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Delayed toxicity following acute ingestion of valpromide

Centre Antipoison, 162 Avenue Lacassagne, 69424 Lyon cedex 03, France, christine.payen{at}chu-lyon.fr

P Frantz

Centre Antipoison, 162 Avenue Lacassagne, 69424 Lyon cedex 03, France

O Martin

Département d'Urgences et Réanimation Médicale, Hôpital Edouard Herriot, 69437 Lyon cedex 03, France

F Parant

M Moulsma

Laboratoire de Pharmacotoxicologie, Hôpital Edouard Herriot, 69437 Lyon cedex 03, France

C Pulce

J Descotes

Centre Antipoison, 162 Avenue Lacassagne, 69424 Lyon cedex 03, France

As valpromide is a prodrug of valproic acid (valproate), the clinical presentation of overdoses with either valpromide or valproate sodium is generally considered similar. Whereas plasma peak levels and signs of central nervous system depression occur within a few hours after the acute ingestion of regular-release forms of valproate sodium, delayed toxicity and time to peak levels following valpromide ingestion can be seen as shown by the three reported cases. They were initially considered as mild because patients presented with no or only moderate symptoms and serum valproate levels were below or at therapeutic levels on admission more than 3 hours post-ingestion in two of the three patients. Serum valproate levels were not monitored until marked deterioration more than 10 hours after ingestion. At the time of deterioration, serum valproate was at toxic level in the three reported cases. Therefore, large intake of valpromide should be closely monitored because no or moderate symptoms together with low plasma levels in the first few hours after ingestion do not exclude a subsequent severe intoxication. Despite the usual favourable outcome and the poor correlation between plasma levels and toxic symptoms, patients should not be discharged until plasma levels are documented to remain at low levels for at least 10 hours after the ingestion of valpromide and the patient asymptomatic.

Key Words: acute poisoning • delayed toxicity • mitochondrial dysfunction • valproic acid • valpromide

Human & Experimental Toxicology, Vol. 23, No. 3, 145-148 (2004)
DOI: 10.1191/0960327104ht430oa


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