

Markiewski MM, DeAngelis RA, Lambris JD: Liver inflammation and regeneration: Two distinct biological phenomena or parallel pathophysiologic processes? Mol Immunol 2006, 43: 45-56. Rutherford A, Chung RT: Acute liver failure: mechanisms of hepatocyte injury and regeneration. Taub R: Liver regeneration: from myth to mechanism. Jones AL: Mechanism of action and value of N -acetylcysteine in the treatment of early and late acetaminophen poisoning: a critical review. 10.1016/j.taap.2005.06.024Īdamson GM, Harman AW: Oxidative stress in cultured hepatocytes exposed to acetaminophen. N Engl J Med 1991, 324: 1852-1857.ĭambach DM, Durham SK, Laskin JD, Laskin DL: Distinct roles of NF-kappaB p50 in the regulation of acetaminophen-induced inflammatory mediator production and hepatotoxicity. Harrison PM, Wendon JA, Gimson AE, Alexander GJ, Williams R: Improvement by acetylcysteine of hemodynamics and oxygen transport in fulminant hepatic failure. Harrison PM, Keays R, Bray GP, Alexander GJ, Williams R: Improved outcome of paracetamol-induced fulminant hepatic failure by late administration of acetylcysteine.


Prescott LF, Park J, Ballantyne A, Adriaenssens P, Proudfoot AT: Treatment of paracetamol (acetaminophen) poisoning with N -acetylcysteine. Yang R, Miki K, He X, Killeen ME, Fink MP: Prolonged treatment with N -acetylcysteine delays liver recovery from acetaminophen hepatotoxicity. This new study raises the issue of whether impairment of regeneration is also a clinical concern for extended NAC use. Concern has been expressed relating to its extended use in late presenters with APAP poisoning and APAP-induced liver failure because of the possibility of changed kinetics of NAC in liver injury, reduced efficacy, and adverse hemodynamic changes (vasodilatation and increased cardiac index). The putative protective mechanisms of NAC in late-APAP poisoning and APAP-induced liver failure remain poorly characterised but include free-radical scavenging, hemodynamic, and cytokine effects. In later years, clinical use of NAC was extended to patients who present more than 10 hours after ingestion and to those with APAP-induced acute liver failure (ALF), and patients in such categories are routinely on NAC infusions for many days, even weeks. NAC has been used since the 1970s, and it effectively manages APAP poisoning by glutathione repletion if administered within 8 to 10 hours of ingestion of the overdose.
