg/handle/10635/130525||ISSN:||00223417||DOI:||10.1002/path.1491|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.