Singer A J, Carracio T R, Mofenson H C
Department of Emergency Medicine, University Medical Center, State University of New York, Stony Brook, USA.
Ann Emerg Med. 1995 Jul;26(1):49-53. doi: 10.1016/s0196-0644(95)70237-7.
It is often taught that acetaminophen-induced liver dysfunction occurs only after a latent period of 24 to 48 hours. This study was designed to evaluate the temporal profile of transaminase levels in patients with acetaminophen-induced hepatotoxicity.
Prospective data collection using standard poison control center data sheets.
Hospitalized patients with acetaminophen exposure who were reported to the Long Island Poison Control Center between January 1993 and June 1994. Patients who presented within 24 hours of ingestion and in whom increased aspartate aminotransferase (AST) levels developed during hospitalization were included in the data analysis. Patients who presented more than 24 hours after ingestion, who had ingested another potentially hepatotoxic agent, or who had ingested acetaminophen over a period of more than 2 hours were excluded.
Of 1,825 patients with reported acetaminophen exposure, 779 had potentially toxic ingestions and were examined in an emergency department. Of 291 patients with toxic acetaminophen levels who were admitted, 36 (12%) had increased levels of AST at some point during hospitalization. All received oral N-acetylcysteine within 2.5 hours of presentation. In 11 of 19 patients who met all inclusion criteria (58%), AST levels were noted to be increased in the 24 hours after ingestion. The median peak AST level was 422 IU/L (range, 74 to 8,538 IU/L). AST levels peaked within 48 hours in 4 patients (21%) and within 72 hours in 18 patients (95%). Six of eight patients with peak AST levels greater than 1,000 IU/L had increased transaminase levels during the 24 hours after acetaminophen ingestion.
Acetaminophen poisoning may cause the serum transaminase level to increase during the 24 hours after ingestion.
