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The prognosis of some of the most prevalent conditions seems to be intricately related to myriad risk factors, largely modifiable, but often leading to irreversible complications when left unmanaged. This study exemplifies the multidisciplinary approach necessary, to successfully control diabetic retinopathy, one of the leading complications of diabetes, and to discuss promising therapies. Based on a Medline Ovid database search, we present a clinical and economic review of the evidence on the epidemiology and risk factors of diabetic retinopathy, its prognosis and economic implications. Among adults aged 20-74, diabetic retinopathy (DR) is the most frequent cause of blindness. However, in both types 1 and 2 DM, improved glycemic control reduces the development and progression of DR. Risk factors of DR include duration of diabetes, pregnancy, renal disease, age, smoking, alcohol, hyperlipidemia and antioxidants. A number of drugs may play a role in DR therapy in the coming few years; eg, somatostatin agonists (sandostatin), corticosteroids (triamcinolone, dexamethasone, fluocinolone), vascular endothelial growth factor inhibitors (pegaptanib, ranibizumab), hyaluronidase and plasmin enzyme. Whether these therapies have a clinically significant impact on DR progression however, remains to be seen.
Increasing prevalence of diabetes mellitus warrants recognition of factors related to asymmetric diabetic retinopathy (DR). This thematic synthesis based on an iterative literature review conducted in Medline and Google Scholar pertaining to diabetes with coexistent asymmetry of retinopathy included 45 original articles, 21 case reports and series, and 18 review articles from 1965 to 2020. Asymmetric DR is defined as proliferative DR (PDR) in one eye and nonproliferative, preproliferative, background, or no DR in the other eye lasting for at least 2 years. It is observed in 5%-10% of patients with PDR. Associated factors can be divided into (i) vascular: carotid obstructive disease, ocular ischemic syndrome, and retinal vascular diseases; (ii) Inflammatory: uveitis, endophthalmitis, and Fuchs' heterochromic cyclitis; (iii) degenerative: posterior vitreous detachment, high myopia and anisometropia, uveal coloboma, retinal detachment, retinitis pigmentosa, and chorioretinal atrophy and scarring; (iv) cataract surgery and vitrectomy; and (v) miscellaneous: elevated intraocular pressure, glaucoma, amblyopia, retinal detachment, and optic atrophy. The gamut of diagnostic modalities for asymmetric DR includes thorough ocular examination, slit-lamp biomicroscopy, fundus photography, fundus fluorescein angiography, optical coherence tomography, and newer modalities such as ultra-widefield fluorescein angiography and optical coherence tomography angiography, along with a complete systemic evaluation and carotid Doppler studies. The differential diagnosis includes other causes of retinal neovascularization that may present in an asymmetric manner, such as sickle cell retinopathy, retinal vein occlusions, and featureless retina. This review discusses in detail the aforementioned considerations and draws a comprehensive picture of asymmetric DR in order to sensitize ophthalmologists to this important condition.
Despite the fact that we still do not understand what causes the development of retinopathy in diabetic subjects, major advances in its treatment have taken place. Photocoagulation clearly reduces the retinopathy although how early treatment should be initiated has not been clearly defined. Vitrectomy is capable of restoring vision in many already blind eyes but at some risk. We are inching closer to an understanding of the pathophysiology of retinopathy with development of retinal endothelial and pericyte cell culture techniques, studies of vascular permeability, flow and angiogenesis. Diabetic retinopathy is more common at early durations of diabetes than previously realized. This may allow for prospective intervention studies, using development of retinopathy as an endpoint. Diabetic retinopathy may be a reasonable index of short-term survival.
Diabetic retinopathy is the major cause of acquired blindness in working-age adults. Studies of the vitreous proteome have provided insights into the etiology of diabetic retinopathy and suggested potential molecular targets for treatments. Further characterization of the protein changes associated with the progression of this disease may suggest additional therapeutic approaches as well as reveal novel factors that may be useful in predicting risk and functional outcomes of interventional therapies. This article provides an overview of the various techniques used for proteomic analysis of the vitreous and details results from various studies evaluating vitreous of diabetic patients using the proteomic approach.
For the past several decades, tremendous efforts have been made to decrease the complications of diabetes, including diabetic retinopathy. New diagnostic modalities like ultrawide field fundus fluorescein angiography and spectral domain optical coherence tomography has allowed more accurate diagnosis of early diabetic retinopathy and diabetic macular edema. Antivascular endothelial growth factors are now extensively used to treat diabetic retinopathy and macular edema with promising results. There remains uncertainty over the long term effects and the socioeconomic costs of these agents.
Diabetic retinopathy (DR) is a serious complication of diabetes, which is fast reaching epidemic proportions worldwide. While tight glycemic control remains the standard of care for preventing the progression of DR, better insights into DR etiology require understanding its genetic basis, which in turn may assist in the design of novel treatments. During the last decade, genomic medicine is increasingly being applied to common multifactorial diseases such as diabetes and age-related macular degeneration. The contribution of genetics to the initiation and progression of DR has been recognized for some time, but the involvement of specific genes and genetic variants remains elusive. Several investigations are currently underway for identifying DR susceptibility loci through linkage studies, candidate gene approaches, and genome-wide association studies. Advent of next generation sequencing and high throughput genomic technologies, development of novel bioinformatics tools and collaborations among research teams should facilitate such investigations. Here, we review the current state of genetic studies in DR and discuss reported findings in the context of biochemical, cell biological and therapeutic advances. We propose the development of a consortium in India for genetic studies with large cohorts of patients and controls from limited geographical areas to stratify the impact of the environment. Uniform guidelines should be established for clinical phenotyping and data collection. These studies would permit identification of genetic loci for DR susceptibility in the Indian population and should be valuable for better diagnosis and prognosis, and for clinical management of this blinding disease.
Purpose: To compare the detection rates of optical coherence tomography (OCT) and fluorescein angiography (FA) in a diabetic macular edema (DME) and the severity of diabetic retinopathy in both color fundus images (CFI) and FA, and to investigate the predictive factors in macular leakages in FA. Methods: This was a retrospective study, and a total of 132 eyes of 77 patients with diabetic retinopathy were enrolled. Macular OCT, FA, and CFI were reviewed and measured. Central foveal thickness was also measured. Results: The severity of diabetic retinopathy in FA was significantly higher than that in CFI (p < 0.001). OCT detected 26 eyes with DMEs, which included the following: 13 eyes with cystoid macular edemas; 13 eyes with serous retinal detachments; 11 eyes with diffuse retinal thickening; 4 eyes with vitreomacular interface abnormalities. In contrast, 72 out of 132 eyes (54.5%) showed macular leakages in FA, which was significantly higher than that detected by OCT (p < 0.001). Compared with FA, the sensitivity and the specificity of OCT in detecting DMEs were 30.6 and 93.3%, respectively. However, central foveal thickness was not significantly different between the patients with non-clinically significant macular edema (CSME, 253.1 ± 26.95 μm) and slight CSME (270.9 ± 37.11 μm, p = 0.204). The mean central foveal thickness in diabetic macular edema (FA) eyes was 271.8 ± 66.02 μm, which was significantly higher than that (253. ± 25.21 μm) in non-DME (FA) eyes (p = 0.039). The central foveal thickness in DME (FA) eyes was significantly lower than that in eyes with DME (OCT) (p = 0.014). After adjusting for age and sex, a logistic regression analysis showed that the classification of diabetic retinopathy in FA was positively associated with macular leakage in FA (p < 0.001). Conclusions: The severity of diabetic retinopathy is underestimated in CFI compared with that in FA. FA can detect latent DMEs, which appeared normal on OCT. The central foveal thickness is not a sensitive parameter for detecting latent DMEs.
Diabetic retinopathy (DR) is characterised by neurovascular degeneration as a result of chronic hyperglycaemia. Proliferative diabetic retinopathy (PDR) is the most serious complication of DR and can lead to total (central and peripheral) visual loss. PDR is characterised by the presence of abnormal new blood vessels, so-called "new vessels," at the optic disc (NVD) or elsewhere in the retina (NVE). PDR can progress to high-risk characteristics (HRC) PDR (HRC-PDR), which is defined by the presence of NVD more than one-fourth to one-third disc area in size plus vitreous haemorrhage or pre-retinal haemorrhage, or vitreous haemorrhage or pre-retinal haemorrhage obscuring more than one disc area. In severe cases, fibrovascular membranes grow over the retinal surface and tractional retinal detachment with sight loss can occur, despite treatment. Although most, if not all, individuals with diabetes will develop DR if they live long enough, only some progress to the sight-threatening PDR stage. OBJECTIVES: To determine risk factors for the development of PDR and HRC-PDR in people with diabetes and DR.
Diabetic retinopathy (DR) and diabetic macular edema (DME) are leading causes of blindness in the working-aged population of most developed countries. The increasing number of persons with diabetes worldwide suggests that DR/DME will continue to be major contributors to vision loss and associated functional impairment for years to come. Early detection of retinopathy in persons with diabetes is critical in preventing visual loss, but current methods of screening fail to identify a sizable number of high-risk patients. The control of diabetes-associated metabolic abnormalities (ie, hyperglycemia, hyperlipidemia, and hypertension) is also important in preserving visual function, as these conditions have been identified as risk factors for both the development and progression of DR/DME. The non-pharmacologic interventions for DR/DME, laser photocoagulation and vitrectomy, only target advanced stages of disease. Several biochemical mechanisms, including increased vascular endothelial growth factor production, protein kinase C beta activation, oxidative stress, and accumulation of intracellular sorbitol and advanced glycosylation end products, may contribute to the vascular disruptions that characterize DR/DME. The inhibition of these pathways holds the promise of the intervention for diabetic retinopathy with higher success rate and also at earlier, non-sight-threatening stages.
Diabetic retinopathy (DR) is the most common complication of diabetes, being the most prevalent reason for blindness among the working-age population in the developed world. Despite constant improvement of understanding of the pathogenesis of DR, identification of novel biomarkers of DR is needed for improvement of patient risk stratification and development of novel prevention and therapeutic approaches. The ubiquitin-proteasome system (UPS) is the primary protein quality control system responsible for recognizing and degrading of damaged proteins. This review aims to summarize literature data on modifications of UPS in diabetes and DR. First, we briefly review the structure and functions of UPS in physiological conditions. We then describe how UPS is involved in the development and progression of diabetes and touch upon the association of UPS genetic factors with diabetes and its complications. Further, we focused on the effect of diabetes-induced hyperglycemia, oxidative stress and hypoxia on UPS functioning, with examples of studies on DR. In other sections, we discussed the association of several other mechanisms of DR (endoplasmic reticulum stress, neurodegeneration etc) with UPS modifications. Finally, UPS-affecting drugs and remedies are reviewed. This review highlights UPS as a promising target for the development of therapies for DR prevention and treatment and identifies gaps in existing knowledge and possible future study directions.
The mean frequency of ophthalmological check-ups should vary between one year in diabetic patients without fundus changes and six months in patients with background retinopathy. Shorter screening intervals are needed in proliferative stages, during gravidity and adolescence and in cases with loss of vision. Fluorescein angiography is indicated if the treatment modality is based on its results (focal laser treatment in significant macular edema or panretinal photocoagulation in early proliferative or severe pre-proliferative stages). Theory and practice differ markedly. A questionnaire sent 1988 to 146 ophthalmologists and internists revealed that in Switzerland probably no more than one-half of all diabetic patients are regularly seen by an ophthalmologist. An actual questionnaire given to all 58 diabetic patients seen within 3 months in our eye clinic shows that about one quarter of the patients were not aware of the risk of diabetic eye disease.
Although hyperglycemia is the main instigator in the development of diabetic retinopathy, elevated circulating levels of a non-protein amino acid, homocysteine, are also associated with an increased risk of retinopathy. Homocysteine is recycled back to methionine by methylenetetrahydrofolate reductase (MTHFR) and/or transsulfurated by cystathionine β-synthase (CBS) to form cysteine. CBS and other transsulfuration enzyme cystathionine-γ-lyase (CSE), through desulfuration, generates H2S. Methionine cycle also regulates DNA methylation, an epigenetic modification associated with the gene suppression. The aim of this study was to investigate homocysteine and its metabolism in diabetic retinopathy.
The apoptosis of human umbilical vein endothelial cells has been reportedly induced by the protein transthyretin (TTR). In human ocular tissue, TTR is generally considered to be secreted mainly by retinal pigment epithelial cells (hRPECs); however, whether TTR affects the development of neovascularization in diabetic retinopathy (DR) remains unclear.
Diabetes and gestational diabetes (GD) are areas of concern worldwide. GD can eventually lead to serious development of diabetic retinopathy (DR) during pregnancy or worsening of an already existing DR. GD confers future risk of diabetes, both in the mother and fetus, further complicating their lives. DR in pregnant women has been intriguing in terms of understanding the prevalence, assessing risk factors causing pathogenesis, and problems associated with treating them. Pregnancy itself is a risk factor for progression of DR. Physiological changes such as metabolic, vascular, immunologic, and hormonal changes that occur during pregnancy can cause development as well as worsening of DR. This can eventually lead to permanent visual loss if not addressed on time. Timing of laser, choice of treatment for diabetic macular edema with laser, intravitreal anti-vascular endothelial growth factor agents (VEGF), and intravitreal steroids pose a serious challenge in managing these patients without causing damage to the mother and fetus. This review article showcases the prevalence, risk factors, and pathogenesis, outlines the management of DR in pregnancy, and recommends guidelines based on the available evidence. PubMed and MEDLINE searches were performed pertaining to the prevalence of GD in India, DR in pregnancy, risk factors for progression of DR, role of vasoactive mediators in DR, role of angiopoietic factors in DR, hormonal influence of DR, role of growth factors in DR, use of fluorescein and indocyanine green angiography, retinal lasers, anti-VEGF agents, intravitreal steroids, anesthesia, and retinal surgery, all pertaining to pregnancy and guidelines and recommendations for managing DR in pregnancy.
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