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March 1973


Author Affiliations

Chief Resident Division of Otolaryngology The Johns Hopkins Hospital Baltimore 21205

Arch Otolaryngol. 1973;97(3):300. doi:10.1001/archotol.1973.00780010308020

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To the Editor. —I am writing to comment upon the paper "Ototoxicity of Ethacrynic Acid" by Dr. Jiri Prazma et al (Archives 95:448-456, 1972).

The electrophysiologic data presented impressively indict ethacrynic acid as an ototoxic agent; however, it is misleading to synthesize data obtained from the guinea pig, cat, and dog since ethacrynic acid has species specificity.

Dr. Prazma develops the concept that cochlear potential decreases may be related to electrolyte changes in the cochlea. In support of this, he states:

Wilson and Juhn12 and Cohn13 et al showed that ethacrynic acid caused a marked increase in potassium in perilymph. The same authors also reported a decrease in the concentration of potassium from 145 to 25 mEq/liter in endolymph. All the above data seem to show that ethacrynic acid inhibits active ion transport in the ductus cochlearis, reversing the K and Na concentrations, and thereby producing a drop

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