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At least 19 recordsLinked to original sources
PubMed1985

Factors influencing the development of visual loss in advanced diabetic retinopathy. Diabetic Retinopathy Study (DRS) Report No. 10.

Natural history data from the Diabetic Retinopathy Study were examined by multivariate methods to determine which baseline characteristics could predict the occurrence of severe visual loss (SVL) in eyes originally assigned to no treatment. The presence and extent of new blood vessels on the optic disc (NVD) had the strongest association with SVL. Several other ocular characteristics also were strongly associated with visual outcome. In the absence of NVD at baseline, the degree of intraretinal hemorrhages and microaneurysms (HMA) had the strongest association with development of SVL. Macular edema was a factor in determining visual loss to 20/200 but not SVL (less than 5/200). Among systemic characteristics, urinary protein was the best predictor of visual outcome, but none were as good as the major ocular variables.

Blindness↗
PubMed1987

Intraocular pressure following panretinal photocoagulation for diabetic retinopathy. Diabetic Retinopathy Report No. 11.

Data collected during the first five years after randomization in the Diabetic Retinopathy Study were analyzed to determine the effect of panretinal photocoagulation on intraocular pressure (IOP). At each follow-up visit, median IOP was identical for the treated and untreated eyes. Mean IOP rose slightly in each group. The proportion of untreated eyes with IOP above 30 mm Hg at two consecutive visits was twice that of the treated eyes (2% vs 1%). These data show that panretinal photocoagulation reduces the risk of subsequent intraocular hypertension, apparently by preventing the development of neovascular glaucoma.

Argon↗
PubMed1989

Factors associated with visual outcome after photocoagulation for diabetic retinopathy. Diabetic Retinopathy Study Report #13.

Six risk factors for severe visual loss despite panretinal (scatter) photocoagulation were identified by analyzing data collected during the first 5 years after randomization in the Diabetic Retinopathy Study. Proportional hazards regression revealed NVD (neovascularization on/around the optic disc) to be the most important risk factor. The risk of severe visual loss rose with increasing NVD, hemorrhages/microaneurysms, retinal elevation, proteinuria, and hyperglycemia and fell with increasing "treatment density." These results are similar to previous DRS findings on untreated eyes. The importance of "treatment density" as an independent predictor of visual outcome is a new finding and lends support to the common clinical practice of repeating photocoagulation if initial treatment does not reduce or stabilize retinal neovascularization.

Aged↗
PubMed2005

Potential utility of statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in diabetic retinopathy.

Diabetic retinopathy is a common and potentially devastating microvascular complication in diabetes and is a leading cause of acquired blindness among the people of occupational age. However, therapeutic options for the treatment of proliferative diabetic retinopathy, photocoagulation and vitrectomy, are limited by considerable side effects. Therefore, to develop novel therapeutic strategies that specifically target diabetic retinopathy is desired for patients with diabetes. In diabetes mellitus, the formation and accumulation of advanced glycation end products (AGEs) progress. There is a growing body of evidence to show that AGEs-their receptor (RAGE) interactions are involved in the development and progression of diabetic retinopathy. Statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, have been recently shown to reduce the risk for cardiovascular events in diabetic patients with or without coronary artery disease. However, the efficacy of statin therapy for diabetic retinopathy is not fully investigated. We have recently found that protein prenylation is crucial for the AGE-RAGE signaling in microvascular endothelial cells. By blocking the protein prenylation, cerivastatin completely prevented the AGE-RAGE-elicited angiogenesis via suppression of vascular endothelial growth factor (VEGF). These observations let us to speculate that statins might be a promising remedy for treating patients with diabetic retinopathy by acting as a potential inhibitor of the AGE-RAGE signaling pathway in microvascular endothelial cells. In this paper, we would like to propose the possible ways of testing our hypotheses. (1) Does treatment with statins decrease the risk for the development and progression of diabetic retinopathy in patients with normocholesterolemia? (2) If the answer is yes, is this beneficial effect of statins superior to that of other cholesterol-lowering agents with equihypolipidemic properties? (3) Does statin treatment suppress retinal VEGF expression in diabetic patients? (4) Does treatment with pyridoxamine, a post-Amadori inhibitor of AGE formation, attenuate the beneficial effects of statins on diabetic retinopathy? These clinical studies could clarify whether the use of statins is of benefit in patients with AGE-RAGE-related disorders such as diabetic retinopathy, even in the absence of hypercholesterolemia.

Acyl Coenzyme A↗
PubMed2000

Management of diabetic retinopathy.

Diabetic retinopathy remains a major cause of blindness despite increased understanding of this disease and identification of successful treatments. The Diabetic Retinopathy Study identified risk factors associated with a high risk of blindness and confirmed the benefits of panretinal photocoagulation. The Early Treatment Diabetic Retinopathy Study defined the retinal characteristics, indications of treatment and results of laser treatment of clinically significant macular oedema. The Diabetic Retinopathy Vitrectomy study established the benefits and timing of vitrectomy for non-clearing vitreous haemorrhage and severe proliferative diabetic retinopathy. The Diabetes Control and Complications Trial and the United Kingdom Prospective Diabetes Study have also demonstrated the value of tight control of blood sugar and blood pressure in diabetic retinopathy. These studies developed specific recommendations for the management of diabetic retinopathy. Optimum use of this information can minimize visual loss due to diabetic retinopathy.

Diabetic Retinopathy↗
PubMed2005

Does hypertension play a role in diabetic retinopathy?

Diabetic retinopathy is a common complication of diabetes. It represents one of the frequent causes of visual disability among diabetic subjects during the period of active life. The risk factors for diabetic retinopathy are poor glycemic control, hypertension, duration of diabetes, hyperlipidemia and proteinuria. It has been observed that prevalence of hypertension is higher in diabetic subjects than in the general population and as it also plays a major role in the progression of diabetic retinopathy, so tight control of hypertension is mandatory. The possible mechanisms by which hypertension affects diabetic retinopathy are haemodynamic (impaired autoregulation and hyperperfusion) and secondly through VEGF (Vascular Endothelial Growth Factor), as it has been observed that hypertension independent of hyperglycaemia upregulates the VEGF expression in retinal endothelial cells and ocular fluids. The level of control of blood pressure are debatable but nearer the blood pressure to the normal levels, better the chances of preventing the onset and progression of diabetic retinopathy. The lowering of blood pressure to a normal range is more important than the type of antihypertensive medication used. Diabetic retinopathy is one of the important causes of visual disability in diabetic subjects during the period of active life. It is characterized by gradually progressive alterations in the retinal microvasculature, leading to increased vasopermeability, areas of retinal occlusion and retinal neovascularization. The complications associated with increased vasopermeability and uncontrolled neovascularization can result in severe and permanent visual loss.

Comorbidity↗
PubMed2004

Increased levels of platelet-derived microparticles in patients with diabetic retinopathy.

Diabetic retinopathy is caused by capillary occlusions. Platelet-derived microparticles (PMPs) stimulate the coagulation cascade and increase leukocyte and endothelial cell adhesions, both of which are key events in the development of diabetic retinopathy. However, the correlation between the levels of PMPs and diabetic retinopathy has not been precisely determined. The PMPs levels and the expression of platelet CD62P and CD63 were measured in 92 diabetic patients. The level of PMPs was significantly correlated with the expression of CD62P (r = 0.76, P < 0.0001) and CD63 (r = 0.71, P < 0.0001). The mean level of PMPs in diabetics (507+/-15/10(4) platelets (plt), mean+/-S.E.) was significantly higher than that in normal. The PMPs levels increased with the progression of the diabetic retinopathy; 480+/-28/10(4) plt in diabetic patients without retinopathy (n = 25), 504+/-40/10(4) plt with mild or moderate non-proliferative diabetic retinopathy (n = 13), 512+/-29/10(4) plt with severe non-proliferative diabetic retinopathy (n = 25), and 528+/-25/10(4) plt with proliferative diabetic retinopathy (n=29). The PMPs level in patients with non-perfused retinal areas (582+/-27/10(4) plt, n = 24) was significantly higher than patients without non-perfused areas (469+/-23/10(4) plt, n = 30; P = 0.0096) and without diabetic retinopathy (P = 0.024). These high correlations indicate that increased levels of PMPs may accelerate diabetic retinopathy.

Adult↗
PubMed2004

Advanced glycation and advanced lipoxidation: possible role in initiation and progression of diabetic retinopathy.

Diabetic retinopathy remains the most common microvascular complication suffered by diabetic patients and is the leading cause of registerable blindness in the working population of developed countries. The clinicopathological lesions of diabetic retinopathy have been well characterised and although a multitude of pathogenic mechanisms have been proposed, the underlying dysfunctional biochemical and molecular pathways that lead to initiation and progression of this complication remain largely unresolved. There is little doubt that the pathogenesis of diabetic retinopathy is highly complex and there is a pressing need to establish new therapeutic regimens that can effectively prevent or limit retinal microvascular cell dysfunction and death which is characteristic of the vasodegenerative stages of diabetic retinopathy. The formation and accumulation of advanced glycation endproducts (AGEs) and/or advanced lipoxidation endproducts (ALEs) are among several pathogenic mechanisms that may contribute to diabetic retinopathy. AGEs/ALEs can form on the amino groups of proteins, lipids and DNA through a number of complex pathways including non-enzymatic glycation by glucose and reaction with metabolic intermediates and reactive dicarbonyl intermediates. These reactions not only modify the structure and function of proteins, but also cause intra-molecular and intermolecular cross-link formation. AGEs/ALEs are known to accumulate in the diabetic retina where they may have important effects on retinal vascular cell function, as determined by a growing number of in vitro and in vivo studies. Evidence now points towards a pathogenic role for advanced glycation/lipoxidation in the initiation and progression of diabetic retinopathy and this review will examine the current state of knowledge of AGE/ALE-related pathology in the diabetic retina at a cellular and molecular level. It will also outline how recent pharmaceutical strategies to inhibit AGE/ALE formation or limit their pathogenic influence during chronic hyperglycaemia may play a significant role in the treatment of diabetic retinopathy.

Animals↗
PubMed2006

[Recent advances in the studies of genetic polymorphisms in diabetic retinopathy].

Diabetic retinopathy is one of the most serious complications of diabetes mellitus, which affects the health and life quality seriously. The development of procedures for prevention and treatment of diabetic retinopathy is one of the most important problems that should be solved. Epidemiological studies indicate that the development of diabetic retinopathy is not only determined by duration of diabetes and blood glucose control; individual diversities also play an important role. Some patients have a long course of disease and poor control of blood glucose, but they do not have diabetic retinopathy or only show slight pathological changes after a long term follow-up. Other patients only have a short term disease and well control of blood glucose, but they develop serious proliferative diabetic retinopathy. These patients usually have a positive family history. This phenomenon may relate to various genetic liabilities. This review introduce the recent advances in the studies of genetic polymorphisms in diabetic retinopathy.

Diabetic Retinopathy↗
PubMed2003

Proposed international clinical diabetic retinopathy and diabetic macular edema disease severity scales.

PURPOSE: To develop consensus regarding clinical disease severity classification systems for diabetic retinopathy and diabetic macular edema that can be used around the world, and to improve communication and coordination of care among physicians who care for patients with diabetes. DESIGN: Report regarding the development of clinical diabetic retinopathy disease severity scales. PARTICIPANTS: A group of 31 individuals from 16 countries, representing comprehensive ophthalmology, retina subspecialties, endocrinology, and epidemiology. METHODS: An initial clinical classification system, based on the Early Treatment Diabetic Retinopathy Study and the Wisconsin Epidemiologic Study of Diabetic Retinopathy publications, was circulated to the group in advance of a workshop. Each member reviewed this using e-mail, and a modified Delphi system was used to stratify responses. At a later workshop, separate systems for diabetic retinopathy and macular edema were developed. These were then reevaluated by group members, and the modified Delphi system was again used to measure degrees of agreement. MAIN OUTCOME MEASURES: Consensus regarding specific classification systems was achieved. RESULTS: A five-stage disease severity classification for diabetic retinopathy includes three stages of low risk, a fourth stage of severe nonproliferative retinopathy, and a fifth stage of proliferative retinopathy. Diabetic macular edema is classified as apparently present or apparently absent. If training and equipment allow the screener to make a valid decision, macular edema is further categorized as a function of its distance from the central macula. CONCLUSIONS: There seems to be a genuine need for consistent international clinical classification systems for diabetic retinopathy and diabetic macular edema that are supported with solid evidence. The proposed clinical classification systems provide a means of appropriately categorizing diabetic retinopathy and macular edema. It is hoped that these systems will be valuable in improving both screening of individuals with diabetes and communication and discussion among individuals caring for these patients.

Diabetic Retinopathy↗
PubMed2004

Growth factors and protein kinase C inhibitors as novel therapies for the medical management diabetic retinopathy.

Diabetic retinopathy is a leading cause of acquired visual loss. Current treatment modalities are not effective in all cases and may have side effects. Investigation of the biochemical basis of diabetic retinopathy suggests that future treatments may reverse or halt the progression of diabetic retinopathy, or actually prevent the development of diabetic retinopathy. Pharmacological manipulation of protein kinase C and various growth factors may form the basis of future treatments for diabetic retinopathy.

Angiogenic Proteins↗
PubMed2006

Elevation of monocyte-derived microparticles in patients with diabetic retinopathy.

Diabetic retinopathy is associated with microvascular damage and capillary occlusions which are common features of the microangiopathy in diabetes. Monocyte-derived microparticles (MDMPs) are released from activated monocytes and enhance the procoagulant activity, and also activate adhesion reactions. These are key events in the development of capillary occlusion. The MDMPs level in the blood, and platelet activation markers (platelet-derived microparticles (PDMPs), CD62P and CD63) were measured by flow cytometry in 72 diabetic patients. The plasma levels of intracellular adhesion molecule-1 (ICAM-1) and P-selectin were analyzed by ELISA. The level of MDMPs was significantly correlated with the levels of PDMPs (r=0.52, P<0.001), CD62P (r=0.37, P=0.001), CD63 (r=0.31 and P=0.007), P-selectin (r=0.38, P=0.001), and ICAM-1 (r=0.31, P=0.009). The MDMPs level increased with the progression of the diabetic retinopathy: 81+/-14/10(4)platelets (plts) in patients without retinopathy (n=10); 88+/-8/10(4)plts with mild or moderate non-proliferative diabetic retinopathy (NPDR, n=12); 95+/-8/10(4)plts with severe NPDR (n=24); and 112+/-9/10(4)plts with proliferative diabetic retinopathy (PDR) (n=26). The MDMPs level in patients with areas of capillary occlusion (123+/-10/10(4)plts, n=25) was significantly higher than that in patients without areas of capillary occlusion (84+/-5/10(4)plts, n=25; P=0.0008). These correlations suggest that increased levels of MDMPs may accelerate the progression of diabetic retinopathy.

Adult↗
PubMed1992

Current management of diabetic retinopathy.

Diabetic retinopathy progresses through three distinct stages. A rational approach to management is based on an understanding of the pathophysiology of each stage. Based on the results of national multicentered clinical trials of laser photocoagulation and other treatments, advances in our understanding of the pathogenesis and treatment can now make a dramatic impact on blindness in the diabetic population: Panretinal laser photocoagulation treatment can reduce the risk of vision loss from high-risk proliferative diabetic retinopathy by at least 50%. Laser photocoagulation treatment of clinically significant diabetic macular edema can reduce the risk of vision loss by more than 50%. Vitrectomy can restore useful vision to some patients with severe diabetic retinopathy and vitreous hemorrhage with or without an accompanying traction retinal detachment. Diabetes 2000 is a new project sponsored by the American Academy of Ophthalmology, the goal of which is to eliminate preventable blindness from diabetes by the year 2000. As its name implies, Diabetes 2000 will be a long-term project aimed at a specific disease--diabetic retinopathy and its complications. It will provide the latest research findings to ophthalmologists and primary care physicians as the first priority, followed by the education of patients and the general public. Recent advances and treatment guidelines for the medical and surgical treatment of diabetic eye disease will be emphasized through the continuing education of ophthalmologists, other physicians, and allied health professionals. In later phases, educational programs for diabetic persons and the public will be developed. Ultimately, improved access of diabetic patients to ophthalmologic care and a close working relationship between ophthalmologists and primary care physicians will ensure early detection of diabetic retinopathy and the timely delivery of state-of-the-art treatments.

Aspirin↗
PubMed2004

A central role for inflammation in the pathogenesis of diabetic retinopathy.

Diabetic retinopathy is a leading cause of adult vision loss and blindness. Much of the retinal damage that characterizes the disease results from retinal vascular leakage and nonperfusion. Diabetic retinal vascular leakage, capillary nonperfusion, and endothelial cell damage are temporary and spatially associated with retinal leukocyte stasis in early experimental diabetes. Retinal leukostasis increases within days of developing diabetes and correlates with the increased expression of retinal intercellular adhesion molecule-1 (ICAM-1) and CD18. Mice deficient in the genes encoding for the leukocyte adhesion molecules CD18 and ICAM-1 were studied in two models of diabetic retinopathy with respect to the long-term development of retinal vascular lesions. CD18-/- and ICAM-1-/- mice demonstrate significantly fewer adherent leukocytes in the retinal vasculature at 11 and 15 months after induction of diabetes with STZ. This condition is associated with fewer damaged endothelial cells and lesser vascular leakage. Galactosemia of up to 24 months causes pericyte and endothelial cell loss and formation of acellular capillaries. These changes are significantly reduced in CD18- and ICAM-1-deficient mice. Basement membrane thickening of the retinal vessels is increased in long-term galactosemic animals independent of the genetic strain. Here we show that chronic, low-grade subclinical inflammation is responsible for many of the signature vascular lesions of diabetic retinopathy. These data highlight the central and causal role of adherent leukocytes in the pathogenesis of diabetic retinopathy. They also underscore the potential utility of anti-inflammatory treatment in diabetic retinopathy.

Animals↗