The Temporal Profile of Increased Transaminase Levels in Patients With Acetaminophen-Induced Liver Dysfunction☆,☆☆,★
Section snippets
INTRODUCTION
Acetaminophen is the single most common cause of poisoning requiring hospital admission and medical management.1 Although serum levels of the hepatic transaminases correlate poorly with ultimate outcome, they are often used to identify liver dysfunction in acetaminophen overdose.2, 3 Acetaminophen overdose has been characterized by an initial stage of gastrointestinal irritation followed by a latent stage lasting 24 to 48 hours before increase of transaminase levels.4 Hepatic transaminases peak
MATERIALS AND METHODS
We prospectively collected data on all hospitalized patients with acetaminophen overdose whose cases were reported to the Long Island Poison Control Center (LIPCC) between January 1993 and June 1994. Data included age, sex, ingestant, estimated amount of ingestant, estimated time of ingestion, coingestants, and pertinent information about the patient's medical history and medications. We used standard LIPCC data sheets to record data. During the study period, all LIPCC personnel were informed
RESULTS
During the study period, 1,825 cases of acetaminophen exposure were reported. Of this total, 779 patients had ingested potentially toxic amounts and were seen in an ED. Two hundred ninety-one of these patients had acetaminophen levels in the toxic range, and they were admitted. Increased serum transaminase levels developed during hospitalization in 36 patients; each had received the standard oral loading dose of N-acetylcysteine followed by 17 maintenance doses. Of the 36 patients, only 19 met
DISCUSSION
Acetaminophen is the most commonly reported potentially toxic ingestant in children and in adults. In 1992, 102,043 cases of acetaminophen ingestion were reported to poison centers in the United States, of which 44,876 were evaluated in a health care facility.1 Acetaminophen toxicity has been divided into various stages.4, 10 After an initial stage of gastrointestinal irritation, a latent phase of 24 to 48 hours elapses before serum hepatic transaminase levels increase. Transaminase levels then
CONCLUSION
Our findings suggest that acetaminophen poisoning may cause serum transaminase levels to increase within 24 hours and to peak within 48 to 72 hours of ingestion. It should not be assumed that patients with acetaminophen overdose who present with increased transaminase levels have ingested acetaminophen more than 24 hours earlier. Therefore they may still benefit from treatment with acetylcysteine.
Acknowledgements
The authors thank Judd E Hollander, MD, for reviewing this manuscript and for his helpful comments.
References (15)
- et al.
1992 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System
Am J Emerg Med
(1993) - et al.
Liver damage after paracetamol overdose: Comparison of liver-function tests, fasting serum bile acids, and liver histology
Lancet
(1975) - et al.
Hepatic damage and death from overdose of paracetamol
Lancet
(1973) - et al.
Acetaminophen overdose
Emerg Med Clin North Am
(1984) - et al.
Plasma half-life and hepatic necrosis in patients with paracetamol overdosage
Lancet
(1971) - et al.
Acetaminophen concepts and controversies
Emerg Med Clin North Am
(1994) Utility and reliability of emergency toxicologic testing
Emerg Med Clin North Am
(1990)
Cited by (79)
Acetaminophen toxicity
2020, Toxicology Cases for the Clinical and Forensic LaboratoryEffect of hemolysis, icterus, and lipemia on three acetaminophen assays: Potential medical consequences of false positive results
2018, Clinica Chimica ActaCitation Excerpt :Significant increase of bilirubin in patients with acute acetaminophen overdose was uncommon during the first 48 h [15]. In patients with acute acetaminophen overdose, the manifestations of hepatotoxicity might not appear until 24–48 h after the acetaminophen overdose [17,25,26]. The false positive results from bilirubin interference were less likely to affect patients during the early onset of an acute acetaminophen overdose when serum acetaminophen concentrations were high.
Acetaminophen (APAP or N-Acetyl-p-Aminophenol) and Acute Liver Failure
2018, Clinics in Liver DiseaseCitation Excerpt :The clinical course of APAP hepatotoxicity in patients with a single overdose can be classically divided into 4 consecutive stages (Table 3), although it should be noted that the course is variable and influenced by several factors, such as dose and formulation of APAP, coingested drug, and preexisting liver disease.1 APAP hepatotoxicity is characterized by marked acute elevation of serum aminotransferase (often >3000 IU/L), which typically is noted within 24 to 36 hours, and peaks approximately 72 hours after overdose.57 The aspartate aminotransferase (AST) can be >10,000 IU/L, and typically more elevated than the ALT.36
Evaluation of three-dimensional cultured HepG2 cells in a nano culture plate system: An in vitro human model of acetaminophen hepatotoxicity
2014, Journal of Pharmacological Sciences
- ☆
From the Department of Emergency Medicine, University Medical Center, State University of New York, Stony Brook*; and the Long Island Regional Poison Control Center, Winthrop University Hospital, Mineola, New York.‡
- ☆☆
Address for reprints: Adam J Singer, MD, Department of Emergency Medicine, University Hospital, Room L4-515, State University of New York, Stony Brook, New York 11794-7400, 516-444-2499, Fax 516-444-3919
- ★
Reprint no. 47/1/65740