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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: Prolonged treatment with N-acetylcystine delays liver recovery from acetaminophen hepatotoxicity. | Available online http ccforum.eom content 13 2 R55 Research Prolonged treatment with N-acetylcystine delays liver recovery from acetaminophen hepatotoxicity Runkuan Yang1 Keita Miki1 Xin He2 Meaghan E Killeen1 and Mitchell P Fink1 Department of Critical Care Medicine University of Pittsburgh Medical School 3550 Terrace Street Pittsburgh PA 15261 USA department of Pathology University of Pittsburgh Medical School 3550 Terrace Street Pittsburgh PA 15261 USA Corresponding author Runkuan Yang Yangr@ccm.upmc.edu Received 3 Jan 2009 Revisions requested 21 Feb 2009 Revisions received 23 Mar 2009 Accepted 9 Apr 2009 Published 9 Apr 2009 Critical Care 2009 13 R55 doi 10.1186 cc7782 This article is online at http ccforum.com content 13 2 R55 2009 Yang et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Open Access Abstract Introduction Acetaminophen APAP toxicity is the most common cause of acute liver failure in the US and Europe. Massive hepatocyte necrosis is the predominant feature of APAP-induced acute liver injury ALI . Liver regeneration is a vital process for survival after a toxic insult it occurs at a relative late time point after the injurious phase. Currently N-acetylcysteine NAC a glutathione precursor is the antidote for acetaminophen overdose. However NAC is effective only for patients who present within hours of an acute overdose and is less effective for late-presenting patients. It is possible that in delayed patients previously reduced endogenous glutathione GSH level has restored and prolonged treatment with NAC might be toxic and impair liver regeneration. Therefore we hypothesize that prolonged treatment with NAC impairs liver regeneration in ALI induced by APAP. Methods ALI was induced in C57BL 6 male mice