tailieunhanh - Báo cáo y học: "Advanced glycation endproducts in sepsis and mechanical ventilation: extra or leading man"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Advanced glycation endproducts in sepsis and mechanical ventilation: extra or leading man? | Available online http content 13 4 164 Commentary Advanced glycation endproducts in sepsis and mechanical ventilation extra or leading man Marcus Baumann Department of Nephrology Klinikum rechts der Isar Technical University Munich Ismaninger Str. 22 81675 Munich Germany Corresponding author Marcus Baumann Published 14 July 2009 This article is online at http content 13 4 164 2009 BioMed Central Ltd Critical Care 2009 13 164 doi cc7939 See related research by Kneyber et al. http content 13 3 R87 Abstract Advanced glycation endproducts AGEs are primarily known as a complication in diabetic patients through their mediation of the inflammatory response. However a variety of studies have demonstrated enhanced formation of AGEs in cardiovascular disorders. Despite the large number of AGEs produced during the Maillard reaction recent focus is on the major non-crosslinking AGE NE-carboxymethyllysine. Kneyber and colleagues focused on sepsis-induced cardiac dysfunction and investigated whether myocardial inflammation is associated with enhanced cardiac AGE deposition and whether this is further enhanced by mechanical ventilation. They showed that both conditions are associated with enhanced AGE deposition and myocardial inflammation. Therefore AGEs may participate in the inflammatory response related to cardiac dysfunction in critically ill patients. Moreover life-saving ventilation stimulates AGE formation in these patients. This interesting study raises the question of whether AGEs in critically ill patients are a driving force of the disease. Advanced glycation endproducts The advanced glycation endproduct AGE N -carboxy-methyllysine CML as recently investigated by Kneyber and colleagues 1 can be formed either from glucose via ketoamine or glyoxal or from lipids by oxidation via glyoxal. This may explain why the pathophysiological role of AGEs is not restricted to diabetes in which condition they have