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Hepatotoxicity in acute iron poisoningDepartment of Pediatrics and Pharmacology, University of Manitoba, Children's Hospital, 840 Sherbrook Street, Winnipeg, MB, R3A 1S1, Canada
Department of Pediatrics and Pharmacology, University of Manitoba, Children's Hospital, 840 Sherbrook Street, Winnipeg, MB R3A 1S1, Canadamtenenbein{at}hsc.mb.ca Although liver injury is a recognized consequence of acute iron poisoning, its description is limited to several case reports. It appears to be dose-related, however, there are published reports of severe iron poisoning without liver injury. The purpose of this study is to examine the hypothesis that this is a dose-related phenomenon and to identify the serum iron concentration of risk for this outcome. The design of this study is a retrospective review of our hospital's experience over 20 years. Extracted data included demographics, time of ingestion, highest serum iron concentration and highest hepatic transaminase activity. Iron poisoning was defined as a serum iron concentration / 300 mg/dL (55 mmol/L) within 12 hours of ingestion. Hepatotoxicity was defined as a serum transaminase (either ALT or AST) / 150 U/L. Severe hepatotoxicity was defined as / 1000 U/L. Seventy-three patients (1 / 704 mg/dL (55 / 48 years old) participated in the study and of these patients 60 (47 female) did not have hepatotoxicity. Their serum iron concentrations were 300 / 128 mmol/L). Thirteen patients had hepatotoxicity and of these patients, nine had severe liver injury. Severe injury was associated with serum iron concentrations well in excess of 1000 mg/dL (182 mmol/L). Our data support hepatotoxicity due to iron poisoning as a doserelated phenomenon with clinically important cases unlikely with a serum iron concentration of B / 700 mg/dL (128 mmol/L) within the first 12 hours. Clinically important hepatotoxicity occurs with values in excess of 1000 mg/dL (182 mmol/L).
Key Words: hepatotoxicity iron poisoning
Human & Experimental Toxicology, Vol. 24, No. 11,
559-562 (2005) |
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