Pathogenetic mechanisms in anterior proliferative vitreoretinopathy.

A clinicopathologic study of ten consecutive patients (ten eyes) undergoing surgery for rhegmatogenous retinal detachment with anterior proliferative vitreoretinopathy and a subsequent histopathologic, immunohistochemical, and ultrastructural study of ten enucleated eyes with anterior proliferative vitreoretinopathy were performed in order to elucidate relevant pathogenetic mechanisms. Our findings suggest that the pathogenetic evolution of anterior proliferative vitreoretinopathy occurs in three consecutive stages: (1) traction on the ciliary body and peripheral retina induced by fibrocellular contraction of the vitreous base; (2) incorporation of tractionally denuded components of the ciliary body and peripheral retina into the fibrocellular membranes overlying the vitreous base; and (3) proliferation of the incorporated components and fibrovascular ingrowth from the uvea, the retina, or both, into the fibrocellular membranes. Tractional disruption of the epithelium of the ciliary body pars plicata and breakdown of the ciliary blood-aqueous barrier are the principal pathogenetic mechanisms of chronic intractable hypotony and the post-vitrectomy fibrin syndrome in anterior proliferative vitreoretinopathy.     

Energy metabolic function in diabetic angioretinopathy

Electron-microscopic and ultrahistochemical investigations of biopsies of the conjunctiva as well as of iris and retina of 46 patients with diabetes mellitus have revealed disturbances in the ultrastructure, bioenergetics and activity of enzyme processes of the cell at different stages of diabetic angioretinopathy. The increase in activity of peroxide oxidation of lipids in progression of retinopathy is recorded. It is recommended to use antioxidants and agents increasing oxidation-reduction processes.     

Pathogenetic mechanisms of glaucoma not related to intraocular pressure

The pathogenesis of the diseases termed open-angle glaucoma remains elusive but progress is being made in understanding more clearly the optic nerve head, vascular, and cellular mechanisms that are associated with them. Even though the greatest risk factors remain intraocular pressure, age, race and refractive error, the association with vascular disease continues to unfold in the literature. Clinical and laboratory studies, although not addressing mechanisms directly as far as we know, continue to probe potential pathways that will ultimately lead to subsets of open-angle glaucoma. Only when this is accomplished will we be able to focus therapy at pathogenesis rather than at risks.     

Pathogenetic mechanisms of optic nerve lesions in acute vascular optic neuropathies

The authors analyze the findings of histomorphologic and immunomorphologic studies of 20 cadaver optic nerves from subjects with a history of acute vascular optic neuropathies due to atherosclerosis, eventuating in optic nerve atrophy: 13 atrophic optic nerves and 7 pair nerves from clinically normal eyes of the same patients were examined. The blood sera of 30 patients suffering from acute vascular optic neuropathies were tested. Noteworthy that vascular optic neuropathy associated with atherosclerosis is a bilateral process. Vascular insufficiency due to sclerotic changes in vessels of various diameters undoubtedly contributes to the pathogenesis of the optic nerve impairments in the involved and clinically healthy eyes. The developing immune status disorders and autoimmune processes also contribute to the genesis of sclerotic shifts in the vessels and optic nerve atrophy in both eyes.     

Advances in the management of diabetes mellitus

This article shall highlight several areas where recent developments have made, and may make in the future, practical advances to diabetes care. These advances have been in the areas of insulin therapy, glucose monitoring, identifying pre-diabetics and using immunosuppressive agents in pre-diabetes and early diabetes, pancreatic transplantation, and managing acute and chronic complications of diabetes.     

Advances in the management of diabetes mellitus

This article shall highlight several areas where recent developments have made, and may make in the future, practical advances to diabetes care. These advances have been in the areas of insulin therapy, glucose monitoring, identifying pre-diabetics and using immunosuppressive agents in pre-diabetes and early diabetes, pancreatic transplantation, and managing acute and chronic complications of diabetes.     

Management of diabetes mellitus

The past decade has seen a rapid advancement in our understanding of diabetes and in our ability to treat it. A new diagnostic classification has been established. Guidelines for diet therapy have been revised. New oral hypoglycemic agents have been approved for use, and the rationale for using oral agents expanded. Insulin therapy has been expanded by development of human insulin and new modes of injection, including insulin pumps. Several new techniques are available for monitoring control of diabetes.     

Pupil responsiveness in diabetes mellitus

The authors compared pupil responsiveness to light, convergence, and the effects of topical cocaine 4%, epinephrine 1%, phenylephrine 1%, homatropine 10%, and pilocarpine 1% in a group of 62 diabetics with a sex- and age-matched group of normal subjects. The duration of disease, metabolic control, and type of diabetes mellitus, the presence and severity of diabetic retinopathy, and evidence of systemic vegetative neuropathy were considered. It was found that sympathetic denervation was related significantly to the duration of disease and to the development of systemic autonomic neuropathy. There were also signs of iris myopathy in the pupil alterations of long-standing diabetics, explaining the poor pupil responsiveness to mydriatics occasionally found in these patients. Pupillary autonomic diabetic neuropathy should be considered an early and major sign of the development of systemic vegetative diabetic disease.