Correspondence

Central Nervous System Depression after Ingestion of RenewTrient

N Engl J Med 1999; 340:570February 18, 1999

Article

To the Editor:

Citing a high median lethal dose to suggest that γ-butyrolactone is not a poison, Gorton (Sept. 17 issue)1 obscures the unfortunate fact that the doses and the circumstances under which many people are misusing the substance can result in coma or death. The median lethal dose of 4.28 g per kilogram of body weight places γ-butyrolactone in the “moderately toxic” category,2 along with other chemicals such as rubbing alcohol and antifreeze. Does Gorton want to suggest that these are not “poisons”?

It is difficult to understand Gorton's attempt to differentiate “coma” from “deep sleep.” If users pass out after the ingestion of γ-butyrolactone and fatally choke on their vomitus, are we to say they died in their sleep? Regardless of what you call it, deeply depressed consciousness can lead to serious complications such as vomiting with pulmonary aspiration of gastric contents or asphyxia due to improper neck positioning.

Kent R. Olson, M.D.
Jo Ellen Dyer, Pharm.D.
Christine Haller, M.D.
California Poison Control System, San Francisco, CA 94110

2 References

1. 1

   Gorton C. Butyrolactone-induced central nervous system depression after ingestion of RenewTrient, a “dietary supplement.“ N Engl J Med 1998;339:848-848
   Full Text | Web of Science | Medline

2. 2

   Gosselin RE, Hodge HC, Smith RP, et al. Clinical toxicology of commercial products. 4th ed. Baltimore: Williams & Wilkins, 1976.
   

To the Editor:

Gorton's endorsement of the antidotal efficacy of physostigmine is most disturbing. Physostigmine, a carbamate-type cholinesterase inhibitor, raises the synaptic acetylcholine concentration by preventing its metabolism. Physostigmine therefore has analeptic, or nonspecific arousal, properties not unlike those of caffeine or other stimulants.1 More than 30 years ago the use of analeptic agents was abandoned for the treatment of sedative–hypnotic poisoning owing to their associated morbidity and mortality.2 The recommendation that physostigmine may quickly reverse the clinical effects of γ-butyrolactone is outdated and potentially dangerous. The intravenous administration of physostigmine at the recommended dose (2 mg) may produce seizures, bradycardia, or cholinergic crisis. The only appropriate remaining indication for the use of physostigmine in poisoned patients is for reversal of the anticholinergic syndrome associated with certain drugs. In these cases the administration of physostigmine should be performed very slowly and under continual observation.

Lewis S. Nelson, M.D.
New York City Poison Control Center, New York, NY 10016

Mary Ann Howland, Pharm.D.
St. John's University College of Pharmacy, Jamaica, NY 11439

Robert S. Hoffman, M.D.
New York City Poison Control Center, New York, NY 10016

2 References

1. 1

   Nattel S, Bayne L, Ruedy J. Physostigmine in coma due to drug overdose. Clin Pharmacol Ther 1979;25:96-102
   Web of Science | Medline

2. 2

   Clemmesen C, Nilsson E. Therapeutic trends in the treatment of barbiturate poisoning: the Scandinavian method. Clin Pharmacol Ther 1961;2:220-229
   Web of Science | Medline

Citing Articles (1)

Citing Articles

1. 1

   Ward Dean. (2000) Physostigmine Treatment of γHydroxybutyric Acid Overdose: Appropriate or Inappropriate Use of a Reversal Agent?. Mayo Clinic Proceedings 75:8, 872
   CrossRef