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      Diabetic vitreopathy--findings using the celloidin embedding technique.

      Ophthalmologica. Journal international d'ophtalmologie. International journal of ophthalmology. Zeitschrift für Augenheilkunde
      Adolescent, Aged, Aging, physiology, Child, Collodion, Diabetes Complications, Diabetes Mellitus, Type 2, Eye Diseases, etiology, pathology, Humans, Microscopy, Electron, Microscopy, Electron, Scanning, Middle Aged, Tissue Adhesives, Tissue Embedding, Vitreous Body, Vitreous Detachment

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          Abstract

          To evaluate the role of the vitreous in diabetic eyes, autopsy eyes from diabetic patients have been examined by means of light and electron microscopy. Twenty-five eyes were obtained from 19 patients. The duration of diabetes was from 8 to 26 years (average 17 years). All patients had type II diabetes. The glycerol-dehydrated globes were embedded in celloidin and hardened with chloroform. For light microscopy, areas of interest were cut from 200-microm-thick celloidin sections and embedded in paraffin, and 10-microm sections were cut. Such 200-microm and 10-microm sections were also used for scanning electron microscopy. For transmission electron microscopy, areas of interest were cut from thick celloidin sections and embedded in Epon for thin sectioning. The vitreous in diabetic eyes exhibits delayed senile degeneration in case of early onset of diabetes. It shows intensified staining of the vitreous cortex. Posterior detachment is often incomplete without collapse. The vitreous collagen fibers are coarse and aggregated in the centrally located cortical region of the vitreous. Hyalocytes in diabetic eyes have a different shape than normally, and their number seems to be increased. All these structural changes were not demonstrated in nondiabetic eyes. The vitreous in diabetic patients is morphologically different from normal vitreous. Features of the diabetic vitreous are aggregated collagen fibers, increased density of the vitreous cortex and morphological changes of hyalocytes. It is discussed whether these findings arise from nonenzymatic glycosylation of collagen molecules resulting in diabetic vitreopathy.

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