Microglial activation in human diabetic retinopathy.

OBJECTIVE: To investigate microglial activation in human diabetic retinopathy. METHODS: Paraffin sections from 21 eyes of 13 patients with diabetic background, preproliferative, or proliferative retinopathies and 10 normal eyes of 9 individuals were studied with immunolabeling of microglia with antibodies against HLA-DR antigen, CD45, or CD68. RESULTS: In the healthy human eyes, ramified microglial cells were scattered in the inner retinal layers. In eyes with diabetic retinopathy, the microglia were markedly increased in number and were hypertrophic at different stages of the disease. These cells clustered around the retinal vasculature, especially the dilated veins, microaneurysms, intraretinal hemorrhages, cotton-wool spots, optic nerve, and retinal and vitreal neovascularization. In some retinas with cystoid macular edema, microglia infiltrated the outer retina and subretinal space. Cells in the epiretinal membrane were also labeled with microglial markers. CONCLUSIONS: Microglia were activated at different stages of human diabetic retinopathy and optic neuropathy. Microglial perivasculitis was a prominent feature of the disease process. CLINICAL RELEVANCE: Activated microglia and microglial perivasculitis may play a role in vasculopathy and neuropathy in diabetic retinopathy.

Corneal myxoma.

BACKGROUND: Myxomas are rare benign tumors that can be found most frequently in the heart. We report the clinical and histological findings in a very rare case of corneal myxoma, which is only the sixth case in the literature. CASE: A whitish elevated tumor of the anterior cornea developed in the left eye cornea of a 46-year-old man 2 years after luxation of the patient's lens into the anterior chamber and subsequent endothelial decompensation. The tumor covered the entire surface of the cornea except for the outer limbal periphery at Schwalbe's line. OBSERVATIONS: Histologically, the hypocellular tumor was characterized by scattered spindle- and stellate-shaped cells with wavy, randomly oriented collagen fibers in a myxomatous ground substance staining positively for acid mucopolysaccharides. Bowman's layer was absent. Immunohistochemically, the tumor cells were positive for vimentin. Ultrastructurally, the tumor cells had features characteristic of keratocytes with no basement membrane, much rough endoplasmic reticulum and vacuoles containing mucoid-like material. CONCLUSIONS: The ultrastructural observations support the hypothesis of a cellular origin of the myxoma from keratocytes. The tumor growth was most probably stimulated by chronic endothelial failure and bullous keratopathy.