Pathophysiology Of Diabetic Retinopathy
We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Diabetes is now regarded as an epidemic, with the population of patients expected to rise to 380 million by 2025. Tragically, this will lead to approximately 4 million people around the world losing their sight from diabetic retinopathy, the leading cause of blindness in patients aged 20 to 74 years. The risk of development and progression of diabetic retinopathy is closely associated with the type and duration of diabetes, blood glucose, blood pressure, and possibly lipids. Although landmark cross-sectional studies have confirmed the strong relationship between chronic hyperglycaemia and the development and progression of diabetic retinopathy, the underlying mechanism of how hyperglycaemia causes retinal microvascular damage remains unclear. Continued research worldwide has focussed on understanding the pathogenic mechanisms with the ultimate goal to prevent DR. The aim of this paper is to introduce the multiple interconnecting biochemical pathways that have been proposed and tested as key contributors in the development of DR, namely, increased polyol pathway, activation of protein kinase C (PKC), increased expression of growth factors such as vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1), haemodynamic changes, accelerated formation of advanced glycation endproducts (AGEs), oxidative stress, activation of the renin-angiotensin-aldosterone syst Continue reading >>
Diabetic Retinopathy
Pregnancy can impair blood glucose control and thus worsen retinopathy. Nonproliferative retinopathy (also called background retinopathy) develops first and causes increased capillary permeability, microaneurysms, hemorrhages, exudates, macular ischemia, and macular edema (thickening of the retina caused by fluid leakage from capillaries). Proliferative retinopathy develops after nonproliferative retinopathy and is more severe; it may lead to vitreous hemorrhage and traction retinal detachment. Proliferative retinopathy is characterized by abnormal new vessel formation (neovascularization), which occurs on the inner (vitreous) surface of the retina and may extend into the vitreous cavity and cause vitreous hemorrhage. Neovascularization is often accompanied by preretinal fibrous tissue, which, along with the vitreous, can contract, resulting in traction retinal detachment. Neovascularization may also occur in the anterior segment of the eye on the iris; neovascular membrane growth in the anterior chamber angle of the eye at the peripheral margin of the iris can occur, and this growth leads to neovascular glaucoma. Vision loss with proliferative retinopathy may be severe. Clinically significant macular edema can occur with nonproliferative or proliferative retinopathy and is the most common cause of vision loss due to diabetic retinopathy. Vision symptoms are caused by macular edema or macular ischemia. However, patients may not have vision loss even with advanced retinopathy. The first signs of nonproliferative retinopathy are Hard exudates are discrete, yellow particles within the retina. When present, they suggest chronic edema. Cotton-wool spots are areas of microinfarction of the retinal nerve fiber layer that lead to retinal opacification; they are fuzzy-edged and Continue reading >>
Proliferative Diabetic Retinopathy: Pathophysiology Of Extraretinal Complications And Principles Of Vitreous Surgery
Extraretinal complications of proliferative diabetic retinopathy are caused by neovascular and/or fibrovascular tissue growth and include vitreous hemorrhage, retinal detachment, and other effects damaging the retina and/or optic nerve. Exact features of fibrovascular tissue growth and secondary complications vary widely from case to case. However, the structural pathogenesis of this disease process is consistent because the abnormal tissue nearly always grows along the posterior vitreous surface. Therefore, differing topographic features and secondary complications are dependent on: (1) the places of origin and amount of fibrovascular proliferation, and (2) the location and extent of any posterior vitreous separation. The latter influences the configuration of the fibrovascular tissue growth and determines the effect on the underlying and adjacent retina. Surgical treatment of proliferative diabetic retinopathy is based on this fundamental structural pathophysiology. The principles of surgery are to minimize damaging effects by reversing the optical and structural complications and preventing recurrence of similar problems. Therefore, the objectives of surgery are to remove any intravitreal opacities and to excise the posterior vitreous surface. To achieve these objectives, various specialized techniques are required, depending on the complexity of the vitreoretinal anatomy in each case. Still, when the objectives are achieved, the operation has similar beneficial immediate and long-term effects in most eyes. This paper discusses and illustrates the structural pathology of proliferative diabetic retinopathy and the principles and methods of surgical therapy, and it presents the results obtained and the complications encountered. The Ophthalmic Communications Society, Continue reading >>
Mechanism Of Diabetic Retinopathy
The retina Enlarge Light enters the eye from the left in this diagram...shown by the yellow arrow. It passes through the clear jelly of the eye (the vitreous) to reach the retina (pink) Retinopathy is a disease of the retina, occurring in about a quarter of people with diabetes. How does the eye 'work'? Light enters the eye from the front, and passes through the eye to hit the retina, just like in a camera. The retina contains cells that convert the light into the electric signals, and these signals are then sent on to the brain so we can see. Two types of diagram are used in the descriptions in this section about retinopathy. First, a side or 'cut through' view of the eye, like a cut through drawing of a camera as opposite (upper picture). Second, the view the doctor sees when he looks into your eye, like a map, with the blood vessels spreading out from the centre (the optic nerve). The yellow dot is the fovea, where light is focused. The red & blue lines are the larger retinal blood vessels spreading out from the optic nerve. How does the retina work? Light ...in yellow... falls onto the retina. The retinal cells are rods (the long straight cells) and cones (the cells with the pointed end). There are tiny blood vessels (capillaries) on the surface of the retina ...the red ovals enlarge The retinal cells stand next to each other, a bit like houses in a street. The main cells are the rods and cones: these are the cells that take up light and convert it into electrical messages, which are then sent onto the brain. These cells receive their oxygen and other nutrients from tiny blood vessels nearby. These blood vessels are like pipes which pass nearby the cells; imagine a largish pipe passing past your house, containing blood. The walls of these pipes/blood vessels are ver Continue reading >>
Ijms | Special Issue : Diabetic Retinopathy: Mechanisms Underlying Pathophysiology And Therapies
Interests: neuroscience; physiology of the retina and central nervous system; mechanisms of neurodegenerative diseases; calcium signaling; electrophysiology The identification of mechanisms underlying the pathophysiology and therapies of diabetic retinopathy continues to be an area of significant research efforts, attracting scientists from a diverse range of fields, including neuroscience, pharmacology, and medicinal chemistry among several others. With the ultimate goal to generate intervention strategies that slow or even reverse structural and functional degeneration of the retina and that attenuate or eliminate vascular complications input from numerous fields, such as neurology, ophthalmology, and endocrinology appears critically needed as effective therapies for diabetic retinopathy are lacking. Research efforts towards treating or curing diabetic retinopathy are characteristic for how clinical practice, basic and translational research inform each other and how such interactions can result in novel therapeutic strategies of high clinical relevance. Recent methodological advances in synthetic and medicinal chemistry, mass spectrometry, proteomics, drug target discovery and drug development have generated significant developments in this field. Therefore, this Special Issue invites manuscript submissions, namely research and review papers, targeting the gamut of methodological and scientific innovation in this field. Of specific interest to this special issue are papers focused on the discovery and mechanistic characterization of novel drug targets, signaling pathways, and mechanisms of action as they are relevant for diabetic retinopathy. These contributions can be general and broad in their basic science and translational research focus or highly focused on spe Continue reading >>
Diabetic Retinopathy
Practice Essentials Diabetes mellitus (DM) is a major medical problem throughout the world. Diabetes causes an array of long-term systemic complications that have considerable impact on the patient as well as society, as the disease typically affects individuals in their most productive years. [1] An increasing prevalence of diabetes is occurring throughout the world. [2] In addition, this increase appears to be greater in developing countries. The etiology of this increase involves changes in diet, with higher fat intake, sedentary lifestyle changes, and decreased physical activity. [3, 4] Patients with diabetes often develop ophthalmic complications, such as corneal abnormalities, glaucoma, iris neovascularization, cataracts, and neuropathies. The most common and potentially most blinding of these complications, however, is diabetic retinopathy, [5, 6, 7] which is, in fact, the leading cause of new blindness in persons aged 25-74 years in the United States. Approximately 700,000 persons in the United States have proliferative diabetic retinopathy, with an annual incidence of 65,000. An estimate of the prevalence of diabetic retinopathy in the United States showed a high prevalence of 28.5% among those with diabetes aged 40 years or older. [8] (See Epidemiology.) The exact mechanism by which diabetes causes retinopathy remains unclear, but several theories have been postulated to explain the typical course and history of the disease. [9, 10] See the image below. In the initial stages of diabetic retinopathy, patients are generally asymptomatic, but in more advanced stages of the disease patients may experience symptoms that include floaters, distortion, and/or blurred vision. Microaneurysms are the earliest clinical sign of diabetic retinopathy. (See Clinical Presentat Continue reading >>
Pathophysiology And Management Of Diabetic Retinopathy: Pathophysiology Of Diabetic Retinopathy
Fong DS, Aiello L, Gardner TW et al. American Diabetes Association. Diabetic retinopathy. Diabetes Care 26 (1), 226-229 (2003). Mizutani M, Kern TS, Lorenzi M. Accelerated death of retinal microvascular cells in human and experimental diabetic retinopathy. J. Clin. Invest. 97(12), 2883-2890 (1996). Hammes HP, Strodter D, Weiss A, Bretzel RG, Federlin K, Brownlee M. Secondary intervention with aminoguanidine retards the progression of diabetic retinopathy in the rat model. Diabetologia 38(6), 656-660 (1995). Barber AJ, Lieth E, Khin SA, Antonetti DA, Buchanan AG, Gardner TW. Neural apoptosis in the retina during experimental and human diabetes. Early onset and effect of insulin. J. Clin. Invest. 102(4), 783-791 (1998). Abu-El-Asrar AM, Dralands L, Missotten L, Al-Jadaan IA, Geboes K. Expression of apoptosis markers in the retinas of human subjects with diabetes. Invest. Ophthalmol. Vis. Sci. 45(8), 2760-2766 (2004). Abu El-Asrar AM, Dralands L, Missotten L, Geboes K. Expression of antiapoptotic and propapoptotic molecules in diabetic retinas. Eye 21(2), 238-245 (2007). Kern TS, Barber AJ. Retinal ganglion cells in diabetes. J. Physiol. 586(Pt 18), 4401-4408 (2008). Mizutani M, Gerhardinger C, Lorenzi M. Mller cell changes in human diabetic retinopathy. Diabetes 47(3), 445-449 (1998). Krady JK, Basu A, Allen CM et al. Minocycline reduces proinflammatory cytokine expression, microglial activation, and caspase-3 activation in a rodent model of diabetic retinopathy. Diabetes 54(5), 1559-1565 (2005). Decanini A, Karunadharma PR, Nordgaard CL, Feng X, Olsen TW, Ferrington DA. Human retinal pigment epithelium proteome changes in early diabetes. Diabetologia 51(6), 1051-1061 (2008). The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment o Continue reading >>
Diabetic Retinopathy
Print Overview Diabetic retinopathy (die-uh-BET-ik ret-ih-NOP-uh-thee) is a diabetes complication that affects eyes. It's caused by damage to the blood vessels of the light-sensitive tissue at the back of the eye (retina). At first, diabetic retinopathy may cause no symptoms or only mild vision problems. Eventually, it can cause blindness. The condition can develop in anyone who has type 1 or type 2 diabetes. The longer you have diabetes and the less controlled your blood sugar is, the more likely you are to develop this eye complication. Symptoms You might not have symptoms in the early stages of diabetic retinopathy. As the condition progresses, diabetic retinopathy symptoms may include: Spots or dark strings floating in your vision (floaters) Blurred vision Fluctuating vision Impaired color vision Dark or empty areas in your vision Vision loss Diabetic retinopathy usually affects both eyes. When to see a doctor Careful management of your diabetes is the best way to prevent vision loss. If you have diabetes, see your eye doctor for a yearly eye exam with dilation — even if your vision seems fine. Pregnancy may worsen diabetic retinopathy, so if you're pregnant, your eye doctor may recommend additional eye exams throughout your pregnancy. Contact your eye doctor right away if your vision changes suddenly or becomes blurry, spotty or hazy. Causes Over time, too much sugar in your blood can lead to the blockage of the tiny blood vessels that nourish the retina, cutting off its blood supply. As a result, the eye attempts to grow new blood vessels. But these new blood vessels don't develop properly and can leak easily. There are two types of diabetic retinopathy: Early diabetic retinopathy. In this more common form — called nonproliferative diabetic retinopathy (NPDR) Continue reading >>
Pathophysiology And Pathogenesis Of Diabetic Retinopathy
@inbook{27976cae086c4ae3abb384133f826681, title = "Pathophysiology and Pathogenesis of Diabetic Retinopathy", abstract = "Diabetic retinopathy is traditionally viewed as a disease of the retinal blood vessels, although there is increasing evidence that retinal neurons and glial cells are also affected. This article describes the changes in the diabetic retina that precede the development of clinical diabetic retinopathy, including changes in the rate of retinal blood flow, alterations in the electroretinogram and breakdown of the integrity of the blood-retinal barrier. The long term lesions of diabetic retinopathy are characterised by a complex array of vasodegenerative changes that lead directly to areas of retinal ischaemia. This frequently triggers the onset of macular oedema and/or the proliferative stages of diabetic retinopathy with risk of visual impairment and blindness. Neurodegeneration has also been reported in the retina during both human and experimental diabetic retinopathy, although presently it remains unclear to what extent such changes contribute to visual loss in diabetic retinopathy.", author = "Heping Xu and Tim Curtis and Alan Stitt", N2 - Diabetic retinopathy is traditionally viewed as a disease of the retinal blood vessels, although there is increasing evidence that retinal neurons and glial cells are also affected. This article describes the changes in the diabetic retina that precede the development of clinical diabetic retinopathy, including changes in the rate of retinal blood flow, alterations in the electroretinogram and breakdown of the integrity of the blood-retinal barrier. The long term lesions of diabetic retinopathy are characterised by a complex array of vasodegenerative changes that lead directly to areas of retinal ischaemia. This Continue reading >>
Diabetic Retinopathy Biomolecules And Multiple Pathophysiology - Sciencedirect
Volume 9, Issue 1 , JanuaryMarch 2015, Pages 51-54 Diabetic retinopathy Biomolecules and multiple pathophysiology Author links open overlay panel HaseebAhsan Get rights and content One of the major complications in patients with diabetes is diabetic retinopathy (DR), a leading cause of blindness worldwide. It causes visual impairment and finally blindness, a result of long-term accumulated damage to the small blood vessels in the retina. It takes several years before any clinical symptoms of retinopathy appear in diabetic patients. Consequently, glycemic control, blood pressure and lipid-lowering therapy have all shown benefits in reducing the incidence and progression of DR. A number of hyperglycemia-induced metabolic stresses have been implicated in the pathophysiology of DR. The microvasculature of the retina responds to hyperglycemia through a number of biochemical changes, including the activation of protein kinase C (PKC), increased advanced glycation end-products (AGEs) formation, polyol pathway and oxidative stress. There is an accumulating body of evidence indicating that inflammation and neurodegeneration play an important role in the pathogenesis of DR. Continue reading >>
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Diabetic Retinopathy
Diabetic retinopathy, also known as diabetic eye disease, is a medical condition in which damage occurs to the retina due to diabetes and is a leading cause of blindness.[1] It affects up to 80 percent of people who have had diabetes for 20 years or more.[2] At least 90% of new cases could be reduced if there were proper treatment and monitoring of the eyes.[3] The longer a person has diabetes, the higher his or her chances of developing diabetic retinopathy.[4] Each year in the United States, diabetic retinopathy accounts for 12% of all new cases of blindness. It is also the leading cause of blindness for people aged 20 to 64 years.[5] Signs and symptoms[edit] Normal vision The same view with diabetic retinopathy. Emptied retinal venules due to arterial branch occlusion in diabetic retinopathy (fluorescein angiography) Diabetic retinopathy often has no early warning signs. Even macular edema, which can cause rapid vision loss, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive. In some cases, the vision will get better or worse during the day. In the first stage which is called non-proliferative diabetic retinopathy (NPDR) there are no symptoms, the signs are not visible to the eye and patients will have 20/20 vision. The only way to detect NPDR is by fundus photography, in which microaneurysms (microscopic blood-filled bulges in the artery walls) can be seen. If there is reduced vision, fluorescein angiography can be done to see the back of the eye. Narrowing or blocked retinal blood vessels can be seen clearly and this is called retinal ischemia (lack of blood flow). Macular edema in which blood vessels leak their contents into the macular regi Continue reading >>
Pathophysiology Of Diabetic Retinopathy
[1] A. G. Burditt, F. I. Caird, and G. J. Draper, e natural history of diabetic retinopathy, e Quarterly Journal of Medicine, vol. [2] R. Klein, B. E. K. Klein, and S. E. Moss, e Wisconsin epi- demiologic study of diabetic retinopathy. IV. Diabetic macular edema, Ophthalmology, vol. 91, no. 12, pp. 14641474, 1984. [3] R. Klein, B. E. K. Klein, and S. E. Moss, Epidemiology of proliferative diabetic retinopathy, Diabetes Care, vol. 15, no. 12, [4] D. R. Matthews, I. M. Stratton, S. J. Aldington, R. R. Holman, and E. M. Kohner, Risks of progression of retinopathy and vision loss related to tight blood pressure control in type 2 diabetes mellitus: UKPDS 69, Archives of Ophthalmology, vol. [5] N. H. White, P. A. Cleary, W. Dahms et al., Benecial eects of intensive therapy of diabetes during adolescence: Outcomes aer the conclusion of the Diabetes Control and Complications Trial (DCCT), e Journal of Pediatrics, vol. 139, no. 6, pp. [6] K. H. Gabbay, Hyperglycemia, polyol metabolism, and com- plications of diabetes mellitus, Annual Review of Medicine, vol. [7] J. H. Kinoshita, A thirty year journey in the polyol pathway, Experimental Eye Research, vol. 50, no. 6, pp. 567573, 1990. [8] K. H. Gabbay, e sorbitol pathway and the complications of diabetes, e New England Journal of Medicine, vol. 288, no. 16, [9] B. S. Szwergold, F. Kappler, and T. R. Brown, Identication of fructose 3-phosphate in the lens of diabetic rats, Science, vol. [10] P. A. Barnett, R. G. Gonzalez, L. T. Chylack, and H. M. Cheng, e eect of oxidation on sorbitol pathway kinetics, Diabetes, [11] B. Lassgue and R. E. Clempus, Vascular NAD(P)H oxidases: specic features, expression, and regulation, American Journal of Physiology, vol. 285, no. 2, pp. R277R297, 2003. [12] R. N. Frank, R. J. Keirn, A. Kennedy, and Continue reading >>
Pathophysiology Of Diabetic Macular Edema
Pathophysiology of Diabetic Macular Edema Joussen A.a,b Smyth N.b,c Niessen C.b aDepartment of Ophthalmology, University of Duesseldorf, Duesseldorf, and bCenter for Molecular Medicine, University of Cologne, Cologne, Germany; cSchool of Biological Sciences, University of Southampton, Southampton, UK I have read the Karger Terms and Conditions and agree. I have read the Karger Terms and Conditions and agree. Buy a Karger Article Bundle (KAB) and profit from a discount! If you would like to redeem your KAB credit, please log in . Save over 20% compared to the individual article price. Buy Cloud Access for unlimited viewing via different devices Immediate access to all parts of this book * The final prices may differ from the prices shown due to specifics of VAT rules. Diabetic maculopathy is the leading cause of visual loss in diabetic patients. The pathogenesisis not fully understood and a satisfactory therapy is currently not available. Malfunctionof the blood-retinal barrier plays a central role in the disease and leads to retinal edema and secondaryphotoreceptor dysfunction. Diabetic vascular leakage and macular edema are regulatedby a distinct combination of direct paracellular transport, alterations in endothelial intercellularjunctions and endothelial cell death. The distribution and relevance of these three factors to diabeticmaculopathy varies over the course of the disease. Cumulative endothelial cell death willbecome more relevant after prolonged diabetic conditions. This article reviews the currentknowledge on the pathogenic mechanisms of diabetic macular edema. Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopyin Continue reading >>
Pathophysiology And Pathogenesis Of Diabetic Retinopathy
Acute and chronic complications of diabetes Creators: Heping Xu , Timothy Curtis , Alan Stitt Diabetic retinopathy is traditionally viewed as a disease of the retinal blood vessels, although there is increasing evidence that retinal neurons and glial cells are also affected. This article describes the changes in the diabetic retina that precede the development of clinical diabetic retinopathy, including changes in the rate of retinal blood flow, alterations in the electroretinogram and breakdown of the integrity of the blood-retinal barrier. The long term lesions of diabetic retinopathy are characterised by a complex array of vasodegenerative changes that lead directly to areas of retinal ischaemia. This frequently triggers the onset of macular oedema and/or the proliferative stages of diabetic retinopathy with risk of visual impairment and blindness. Neurodegeneration has also been reported in the retina during both human and experimental diabetic retinopathy, although presently it remains unclear to what extent such changes contribute to visual loss in diabetic retinopathy. Early functional changes in the diabetic retina The earliest suggestion that retinal perfusion may be altered in diabetes came from studies in the 1930s which showed that the calibre of retinal vessels is increased in diabetes. Direct evidence for changes in retinal perfusion during diabetes came nearly 40 years later with the development of techniques for measuring blood flow from fluorescein angiograms [1] . Various techniques have been used since then to measure blood flow in the retina of individuals with diabetes, including the blue-field entoptic technique [2] , laser Doppler flowimetry [3] and laser speckle imaging [4] . Despite some discrepancies between studies, in general individuals wit Continue reading >>
The Diabetic Retina: Anatomy And Pathophysiology
The Diabetic Retina: Anatomy and Pathophysiology Throughout the world diabetic retinopathy (DR) has emerged as a major cause of permanent loss of vision among people over the age of 20 years. Retinopathy has generally been considered a vasculopathy that results from breakdown of the blood-retinal barrier and closure of retinal capillaries. Recent evidence, however, suggests that DR begins as a neuro-retinopathy with vascular changes occurring later during the disease. Vascular Endothelial Growth FactorDiabetic RetinopathyRetinal Pigment EpitheliumMacular EdemaVascular Endothelial Growth Factor Level These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Abiko T, Abiko A, Clermont AC, et al. Characterization of retinal leukostasis and hemodynamics in insulin resistance and diabetes: role of oxidants and protein kinase-C activation. Diabetes. 2003;52(3):82937. PubMed CrossRef Google Scholar Adamiec-Mroczek J, Oficjalska-Myczak J. Assessment of selected adhesion molecule and proinflammatory cytokine levels in the vitreous body of patients with type 2 diabetes role of the inflammatory-immune process in the pathogenesis of proliferative diabetic retinopathy. Graefes Arch Clin Exp Ophthalmol. 2008;246:166570. PubMed CrossRef Google Scholar Adamis AP, Berman AJ. Immunological mechanisms in the pathogenesis of diabetic retinopathy. Semin Immunopathol. 2008;30(2):6584. PubMed CrossRef Google Scholar Adamis AP, Miller JW, Bernal MT, et al. Increased vascular endothelial growth factor levels in the vitreous of eyes with proliferative diabetic retinopathy. Am J Ophthalmol. 1994;118:44550. PubMed CrossRef Google Sch Continue reading >>
