The antidote to acetaminophen overdose, N-acetylcysteine (NAC), is most effective when given within 8 hours of ingesting acetaminophen and can prevent liver failure, if given early enough, by replenishing the stores of glutathione in the liver to detoxify NAPQI.

The fasting state, poor nutrition, and/or anorexia nervosaĪn overdose of acetaminophen can seriously damage the liver.

The anti-tuberculosis drug isoniazid (INH, Nydrazid, Laniazid).

Anti-seizure medications, such as phenobarbital, phenytoin (Dilantin), and carbamazepine (Tegretol).

The following may also lower the threshold for acetaminophen-caused hepatotoxicity: The amount of toxic metabolite produced and the ability of the liver to remove this metabolite before it binds to liver protein influence the extent of liver injury (Hodgman & Garrard, 2012). When acetaminophen is taken in therapeutic doses, this metabolite is safely broken down by the liver and then excreted in the urine however, when liver function is impaired (eg, in alcoholics), or if an excessive amount of acetaminophen is ingested, high concentrations of NAPQI accumulate and bind with liver proteins, causing cellular injury (McGill et al., 2012).

The mechanism of liver injury is not related to acetaminophen itself, but to the conversion of small amounts of acetaminophen into a toxic metabolite called N-acetyl-p-benzoquinone imine (NAPQI) (Wikipedia, 2018c). The liver helps break down and remove many chemicals or drugs that enter the body however, taking too much acetaminophen overloads the liver’s ability to process the drug effectively (Jaeschke et al., 2012).

78,000 emergency department visits per yearĪcetaminophen overdose and hepatotoxicity is the leading cause of ALF in the United States.Summarizing data related to acetaminophen-associated overdoses from 2016, there were an estimated:

Acetaminophen antidote