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ROBERT D. WEEKLEY, M.D.; ALBERT M. POTTS, M.D.; JOSE REBOTON, M.D.; RUPERT H. MAY, M.D.

Arch Ophthalmol. 1960;64(1):65-76.

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

Introduction

Within the last 40 years a series of entities have been recognized which have their origin in the administration of a drug and which present an ophthalmoscopic picture somewhat resembling retinitis pigmentosa. The first of these followed the intravenous administration for puerperal sepsis of an iodine-potassium iodide compound known under the trade name of Septojod.³² It was later shown experimentally that the substance responsible for the eye effects was the iodate ion and that the pathological findings^29,31 involved acute necrosis of the neural portion of the retina and pigment epithelium. In the experimental animal, retinae, so damaged, took up colored dyes more easily than did the normal fundi.³⁴

More recently it was demonstrated in experimental animals that intravenous injection of sublethal doses of diphenylthiocarbazone (Dithizon) caused diabetes and a type of retinopathy similar to that from iodate.^4,8,16,38 A synthetic antimalarial drug, chloroquine, reportedly produced great . . . [Full Text PDF of this Article]

Author Affiliations
Cleveland

From the Departments of Ophthalmology, Cleveland Metropolitan General Hospital and Western Reserve University School of Medicine, and from the Cleveland Psychiatric Institute and Hospital.

Footnotes
Submitted for publication March 18, 1960.

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