Acetaminophen alone depleted intracellular glutathione, and led to a progressive decrease in the biliary excretion of glutathione and glutathione disulfide. N -Acetylcysteine alone did not affect the biliary excretion of glutathione disulfide.
However, when administered after acetaminophen. N -acetylcysteine produced a marked increase in the biliary excretion of glutathione disulfide from 1. Animals treated with acetaminophen and N -acetylcysteine excreted 2. In conclusion, exogenous N -acetylcysteine does not form significant amounts of conjugate with the reactive metabolite of acetaminophen in the rat in vivo but increases glutathione synthesis, thus providing more substrate for the detoxification of the reactive metabolite in the early phase of an acetaminophen intoxication when the critical reaction with vital macromolecules occurs.
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Copyright notice. This article has been cited by other articles in PMC. Abstract N -Acetylcysteine is the drug of choice for the treatment of an acetaminophen overdose. UK, remember your settings and improve government services. We also use cookies set by other sites to help us deliver content from their services. You can change your cookie settings at any time. New simplified guidance on treating paracetamol overdose with intravenous acetylcysteine including an updated treatment nomogram.
Paracetamol overdose can result in liver damage which may be fatal. After this time efficacy falls substantially, affording only a very limited window of time in which to successfully prevent serious hepatotoxicity.
New simplified guidance on the treatment of acute paracetamol overdose with acetylcysteine is now in place, following an evidence-based review by the Commission on Human Medicines CHM. Previously, healthcare professionals treating paracetamol overdose were advised to assess for risk factors of hepatotoxicity such as chronic alcohol consumption, co-medications and poor nutritional intake. This resulted in two lines on the treatment nomogram — 1 for patients with risk factors and 1 for those without.
The CHM review found that the evidence base to support the use of risk factors was poor and inconsistent, and that many of the risk factors for hepatotoxicity were imprecise and difficult to determine with sufficient certainty in clinical practice.
CHM concluded that there was insufficient evidence of efficacy to add information about the off-label shortened 2-bag dose regimen used in the SNAP study to the product information for NAC. The pattern of potential adverse drug reactions associated with NAC is well established, and no new safety issues have been identified since the guidance. The authorised NAC product information reflects the safety profile. CHM concluded that the benefits of the authorised 3-bag dose regimen continue to outweigh the risks.
As with all medicines, suspected adverse reactions should continue to be reported to us on a Yellow Card. As a result of the review, in line with current clinical guidance, prescribing information for NAC is being updated to advise that continued treatment with NAC beyond 21 hours may be necessary depending on the clinical evaluation of the individual patient.
Bateman DN, et al. Reduction of adverse effects from intravenous acetylcysteine treatment for paracetamol poisoning: a randomised controlled trial. Lancet ; — If timing of ingestion is unreliable then consider treating with acetylcysteine regardless of whether the plasma level is above or below the treatment line. The nomogram becomes less reliable after 15 hours. Hypersensitivity and anaphylaxis reaction Hypersensitivity and anaphylaxis reactions with acetylcysteine are not contraindications as the benefit of treatment still outweighs the risk of not treating.
True anaphylaxis is rare with acetylcysteine. Hypersensitivity reactions are directly proportional to the serum acetylcysteine level and most common during the 1st infusion.
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