NAC: still the way to go

Abstract

We would like to thank Yang and colleagues for their attempt to determine the possibility of delayed hepatic recovery with N-acetylcysteine (NAC) administration in acetaminophen-induced hepatotoxicity [1]. We are concerned, however, about the possible consequences that may arise from their conclusions. Owing to the wide availability of acetaminophen, intentional and unintentional overdoses are one of the leading causes of liver failure in the world [2]. NAC is currently a highly effective and safe antidote to treat acute acetaminophen overdose, and is most efficacious when administered within 8 hours of ingestion [3]. Furthermore, one landmark study showed that even in patients who presented with delayed acetaminophen-induced fulminant hepatic failure, intravenous NAC administration improved survival versus control individuals (48% vs. 20%) [4]. Another study found that the infusion of acetylcysteine in patients with acetaminophen-induced liver failure resulted in an increase in mean oxygen delivery and in an increased mean arterial pressure [5]. It is difficult to believe that the mouse model of Yang and colleagues has any correlation to humans, since the already established human data are so overwhelmingly positive. The amount of acetaminophen administered in their study caused hepatotoxicity but did not induce death, and therefore is not applicable to real-life situations where people may ingest potentially fatal doses of acetaminophen. It is not clear to us why the authors came to explore this study topic. The conclusions drawn from their article are potentially dangerous and should be viewed with caution and scepticism.