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Jose S. Pulido, MD
Milwaukee, Wis

Thomas K. Shires, PhD
Iowa City, Iowa

Harry W. Flynn, Jr, MD
Miami, Fla

M. Bridget Zimmerman, PhD; James C. Folk, MD; Michael H. Scott
Iowa City, Iowa

Arch Ophthalmol. 1992;110(12):1683-1684.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—We read with interest the article by Campochiaro and Conway¹ as well as the subsequent related correspondence.^2,3 Part of the problem with the determination of aminoglycoside toxicity has been that toxic doses have been established in rabbit eyes by relying on electroretinographic (ERG) changes, histopathologic changes, or both. Intravitreal antibiotic studies have attempted to determine the threshold for toxic doses. These studies have looked for a dose that consistently caused toxicity and labeled this dose as the toxic dose.

In most biologic systems, tissues respond in log-dose fashion to pharmacologic agents. A log dose-response curve shows that a certain percentage of eyes will have an adverse response to a dose of tested drug that would not cause an adverse response to others. For an aminoglycoside-toxicity model, the clinical observation has been made that macular infarction can occur at lower doses than the threshold dose obtained . . . [Full Text PDF of this Article]

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