Cysteamine for Paracetamol Overdosage

Prescott, L. F.; Matthew, Henry; Todd, J.G.

doi:10.1016/s0140-6736(74)91316-6

Cited by 32 publications

(12 citation statements)

References 2 publications

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“…We first reported the successful use of cysteamine (Prescott, Newton, Swainson, Wright, Forrest & Matthew, 1974), and there have been numerous subsequent reports confirming protection against severe liver damage by cysteamine, methionine and N-acetylcysteine (Prescott, Park, Sutherland, Smith & Proudfoot, 1976;Crome, Vale, Volans, Widdop & Goulding, 1976; Rumack & Peterson, 1978;Prescott, Illingworth, Critchley, Stewart, Adam & Proudfoot, 1979;and others). Early treatment is essential, as the critical time interval between overdosage and treatment for complete protection against severe liver damage is 8 hours.…”

Section: Paracetamolmentioning

confidence: 97%

Hepatotoxicity of mild analgesics.

Prescott¹

1980

Brit J Clinical Pharma

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1 Hepatotoxicity is rare when mild analgesics are used in normal therapeutic doses. 2 The potential of aspirin and salicylates to cause hepatotoxicity has been only recently recognized. 3 Salicylate hepatitis is often asymptomatic, and may only be revealed by finding elevated levels of aminotransferases. 4 Most cases have occurred in children or young adults with connective tissue diseases, who take high doses of salicylates for long periods. 5 Hepatic injury is not recognized as a complication of acute aspirin poisoning. 6 Following overdosage of paracetamol, a toxic intermediate metabolite causes acute hepatic necrosis which may be fatal. 7 Cysteamine, methionine and N‐ acetylcysteine confer protection against this severe liver damage, but the time between overdosage and treatment is critical. 8 The chronic therapeutic use of paracetamol should be considered a potential but very rare cause of active chronic hepatitis. 9 There is no clear evidence of phenacetin hepatotoxicity in man. 10 Phenylbutazone may cause liver injury and other analgesics can cause hypersensitivity reactions in which the liver is involved.

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Section: Paracetamolmentioning

confidence: 97%

Hepatotoxicity of mild analgesics.

Prescott¹

1980

Brit J Clinical Pharma

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“…Acetylcysteine was first suggested as an anti-dote for acetaminophen toxicity in 1974 20. Subsequently, several case series described good outcomes for patients with acetaminophen overdose who were treated on the basis of the presence of a toxic blood concentration with either intravenous21,22 or oral6,23–25 acetylcysteine.…”

Section: Clinical Evidencementioning

confidence: 99%

Acetylcysteine for Acetaminophen Poisoning

Heard¹

2008

N Engl J Med

371

278

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A 25-year-old man presents to the emergency department with a toothache. During the evaluation, the physician determines that the patient has been taking large doses of over-the-counter acetaminophen along with an acetaminophen-hydrocodone product for the past 5 days. His daily dose of acetaminophen has been 12 g per day (maximum recommended dose, 4 g per day). He has no other medical problems and typically consumes two beers a day. The patient has no symptoms beyond his toothache, is not icteric, and has no hepatomegaly or right-upper-quadrant tenderness. His serum acetaminophen concentration 8 hours after the most recent dose is undetectable. His serum alanine aminotransferase concentration is 75 IU per liter, his serum bilirubin concentration is 1.2 mg per deciliter (20.5 μmol per liter), and his international normalized ratio (INR) is 1.1. The emergency department physician contacts the regional poison-control center, which recommends treatment with acetylcysteine.

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“…Treatment is based on the phnciple of preventing gluthathione depletion with glutathione precursors, as glutathione itself does not enter cells readily (Prescott & Matthew 1974). …”

Section: Clinical Aspects Of Treatmentmentioning

confidence: 99%

Recent Developments in the Management of Paracetamol (Acetaminophen) Poisoning

Janes

Routledge

1992

Drug Safety

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Paracetamol (acetaminophen) poisoning accounts for almost a third of admissions to our district poisons unit, and is the commonest cause of death in such patients. Antidotal treatment may be effective up to 10h after overdose with oral methionine or up to 24h with acetylcysteine (not 15h as previously suggested for the latter). Patients taking paracetamol overdose while also receiving drugs which induce hepatic enzymes are more susceptible to liver damage, and antidotal treatment may be necessary at lower plasma paracetamol concentrations (50% of the normal treatment line). As survival following liver transplantation is now increasing, it is important to identify early prognostic indicators in fulminant hepatic failure, so that those patients with a high chance of fatal outcome can be considered for transplantation. Useful indicators are the presence of acidosis, marked prolongation of prothrombin time or a continued rise in prothrombin time on day 4 after the overdose. There is no evidence that paracetamol or acetylcysteine are teratogenic in pregnancy. Delays in administering acetylcysteine after paracetamol poisoning in pregnancy have been shown to increase the risk of spontaneous abortion and fetal death. Thus, acetylcysteine should be started as early as possible where treatment is indicated.

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Cysteamine for Paracetamol Overdosage

Cited by 32 publications

References 2 publications

Hepatotoxicity of mild analgesics.

Hepatotoxicity of mild analgesics.

Acetylcysteine for Acetaminophen Poisoning

Recent Developments in the Management of Paracetamol (Acetaminophen) Poisoning

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