Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Macular edema is the final common pathway of many intraocular and systemic insults. It may develop in a diffuse pattern where the macula appears generally thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with protean underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, diabetic retinopathy, and posterior segment inflammatory disease. As well as clinical suspicion, a wide range of investigations may lead to the diagnosis of macular edema. Fluorescein angiography and optical coherence tomography provide enhanced visualization of the geometry and distribution of macular edema. A variety of approaches to the treatment of macular edema have been attempted, with a variable degree of success. These options have included topical and systemic steroids, topical and oral non-steroidal anti-inflammatory agents and laser photocoagulation treatment. More recently other therapeutic modalities, including immunomodulators, intravitreal injection of triamcinolone, and pars plana vitrectomy have also been employed. Clinical trials are currently looking into the use of a steroid slow-release intravitreal device for the management of macular edema secondary to uveitis and diabetes. This article reviews the clinical entity of macular edema focusing on the current therapeutic strategies for its management.
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PMID:Macular edema. 1532 93

We evaluated the relationships between serum lipid levels and clinically significant macular edema (CSME), hard exudates, and other diabetic retinopathy (DR) end points in a population with type 1 diabetes. We studied data from serum lipids that were measured annually among the 1,441 Diabetes Control and Complications Trial (DCCT) participants. We used proportional hazards regression models to examine the relationship of the cumulative average of lipid levels (total, LDL, and HDL cholesterol, total-to-HDL cholesterol ratio, and triglycerides) with development of CSME, hard exudate, DR progression, and development of proliferative DR (PDR). In models controlling for primary prevention versus secondary intervention subgroup, randomized treatment assignment, HbA(1c), and other risk factors, both total-to-HDL cholesterol ratio and LDL predicted development of CSME (rate ratio [RR] for extreme quintiles 3.84, P for trend = 0.03 for total-to-HDL cholesterol ratio, and RR 1.95, P for trend = 0.03 for LDL) and hard exudate (RR 2.44, P for trend = 0.0004 for total-to-HDL cholesterol ratio, and RR 2.77, P for trend = 0.002 for LDL). Relationships of lipids with progression of DR and development of PDR were weaker and not significant after adjustment for HbA(1c). Higher serum lipids are associated with increased risk of CSME and retinal hard exudate. Lipid-lowering treatment among type 1 diabetic subjects, recommended to prevent cardiovascular disease, may also decrease risk of CSME, an important cause of vision loss.
Diabetes 2004 Nov
PMID:A prospective study of serum lipids and risk of diabetic macular edema in type 1 diabetes. 1550 69

Diabetes is a risk factor for the development of cataracts. Studies have shown an increased risk of ocular complications in diabetics after cataract surgery, but modern surgical techniques have minimized them, leading to an overall good visual outcome. Macular edema before surgery is the most common condition that limits post-operative visual recovery. Thus, pre-operative laser treatment is needed. Photocoagulation of preproliferative or early proliferative diabetic retinopathy is also advisable, due to the increased risk of iris neovascularization or retinopathy progression after surgery.
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PMID:Cataract surgery and diabetic retinopathy. 1551 69

The effect of lisinopril (an angiotensin-converting enzyme inhibitor) on diabetic macular edema (DME) was investigated by quantitative measurement of macular thickness. In a nonrandomized clinical trial, 19 normotensive type 2 diabetic patients with DME prospectively received oral lisinopril therapy for 2 months. Another 10 normotensive type 2 diabetic patients with similar DME were prospectively followed for two months without treatment. Central macular thickness was measured with a retinal thickness analyzer (RTA). In the lisinopril group, visual acuity improved by two lines or more in two out of 19 eyes (11%), was unchanged in 15 eyes (78%), and deteriorated by two lines or more in two eyes (11%). The mean central macular thickness was significantly reduced after 2 months of treatment (381.3 +/- 121.1 microm) compared with that before administration (475.2 +/- 171.0 microm, P = 0.0093). In the control group, central macular thickness was not significantly decreased after 2 months (458.5 +/- 113.7 microm, P = 0.2178) compared with the baseline value (464.7 +/- 152.2). Fluorescein angiography showed that macular leakage was decreased in 10 patients from the lisinopril group (53%) and was unchanged in nine patients (47%). There was a significant difference of central macular thickness between the patients with and without improvement of macular leakage (P = 0.0040). Lisinopril therapy may reduce macular thickness in patients with DME, as shown by this quantitative study. In addition, quantitative measurement of retinal thickness is useful when evaluating therapeutic agents for DME.
Diabetes Res Clin Pract 2004 Dec
PMID:Quantitative measurement of retinal thickness in patients with diabetic macular edema is useful for evaluation of therapeutic agents. 1553 18

Diabetes is present in 7% of Missourians. Another 52% are at risk. Periodic eye examinations are key to averting vision loss from diabetic retinopathy. Signs of diabetic retinopathy are evident long before vision loss and include microaneurysms, retinal hemorrhage, microvascular and venous caliber abnormalities and neovascularization. Loss of vascular integrity can lead to retinal edema and neovascular growth. Laser ablation of the peripheral retina can curb neovascular growth. It can also help stabilize macular edema.
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PMID:The challenge of preventing vision loss from diabetic retinopathy. 1575 16

Neovascularization leads to blindness in numerous ocular diseases, including diabetic retinopathy, age-related macular degeneration, retinopathy of prematurity, and sickle cell disease. More effective and stable treatments for ocular neovascularization are needed, yet there are major limitations in the present animal models. To develop primate models of diabetic retinopathy and choroidal neovascularization, rhesus monkeys were injected subretinally or intravitreally with an adeno-associated virus (AAV)-2 vector carrying the cDNA encoding human vascular endothelial growth factor (VEGF). Overexpression of VEGF was measured by intraocular fluid sampling over time. Neovascularization was evaluated by ophthalmoscopy through angiography, optical coherence tomography, and ultimately histopathology. Overexpression of VEGF through AAV2 results in rapid development of features of diabetic retinopathy or macular edema, depending on the targeted cell type/mode of production of VEGF and diffusion of VEGF. Nonhuman primate models will be useful in testing long-term safety and efficacy of novel therapeutic agents for blinding neovascular diseases.
Diabetes 2005 Apr
PMID:Nonhuman primate models for diabetic ocular neovascularization using AAV2-mediated overexpression of vascular endothelial growth factor. 1579 54

Since vascular endothelial growth factor (VEGF) has a strong effect on induction of vascular permeability, VEGF is an attractive candidate gene for development of diabetic macular edema (ME). Among the 378 patients with type 2 diabetes studied, 203 patients had no retinopathy, 93 had non-proliferative diabetic retinopathy (NPDR), and 82 had proliferative diabetic retinopathy (PDR). ME was present in 16 patients with NPDR and 47 patients with PDR. We genotyped three VEGF polymorphisms: C-2,578A, G-1,154A, and C-634G. Genotype and allele distribution of C-634G, but not C-2,578A or G-1,154A, were significantly different between patients with and without diabetic retinopathy. Logistic regression analysis revealed that the C-634G genotype was a risk factor for DR (p = 0.002), and furthermore for ME (p = 0.047), independently from severity of DR, with the -634C allele increasing the risk. Macular thickness measured by optical coherence tomography was correlated with the C-634G genotype, with the trend increasing with the presence of more -634C alleles (p = 0.006). Stepwise regression analysis showed that duration of diabetes and presence of the C-634G genotype were independent predictors of macular thickness. In addition, basic transcriptional activity levels associated with the -634C allele were greater compared to those seen with the -634G allele in human glioma and lymphoblastic T-lymphocyte cells. These results demonstrate that the VEGF C-634G polymorphism is a genetic risk factor for ME as well as DR.
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PMID:Functional VEGF C-634G polymorphism is associated with development of diabetic macular edema and correlated with macular retinal thickness in type 2 diabetes. 1596 67

The purpose of this study was to evaluate the Safety and efficacy of the orally administered protein kinase C (PKC) beta isoform-selective inhibitor ruboxistaurin (RBX) in subjects with moderately severe to very severe nonproliferative diabetic retinopathy (NPDR). In this multicenter, double-masked, randomized, placebo-controlled study, 252 subjects received placebo or RBX (8, 16, or 32 mg/day) for 36-46 months. Patients had an Early Treatment Diabetic Retinopathy Study (ETDRS) retinopathy severity level between 47B and 53E inclusive, an ETDRS visual acuity of 20/125 or better, and no history of scatter (panretinal) photocoagulation. Efficacy measures included progression of DR, moderate visual loss (MVL) (doubling of the visual angle), and sustained MVL (SMVL). RBX was well tolerated without significant adverse effects but had no significant effect on the progression of DR. Compared with placebo, 32 mg/day RBX was associated with a delayed occurrence of MVL (log rank, P = 0.038) and of SMVL (P = 0.226). RBX reduction of SMVL was evident only in eyes with definite diabetic macular edema at baseline (10% 32 mg/day RBX vs. 25% placebo, P = 0.017). In multivariable Cox proportional hazard analysis, 32 mg/day RBX significantly reduced the risk of MVL compared with placebo (hazard ratio 0.37 [95% CI 0.17-0.80], P = 0.012). In this clinical trial, RBX was well tolerated and reduced the risk of visual loss but did not prevent DR progression.
Diabetes 2005 Jul
PMID:The effect of ruboxistaurin on visual loss in patients with moderately severe to very severe nonproliferative diabetic retinopathy: initial results of the Protein Kinase C beta Inhibitor Diabetic Retinopathy Study (PKC-DRS) multicenter randomized clinical trial. 1598 21

Retinal neovascularization and macular edema are central features of diabetic retinopathy, a major cause of blindness in working age adults. The currently established treatment for diabetic retinopathy targets the vascular pathology by laser photocoagulation. This approach is associated with significant adverse effects due the destruction of neural tissue and is not always effective. Characterization of the molecular and cellular processes involved in vascular growth and hyperpermeability has led to the recognition that the angiogenic growth factor and vascular permeability factor VEGF (vascular endothelial growth factor) play a pivotal role in the retinal microvascular complications of diabetes. Thus, VEGF represents an important target for therapeutic intervention in diabetic retinopathy. Agents that directly inhibit the actions of VEGF and its receptors show considerable promise, but have not proven to be completely effective in blocking pathological angiogenesis. Therefore, a better understanding of the molecular events that control VEGF expression and mediate its downstream actions is important to define more precise therapeutic targets for intervention in diabetic retinopathy. This review highlights the current understanding of the process by which VEGF gene expression is regulated and how VEGF's biological effects are altered during diabetes. In particular, cellular and molecular alterations seen in diabetic models are considered in the context of high glucose-mediated oxidative stress effects on VEGF expression and action. Potential therapeutic strategies for preventing VEGF overexpression or blocking its pathological actions in the diabetic retina are considered.
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PMID:Vascular endothelial growth factor and diabetic retinopathy: role of oxidative stress. 1602 70

Diabetic eye disease affects quality of life for patients with diabetes by decreasing visual acuity and increasing the risk of blindness. In the course of diabetic retinopathy (DR) the loss of capillary integrity, microaneurysm formation, and ischemia is observed, which in turn drives the progression of DR. The macular edema is the result of fluid accumulation in the retina secondary to capillary leakage and/or microaneurysms. This contributes to loss of vision in DR. There is substantial evidence that control over metabolic factors can effectively prevent the development and progression of DR. For many patients who fail to achieve the optimal level of metabolic control the standard care should include the early detection and timely treatment of DR. Laser photocoagulation therapy, and vitrectomy are invasive methods, recommended to treat only the late stages of disease. A number of pharmacological agents that could slow the progression of DR in earlier stages are now being tested. It is likely that at least one of these agents, will be effective in reducing the progression of DR and the associated vision loss. With the introduction of these drugs in the coming years, there will be a need for improved screening and monitoring of patients with DR. New technologies are giving patients more access to optimal screening and may make this a more achievable goal.
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PMID:[Diabetic retinopathy. Current opinion on pathophysiology, diagnostics and therapy]. 1622 43


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