Báo cáo y học: "Insulin and the critically ill"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Insulin and the critically ill. | Critical Care June 2002 Vol 6 No 3 Das Letter Insulin and the critically ill Undurti N Das Research Director and Chairman EFA Sciences LLC Norwood Massachusetts USA Correspondence Undurti N Das e-mail undurti@ Published online 18 April 2002 Critical Care 2002 6 262-263 2002 BioMed Central Ltd Print ISSN 1364-8535 Online ISSN 1466-609X Septic shock is the most common cause of death in intensive care units. In the USA alone more than 100 000 deaths occur as a result of septicemia and septic shock per year for review 1 . In a prospective randomized controlled study involving adults admitted to surgical intensive care units and receiving mechanical ventilation 2 intensive insulin therapy substantially reduced mortality and morbidity. Intensive insulin treatment reduced the number of deaths from multiple organ failure with sepsis. Markers of inflammation were found to be less frequently abnormal in the intensive insulin treatment group than in the conventional treatment group although the nature of the inflammatory markers measured was not given. While commenting on this interesting study Groeneveld and coworkers 3 outlined the possible mechanisms that could be responsible for this beneficial action of insulin in the critically ill. I was the first to suggest that the beneficial action of insulin administered in the form of a glucose-insulin-potassium regimen in patients with acute myocardial infarction especially those who are poor candidates for thrombolytic therapy and in whom the risk of bleeding is high can be ascribed to its ability to suppress the production and harmful actions of tumor necrosis factor-a macrophage migration inhibitory factor and free radicals 1 4 5 . Recent studies have provided further evidence for the antiinflammatory actions of insulin. For instance insulin infusion decreased concentrations of intranuclear NF-kB in mononuclear cells increased levels of its inhibitor and decreased the generation of reactive oxygen species and levels

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