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Fulminant hepatic failure in an adolescent
THE JOURNAL OF PEDIATRICS JULY 2001
LETTERS
Fulminant hepatic failure in an adolescent To the Editor: I read with great interest the Grand Rounds article regarding a 15-year-old boy with fulminant hepatic failure (FHF) presented as being due to mushroom poisoning.1 However, the history of this patient is not very convincing because of a lack of information. The fact that the patient’s friends, who also drank the mushroom tea, had no symptoms weakens the hypothesis of mushroom poisoning as the cause of FHF. Moreover, other important causes of FHF, although reviewed and summarized in Table III, are no longer considered by the authors as possible causes in the discussion. I assume that screening for viral infection had been performed, but the results are not mentioned in the text. As to drug toxicity, what was the administered dosage of the 3 drugs—acetaminophen, “antinausea medication,” and loperamide hydrochloride—prescribed for and taken by the patient for 2 days? The supra-therapeutic plasma level of acetaminophen should be taken into consideration and be related to the time of the last ingestion.2,3 Certainly, in this teenager “who admitted to the use of marijuana and alcohol,” acetaminophen toxicity might be an additional risk factor for FHF. Has the use of ecstacy, a well-known cause of FHF
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been ruled out? Finally, what is the generic name of the “antinausea medication”? Some antiemetics are known to be hepatotoxic as well. Maria Casteels-Van Daele, MD Department of Pediatrics University Hospitals Gasthuisberg Katholieke Universiteit Leuven B3000 Leuven Belgium 9/35/116608 doi:10.1067/mpd.2001.116608
REFERENCES 1. Pomerance HH, Barness EG, KohliKumar M, Arnold SR, Steigelfest J. A 15-year-old boy with fulminant hepatic failure. J Pediatr 2000;137:114-8. 2. Insel PA. Para-aminophenol derivatives: acetaminophen. In: Hardman JG, Limbird LE, editors. Goodman & Gilman’s the pharmacological basis of therapeutics. 9th ed. New York: McGraw-Hill; 1996. p. 631-3. 3. Rivera-Penera T, Gugig R, Davis J, McDiarmid S, Vargas J, Rosenthal Ph, et al. Outcome of acetaminophen overdose in pediatric patients and factors contributing to hepatotoxicity. J Pediatr 1997;130:300-4.
Reply To the Editor: We appreciate the interest in our case, which led to the letter from Dr
Casteels-Van Daele. In response to the major question, the evidence in favor of mushroom toxicity, it was stated that the friends who shared the tea did not become ill. Actually, all of them did, but not significantly. Each complained of nausea and vomiting for a brief time. Important in this regard is the fact that the friends drank the true supernatant tea, whereas the patient happened to be left with the “dregs,” which perforce would have a greater concentration of toxins. Although we do not have data on the antinausea and antidiarrheal medications, these were administered after symptoms began. The acetaminophen level reported is within the margin of error for most laboratories, including ours. Herbert H. Pomerance, MD Enid Gilbert Barness, MD Mudra Kohli-Kumar, MD Sonya R. Arnold, MD Jill Steigelfest, MD University of South Florida College of Medicine Tampa, FL 33606 9/35/116609 doi:10.1067/mpd.2001.116609
LETTERS
Fulminant hepatic failure in an adolescent To the Editor: I read with great interest the Grand Rounds article regarding a 15-year-old boy with fulminant hepatic failure (FHF) presented as being due to mushroom poisoning.1 However, the history of this patient is not very convincing because of a lack of information. The fact that the patient’s friends, who also drank the mushroom tea, had no symptoms weakens the hypothesis of mushroom poisoning as the cause of FHF. Moreover, other important causes of FHF, although reviewed and summarized in Table III, are no longer considered by the authors as possible causes in the discussion. I assume that screening for viral infection had been performed, but the results are not mentioned in the text. As to drug toxicity, what was the administered dosage of the 3 drugs—acetaminophen, “antinausea medication,” and loperamide hydrochloride—prescribed for and taken by the patient for 2 days? The supra-therapeutic plasma level of acetaminophen should be taken into consideration and be related to the time of the last ingestion.2,3 Certainly, in this teenager “who admitted to the use of marijuana and alcohol,” acetaminophen toxicity might be an additional risk factor for FHF. Has the use of ecstacy, a well-known cause of FHF
170
been ruled out? Finally, what is the generic name of the “antinausea medication”? Some antiemetics are known to be hepatotoxic as well. Maria Casteels-Van Daele, MD Department of Pediatrics University Hospitals Gasthuisberg Katholieke Universiteit Leuven B3000 Leuven Belgium 9/35/116608 doi:10.1067/mpd.2001.116608
REFERENCES 1. Pomerance HH, Barness EG, KohliKumar M, Arnold SR, Steigelfest J. A 15-year-old boy with fulminant hepatic failure. J Pediatr 2000;137:114-8. 2. Insel PA. Para-aminophenol derivatives: acetaminophen. In: Hardman JG, Limbird LE, editors. Goodman & Gilman’s the pharmacological basis of therapeutics. 9th ed. New York: McGraw-Hill; 1996. p. 631-3. 3. Rivera-Penera T, Gugig R, Davis J, McDiarmid S, Vargas J, Rosenthal Ph, et al. Outcome of acetaminophen overdose in pediatric patients and factors contributing to hepatotoxicity. J Pediatr 1997;130:300-4.
Reply To the Editor: We appreciate the interest in our case, which led to the letter from Dr
Casteels-Van Daele. In response to the major question, the evidence in favor of mushroom toxicity, it was stated that the friends who shared the tea did not become ill. Actually, all of them did, but not significantly. Each complained of nausea and vomiting for a brief time. Important in this regard is the fact that the friends drank the true supernatant tea, whereas the patient happened to be left with the “dregs,” which perforce would have a greater concentration of toxins. Although we do not have data on the antinausea and antidiarrheal medications, these were administered after symptoms began. The acetaminophen level reported is within the margin of error for most laboratories, including ours. Herbert H. Pomerance, MD Enid Gilbert Barness, MD Mudra Kohli-Kumar, MD Sonya R. Arnold, MD Jill Steigelfest, MD University of South Florida College of Medicine Tampa, FL 33606 9/35/116609 doi:10.1067/mpd.2001.116609