The investigations of Ballantyne,1 Friedenwald,2 and Ashton3 have shown that the earliest recognizable (ie, recognizable by ophthalmoscopy or by various histological methods) lesions of diabetic retinopathy are the microaneurysms. While these microaneurysms are universally accepted as the characteristic feature of diabetic retinopathy, no one has been able to explain satisfactorily how and why these microaneurysms develop with such regularity in this disease. Since the pioneering work of Ballantyne, there have been many attempts, in both the clinical and the experimental field, to find the cause for the development of these microaneurysms or at least offer reasonable postulates. More recently Ashton4 and Bloodworth5 have offered interesting theories along these lines; they believe that there is an accumulation of metabolic waste products in the diabetic retina; ie, there is an incomplete or defective metabolism in the diabetic retina.Postulating that the basic lesion before the development
de ROETTH A, PEI YF. Metabolism of the Alloxan Diabetic Rat Retina. Arch Ophthalmol. 1964;71(1):73–76. doi:10.1001/archopht.1964.00970010089014
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