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Ronald Engerman, PhD
Madison, Wis

Arch Ophthalmol. 1993;111(5):584-585.

	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.

—The article by Takahashi and coworkers,¹ published in the September 1992 issue of the ARCHIVES, on experimental retinopathy nicely illustrates the retinal lesions that occur in dogs kept experimentally galactosemic for 4 to 5 years. The authors' suggestion that this is the "... first reliable animal model that demonstrates retinal vascular changees associated with advanced diabetic retinopathy" is, however, misleading. The retinal lesions in galactosemic dogs are anatomically identical with those found in diabetic dogs, as we have pointed out previously, and the neovascularization in either animal model differs at present in an important respect from clinically significant retinal neovascularization in diabetic patients.

In both the diabetic dog and the galactosemic dog, neovascularization is located chiefly within the retina, external to the inner-limiting membrane, rather than on the retina or in the vitreous. The neovascularization, in our experience, is always preceded by vessel nonperfusion or obliteration, and . . . [Full Text PDF of this Article]

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