Purchase this article with an account.
J. Feher, I. Kovacs, M. Artico, M. Mancone, S. Keresz, C. Balacco Gabrieli; Histopathologic Reappraisal of the Early Diabetic Retinopathy. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5371.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Current concept on the diabetic retinopathy assigned a primary role to the endothelial dysfunction responsible for basement membrane thickening, while retinal alterations are considered to be secondary due to either ischemia or exudation. Although type 2 diabetes almost always associated with abnormal lipid metabolism, the role of this latter has not yet been studied. The aim of this study was to reveal initial retinal alterations in type 2 diabetes without or with dyslipidemia
TEM and SEM as well as histochemical studies were performed on 46 enucleated human eyes (23 diabetics and 23 age matched controls). Morphometric studies on the capillary wall and on the inner limiting membrane (ILM) were also performed.
(i) In normal young eyes the capillary wall contains three distinct layers: the inner layer belongs to endothelial cells, the central surrounds pericytes, and the outer layer belongs to the Muller cells.(ii) In early diabetes basement membrane thickening starts at the glial side but not at the endothelial side.Highly electron-dense lysosomes accumulated in the Muller cell cytoplasm which surrounded the retinal capillaries. Proliferation of basement membrane material was also observed in the intercellular space of the Muller cell next to the capillaries.(iii) In the thickened outer layer lipids were accumulated in various extents, but it was particularly evident in diabetic patients with dyslipidemia(iv) The ILM was also thickened and vacuolated.(v) Both capillary wall and ILM thickening was significantly higher in diabetics as compared to age matched controls (p<0.01),(vi) Histochemistry showed accumulation of type II (vitreal/glial) collagen in both localization.
Our study on early diabetic retina added three significant new findings to the current concept:(i) Muller cells initiate to deposit excessive basement membrane material,(ii) Dyslipidemia is a contributing factor to diabetic retinopathy(ii) ILM may have alterations similar to those of the capillary wall.These observations suggested that changes of Muller cell metabolism rather than those of endothelial cells may play primary role in early diabetic retinopathy. Furthermore, metabolic syndrome pathologic point of view has a specific feature, i.e. metabolic retinopathy.
This PDF is available to Subscribers Only