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PubMed · 7469631

Age as a variable in acetaminophen overdose.

R G Peterson·B H Rumack
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Abstract

More than 300 accidental ingestions of acetaminophen products in children 6 years of age and younger have been reported to the Rocky Mountain Poison Center, Denver, during September 1974 to September 1979. Few of these have resulted in toxic reactions, based on clinical examination of the children. This report documents 17 childhood ingestions of acetaminophen in which plasma levels of the substance were measured and liver function was evaluated. Thirteen of these cases occurred as a result of accidental ingestion by children 6 years of age or younger; five of these children had documented plasma levels that were in the toxic range of an adult nomogram and were treated with acetylcysteine. Only minor abnormalities in liver function were observed in the treated children, even when therapy was instituted as late as 20 hours after ingestion.

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AcetaminophenAcetylcysteineAdolescentAdultAge FactorsChildChild, PreschoolFemaleHalf-LifeHumansInfantMaleJournal Article

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BibTeXRIS

R G Peterson, B H Rumack. 1981-02-23. Age as a variable in acetaminophen overdose.. https://doi.org/10.1001/archinte.141.3.390

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PubMed2001

Effect of maximal daily doses of acetaminophen on the liver of alcoholic patients: a randomized, double-blind, placebo-controlled trial.

BACKGROUND: Retrospective reports suggest that therapeutic doses of acetaminophen may be associated with fulminant hepatic failure and death in alcoholic patients. Millions of patients use acetaminophen; the prevalence of alcoholism in the United States is 5% to 10%. OBJECTIVE: To determine if hepatic injury was associated with maximal therapeutic dosing of acetaminophen to chronic alcohol abuse patients immediately following cessation of alcohol intake (the presumed time of maximal vulnerability). METHODS: Patients entering an alcohol detoxification center were enrolled in a randomized, double-blind, placebo-controlled trial. Exclusion criteria were baseline values of aspartate or alanine aminotransferase greater than 120 U/L, international normalized ratio greater than 1.5, serum acetaminophen level greater than 20 mg/L, or a history of ingesting more than 4 g/d of acetaminophen. Acetaminophen, 1000 mg, or placebo was administered orally 4 times daily for 2 consecutive days and liver test results were monitored for 2 more days. Acetaminophen was not administered until the alcohol had been eliminated. RESULTS: There were 102 patients in the acetaminophen-treated group and 99 patients in the placebo-treated (control) group. Demographic data, alcohol history, and baseline blood test results were similar in both groups. The mean (SD) aspartate aminotransferase level on day 4 was 38.0 +/- 26.7 U/L in the acetaminophen-treated group and 37.5 +/- 27.6 U/L in the placebo-treated group. There were 4 patients in the acetaminophen-treated group and 5 in the placebo-treated group who developed an increase in their serum aspartate aminotransferase level to greater than 120 U/L; it did not exceed 200 U/L in any patient. The mean (SD) international normalized ratio on day 4 was 0.96 +/- 0.09 in the acetaminophen-treated group and 0.98 +/- 0.11 in the placebo-treated group. CONCLUSION: Repeated administration of the maximum recommended daily doses of acetaminophen to long-term alcoholic patients was not associated with evidence of liver injury.

Acetaminophen↗
PubMed2001

[Acetaminophen use by chronic alcohol abusers: a therapeutic dose may be too much for the liver].

Two patients, both women aged 31 and 73 years, were admitted with chest pain and coma, respectively. They had very high aspartate aminotransferase levels, accompanied by relatively low alanine aminotransferase levels. The second patient had developed acute liver failure and hepatic encephalopathy. Both patients were chronic alcohol abusers and had taken therapeutic doses of acetaminophen for a couple of days. The marked elevation of the aminotransferase levels and the rapid decline of these levels after discontinuing the use of acetaminophen and alcohol led to the diagnosis of acetaminophen hepatotoxicity. In chronic alcohol abusers, cytochrome P450 2E1 is induced and the amount of glutathione is depleted. This combination causes the formation of a relatively large amount of the radical N-acetyl-p-benzoquinone imine and a low potential to detoxify this metabolite, so that even small amounts of acetaminophen may cause liver damage. It is recommended that chronic alcohol abusers (more than four alcoholic beverages per day) use no more than 2 g acetaminophen per day.

Acetaminophen↗