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SALICYLAMIDE TOXICITY AND SALICYLISM FREE

H. C. MOFENSON, MD
Am J Dis Child. 1964;108(1):109. doi:10.1001/archpedi.1964.02090010111016.
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To the Editor: In reading over Dr. Paul N. Tschetter's article on salicylism (Amer J Dis Child 106:334 [Sept] 1963) I encountered a controversial point in that he implied that salicylamide produces the clinical picture of salicylism.

Salicylamide chemically 2-hydroxybenzamide (Liquiprin) has a LD-50 of 1.4 gm per kg in rats. Toxic dose of this drug causes depression of the central nervous system as opposed to stimulation caused by acetylsalicylic acid. It does not alter the prothrombin time and is not hydrolized to salicylic acid. Therefore, salicylate levels are of no value in determining this drug ingestion. It is excreted as glucuronide of salicylamide.

It would appear that this controversial point is carried over from a previous article by Fruthaler and Snyder (Pediat Clin N Amer 9:41, 1962).

REFERENCES

Little, M., et al:  Salicylamide Pharmacology Fate and Clinical Use , J Pharmacol Exp Ther 101:119-124, 1951;.
Quick, A. J., and Clesceri, L.:  Influence of Acetylsalicylic Acid and Salicylamide on Coagulation of Blood , J Pharmacol Exp Ther 128:95-98, 1960;.

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References

Little, M., et al:  Salicylamide Pharmacology Fate and Clinical Use , J Pharmacol Exp Ther 101:119-124, 1951;.
Quick, A. J., and Clesceri, L.:  Influence of Acetylsalicylic Acid and Salicylamide on Coagulation of Blood , J Pharmacol Exp Ther 128:95-98, 1960;.

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