Correlation of fluorescein angiogram and retinal digest in diabetic retinopathy.
About: This article is published in American Journal of Ophthalmology.The article was published on 1970-03-01. It has received 141 citations till now. The article focuses on the topics: Diabetic retinopathy & Retinal.
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TL;DR: It is shown that chronic, low‐grade subclinical inflammation is responsible for many of the signature vascular lesions of diabetic retinopathy, highlighting the central and causal role of adherent leukocytes in the pathogenesis of diabetes.
Abstract: 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.
1,077 citations
Cites background from "Correlation of fluorescein angiogra..."
...Histolopathological analyses have shown that areas of angiographic non-perfusion in vivo frequently co-localize to regions full of acellular capillaries, that is, basement membrane tubes devoid any viable endothelial cells or pericytes (7)....
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TL;DR: The inflammatory mediators and their relationship to early and late DR are reviewed, and the potential of anti-inflammatory approaches to inhibit development of different stages of the retinopathy is discussed.
878 citations
Cites background from "Correlation of fluorescein angiogra..."
...Capillary nonperfusion and degeneration also are important lesions of the early retinopathy (de Venecia et al., 1976; Kohner and Henkind, 1970), because they have been regarded as causal in the eventual progression to neovascularization (Shimizu et al....
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...Capillary nonperfusion and degeneration also are important lesions of the early retinopathy (de Venecia et al., 1976; Kohner and Henkind, 1970), because they have been regarded as causal in the eventual progression to neovascularization (Shimizu et al., 1981) as summarized in this simple…...
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TL;DR: It is emphasised that although there have been significant advances, there is still a pressing need for a better understanding basic mechanisms enable development of reliable and robust means to identify patients at highest risk, and to intervene effectively before vision loss occurs.
648 citations
TL;DR: Cerebral microvascular pathology in ageing and neurodegeneration is a major concern in the field of neuropathology and Applied Neurobiology.
Abstract: This review of age-related brain microvascular pathologies focuses on topics studied by this laboratory, including anatomy of the blood supply, tortuous vessels, venous collagenosis, capillary remnants, vascular density and microembolic brain injury. Our studies feature thick sections, large blocks embedded in celloidin, and vascular staining by alkaline phosphatase. This permits study of the vascular network in three dimensions, and the differentiation of afferent from efferent vessels. Current evidence suggests that there is decreased vascular density in ageing, Alzheimer's disease and leukoaraiosis, and cerebrovascular dysfunction precedes and accompanies cognitive dysfunction and neurodegeneration. A decline in cerebrovascular angiogenesis may inhibit recovery from hypoxia-induced capillary loss. Cerebral blood flow is inhibited by tortuous arterioles and deposition of excessive collagen in veins and venules. Misery perfusion due to capillary loss appears to occur before cell loss in leukoaraiosis, and cerebral blood flow is also reduced in the normal-appearing white matter. Hypoperfusion occurs early in Alzheimer's disease, inducing white matter lesions and correlating with dementia. In vascular dementia, cholinergic reductions are correlated with cognitive impairment, and cholinesterase inhibitors have some benefit. Most lipid microemboli from cardiac surgery pass through the brain in a few days, but some remain for weeks. They can cause what appears to be a type of vascular dementia years after surgery. Donepezil has shown some benefit. Emboli, such as clots, cholesterol crystals and microspheres can be extruded through the walls of cerebral vessels, but there is no evidence yet that lipid emboli undergo such extravasation.
629 citations
TL;DR: It is postulated that photocoagulative debridement of a disordered retinal pigment epithelium could be a mechanism of action of this treatment of diffuse macular edema.
358 citations
References
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TL;DR: Noteworthy has been the predominant localization of the diabetic microaneurysms in the central and paracentral regions, their random distribution, and their association with punctate hemorrhages and "exudates" in the deep retina.
Abstract: It is generally held that microaneurysms constitute the characteristic lesion of diabetic retinopathy. First observed by MacKenzie and Nettleship in 1879, 1 the microaneurysms were rediscovered by Ballantyne and Loewenstein in 1943 2 and have been described by numerous clinicians and pathologists since that time. Noteworthy has been the predominant localization of the diabetic microaneurysms in the central and paracentral regions, their random distribution, and their association with punctate hemorrhages and "exudates" in the deep retina. It has also been assumed that the microaneurysms and other evidence of angiopathy in diabetic retinas have a bearing on the glomerular changes in diabetic nephropathy 3-5 and that a clarification of the one might yield useful information for the other. As must be evident from the many reviews which have appeared in recent years, 6-12 the pathogenesis of retinal microaneurysms has been a subject of wide speculation based on some firm evidence but
715 citations
TL;DR: Findings were seen in hypertensive and diabetic patients, and, in addition, neovascularization was clearly defined, and some cotton-wool patches, but not hemorrhages, were found to fluoresce.
Abstract: A simple method, with use of intravenous fluorescein, was used for producing and photographing fluorescence in circulating blood of the human retina. Separate arteriolar and venous filling phases, arteriolovenous shunt, sluggish choroidal circulation, stratified flow of fluorescein, and rapid central retinal circulation times were observed in normal retinas. Similar findings were seen in hypertensive and diabetic patients, and, in addition, neovascularization was clearly defined, and some cotton-wool patches, but not hemorrhages, were found to fluoresce. Limitations and applications of the method are discussed.
625 citations
TL;DR: Flat preparations of the retina afford an unusually favorable opportunity to study blood vessel architecture (Ballantyne and Lowenstein 1 ).
Abstract: Flat preparations of the retina afford an unusually favorable opportunity to study blood vessel architecture (Ballantyne and Lowenstein 1 ). The retinal vessels have been visualized in the past by the following methods: 1. injection of India ink into the heart, major arteries, or directly into the retinal artery (Michaelsen, 2 Ashton, 3 Keeney and Barlow, 4 and others); 2. latex injection into the aorta (Janes 5 ); 3. benzidine-peroxidase staining of the red blood cells (Michaelsen 2 ); 4. infusion of silver nitrate with subsequent reduction of the silver to outline the reticular fibers, 6 and 5. staining of the full thickness of
409 citations
TL;DR: The purpose of this paper is to attempt an explanation for some aspects of diabetic retinopathy, based on a relatively new method of histologic visualization of retinal vessels utilizing incubation of the retina in a trypsin solution.
Abstract: The retina is a target organ of diabetes and a unique tissue in which to study one of the major vascular complications of this disease. Nowhere else in the body, with the possible but unproved exception of the conjunctiva, can this vascular disease be observed during life, and from no other tissue has it been possible to prepare whole mounts of the vessels after death in such a way as to permit combined topographic and cytologic study. It is the purpose of this paper to attempt an explanation for some aspects of diabetic retinopathy, based on a relatively new method of histologic visualization of retinal vessels utilizing incubation of the retina in a trypsin solution. While no one sign of diabetic retinopathy is pathognomonic of the disease, the aggregate of signs is highly characteristic. Ophthalmoscopic examination shows microaneurysms, hemorrhages, and white spots (called "exudates") predominantly in the posterior or central portions of the fundus. On the other hand, the larger retinal vessels, those which can be seen with the ophthalmoscope, are not necessarily abnormal. The phenomena requiring explanation are: the pathogenesis of microaneurysms; the involvement of vessels of a size less than that which can be seen with the ophthalmoscope (of capillary or paracapillary dimensions); the relationship, if any, between permeability of vessels and development of hemorrhages and "exudates"; and the preferential involvement of the posterior retina. Hemorrhage into the vitreous and proliferation of vessels into the vitreous also require some consideration, for, although they occur in many conditions, they are particularly frequent and run an especially malignant course in diabetes. Various histologic means have been employed to study diabetic retinopathy. Cross sections and flat sections of the retina have shown the microaneurysms clearly and have indicated that the natural course of these microaneurysms is a progressive thickening and eventual disintegration of their walls. Cross sections have shown
161 citations
TL;DR: Though no toxoplasma parasites have been discovered, and it is perhaps rather late to expect a positive finding, there can be no doubt concerning the diagnosis of toxoplasmosis, the mother's negative serum-reaction is difficult to explain.
103 citations