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At least 595 records · Page 33Linked to original sources
PubMed1977

Closed vitreous surgery: XV. Fibrovascular ingrowth from the pars plana sclerotomy.

Ten eyes developed fibrovascular ingrowth from the sclerotomy following closed vitreous surgery. The complication was detected by examining all patients postoperatively by indirect ophthalmoscopy and biomicroscopy with a three-mirror lens. The average follow-up was 13.2 months. Nine patients had proliferative retinal disease prior to surgery and related systemic disease. In six eyes, useful vision was lost due to the ingrowth. In three eyes, a stabilization occurred. In one eye, that of a 12-year-old girl with an undefined syndrome of cochlear and retinal neovascularization, the ingrowth involuted. Rubeosis iridis was observed in 6 eyes that developed vascular ingrowth as opposed to 11 eyes in a control group of 78 eyes. Eyes with rubeosis iridis should not have vitreous surgery, and careful dissection of the Tenon capsule should be done over the sclerotomy.

Adolescent↗
PubMed1984

Retinal vascular changes in malignant melanoma of the choroid.

A review of fluorescein angiograms from 41 patients with malignant melanoma of the choroid showed that 11 patients (27%) had evidence of retinal vascular abnormalities. Abnormal retinal capillaries were found in eight cases, areas of capillary nonperfusion in seven cases, and microaneurysms in four cases. Lipid exudation, retinal neovascularization, and arteriovenous communication were noted in one case each. Histopathologic studies in eight cases showed extensive degeneration of the overlaying retina in all eight cases and extension through Bruch's membrane by the tumor in four cases. Abnormal capillary architecture was demonstrated by trypsin digest preparations from four cases.

Adult↗
PubMedDate not supplied

[Occurrence of changes in the eye in diabetic retinopathy with significant myopia].

The optic disc and retinal neovascularization are less prominent and less frequent in myopic eyes in patients suffering from diabetes mellitus. The exact mechanisms of this phenomenon are not well known, but there is some evidence that there is a reduced blood flow in myopic eyes which is associated with less damaged microcirculation in eyes of patients with diabetes mellitus. The aim of our study was to evaluate the correlation between myopic refractive error and degree of diabetic retinopathy. We conducted a retrospective study in a group of randomized patients, divided into the following groups according to their refractive error: emmetropia (30 eyes), myopia simplex (30 eyes) and high myopia, over -6.5 dsph (21 eyes). Among patients with high myopia, seven had monocular myopia. All patients suffered from non insulin dependent diabetes mellitus for more than ten years, and their average age was 52.37-3.48 years. We did not observe patients with rubeosis iridis and neovascular glaucoma or patients with myopia less than -2.0 dsph. Our results indicated that there was no significant difference in the appearance of fundus between the studied groups. In all patients the incidence rate of non proliferative and proliferative diabetic retinopathy was the same as well as the absence of retinopathy (Fisher's test). The only exception were the patients with monocular myopia over -13.o dsph who had no signs of diabetic retinopathy in myopic eye, while the other, emmetropic eye, showed various stages of retinopathy, from severe non proliferative to proliferative. Some of the risk factors which influence the incidence rate of ocular complications in diabetic patients are well known, as are duration of diabetes mellitus, blood sugar level, blood pressure, ocular pressure and eye perfusion. On the other hand, it is also known that amblyopia, optic atrophy, low blood pressure in central retinal artery and retinitis pigmentosa are ocular conditions which are not associated with proliferative diabetic retinopathy. It was also noticed that complications of diabetes in high myopic eyes are less prominent than in emmetropic eyes. This finding is in harmony with our results. Sultanov et al. observed diabetic changes in the retina in 40.9% of myopic refraction patients, 65.2% of emmetropia cases and 70.4% of hypermetropia cases. The severity of involvement was less in myopia than in other types of refraction. In medium severe myopia, no proliferative diabetic retinopathy was observed, and in high myopia (10 eyes) no diabetic involvement of the fundus oculi was found. In anisometropia diabetic symptoms on the myopic side were either absent or poorly manifest. The possible cause of such findings could be the changes in retinal perfusion in myopic eyes and eyes in patients with diabetes mellitus. In 1973 a lower blood flow was detected in the retina and the choroid, proportionally to the degree of myopia. In 1982, Perkins indicated that the circulation time and pulsation rate in the central retinal artery in myopic eyes were reduced proportionally to the degree of myopia. In cases with early diabetic retinopathy Coscas detected a lesser blood flow in retinal veins. On the other hand, it has been found that high blood pressure increases the risk of diabetic retinopathy. These data suggest that the reduced blood flow in high myopia is a protective factor regarding the occurrence of complications in diabetes. Anisometropia and amblyopia in cases with monocular myopia, which presents a particular group in our study, could be factors which also prevent the occurrence of proliferative diabetic retinopathy. Instead of conclusion, we would like to point out that pathophysiologic mechanisms of these phenomena are not discussed enough. It is, nevertheless, important to appropriately examine the fundus in patients with high myopia and diabetes mellitus, because if the complications appear, they may be disastrous and must be treated immediately.

Diabetic Retinopathy↗
PubMed2001

Low IGF-I suppresses VEGF-survival signaling in retinal endothelial cells: direct correlation with clinical retinopathy of prematurity.

Retinopathy of prematurity is a blinding disease, initiated by lack of retinal vascular growth after premature birth. We show that lack of insulin-like growth factor I (IGF-I) in knockout mice prevents normal retinal vascular growth, despite the presence of vascular endothelial growth factor, important to vessel development. In vitro, low levels of IGF-I prevent vascular endothelial growth factor-induced activation of protein kinase B (Akt), a kinase critical for endothelial cell survival. Our results from studies in premature infants suggest that if the IGF-I level is sufficient after birth, normal vessel development occurs and retinopathy of prematurity does not develop. When IGF-I is persistently low, vessels cease to grow, maturing avascular retina becomes hypoxic and vascular endothelial growth factor accumulates in the vitreous. As IGF-I increases to a critical level, retinal neovascularization is triggered. These data indicate that serum IGF-I levels in premature infants can predict which infants will develop retinopathy of prematurity and further suggests that early restoration of IGF-I in premature infants to normal levels could prevent this disease.

Base Sequence↗
PubMed1991

A prospective evaluation of anterior retinal cryoablation in neovascular glaucoma.

We report a prospective evaluation of the effect of anterior retinal cryopexy on 62 eyes with neovascular glaucoma. Pain was relieved and anterior chamber inflammatory reaction regressed dramatically in 95%. Iris neovascularization was reduced or regressed in 93.5%. Control of intraocular pressure was clinically significant in 82.3% 1 year after the procedure, especially in patients with pretreatment pressures less than 40 mm Hg on maximal medical therapy. Anterior retinal cryopexy is recommended in eyes with media opacities and as a preliminary procedure for filtering surgery in eyes with neovascular glaucoma.

Adolescent↗
PubMed2005

The role of omega-3 long-chain polyunsaturated fatty acids in health and disease of the retina.

In this work we advance the hypothesis that omega-3 (omega-3) long-chain polyunsaturated fatty acids (LCPUFAs) exhibit cytoprotective and cytotherapeutic actions contributing to a number of anti-angiogenic and neuroprotective mechanisms within the retina. omega-3 LCPUFAs may modulate metabolic processes and attenuate effects of environmental exposures that activate molecules implicated in pathogenesis of vasoproliferative and neurodegenerative retinal diseases. These processes and exposures include ischemia, chronic light exposure, oxidative stress, inflammation, cellular signaling mechanisms, and aging. A number of bioactive molecules within the retina affect, and are effected by such conditions. These molecules operate within complex systems and include compounds classified as eicosanoids, angiogenic factors, matrix metalloproteinases, reactive oxygen species, cyclic nucleotides, neurotransmitters and neuromodulators, pro-inflammatory and immunoregulatory cytokines, and inflammatory phospholipids. We discuss the relationship of LCPUFAs with these bioactivators and bioactive compounds in the context of three blinding retinal diseases of public health significance that exhibit both vascular and neural pathology. How is omega-3 LCPUFA status related to retinal structure and function? Docosahexaenoic acid (DHA), a major dietary omega-3 LCPUFA, is also a major structural lipid of retinal photoreceptor outer segment membranes. Biophysical and biochemical properties of DHA may affect photoreceptor membrane function by altering permeability, fluidity, thickness, and lipid phase properties. Tissue DHA status affects retinal cell signaling mechanisms involved in phototransduction. DHA may operate in signaling cascades to enhance activation of membrane-bound retinal proteins and may also be involved in rhodopsin regeneration. Tissue DHA insufficiency is associated with alterations in retinal function. Visual processing deficits have been ameliorated with DHA supplementation in some cases. What evidence exists to suggest that LCPUFAs modulate factors and processes implicated in diseases of the vascular and neural retina? Tissue status of LCPUFAs is modifiable by and dependent upon dietary intake. Certain LCPUFAs are selectively accreted and efficiently conserved within the neural retina. On the most basic level, omega-3 LCPUFAs influence retinal cell gene expression, cellular differentiation, and cellular survival. DHA activates a number of nuclear hormone receptors that operate as transcription factors for molecules that modulate reduction-oxidation-sensitive and proinflammatory genes; these include the peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and the retinoid X receptor. In the case of PPAR-alpha, this action is thought to prevent endothelial cell dysfunction and vascular remodeling through inhibition of: vascular smooth muscle cell proliferation, inducible nitric oxide synthase production, interleukin-1 induced cyclooxygenase (COX)-2 production, and thrombin-induced endothelin 1 production. Research on model systems demonstrates that omega-3 LCPUFAs also have the capacity to affect production and activation of angiogenic growth factors, arachidonic acid (AA)-based vasoregulatory eicosanoids, and MMPs. Eicosapentaenoic acid (EPA), a substrate for DHA, is the parent fatty acid for a family of eicosanoids that have the potential to affect AA-derived eicosanoids implicated in abnormal retinal neovascularization, vascular permeability, and inflammation. EPA depresses vascular endothelial growth factor (VEGF)-specific tyrosine kinase receptor activation and expression. VEGF plays an essential role in induction of: endothelial cell migration and proliferation, microvascular permeability, endothelial cell release of metalloproteinases and interstitial collagenases, and endothelial cell tube formation. The mechanism of VEGF receptor down-regulation is believed to occur at the tyrosine kinase nuclear factor-kappa B (NFkappaB). NFkappaB is a nuclear transcription factor that up-regulates COX-2 expression, intracellular adhesion molecule, thrombin, and nitric oxide synthase. All four factors are associated with vascular instability. COX-2 drives conversion of AA to a number angiogenic and proinflammatory eicosanoids. Our general conclusion is that there is consistent evidence to suggest that omega-3 LCPUFAs may act in a protective role against ischemia-, light-, oxygen-, inflammatory-, and age-associated pathology of the vascular and neural retina.

Adolescent↗
PubMed2000

Retinal and choroidal neovascularization.

The unique vascular supply of the retina, the ability to visualize the vasculature in vivo, and the ability to selectively express genes in the retina make the retina an ideal model system to study molecular mechanisms of angiogenesis. In addition, this area of investigation has great clinical significance, because retinal and choroidal neovascularization are the most common causes of severe visual loss in developed countries and new treatments are needed. As a result, interest in ocular neovascularization is rapidly growing and there has been considerable recent progress. Use of genetically engineered mice in recently developed murine models provides a means to investigate the role of individual gene products in neovascularization in two distinct vascular beds, the retinal vasculature and the choroidal vasculature. It appears that angiogenesis in different vascular beds has common themes, but also has tissue-specific aspects. This review summarizes recent progress in the field of ocular neovascularization and the prospects that it provides for the development of new treatments.

Adult↗
PubMed2003

Neovascular ingrowth site photothrombosis in choroidal neovascularization associated with retinal pigment epithelial detachment.

PURPOSE: To describe the clinical, angiographic and optical coherence tomography (OCT) findings of patients with choroidal neovascularization (CNV) associated with retinal pigment epithelial detachment (PED) who were treated by neovascular ingrowth site photothrombosis. METHODS: Interventional case reports. After identification of the CNV feeder vessels, two patients had focal photothrombosis of the neovascular ingrowth site using continuous 810-nm laser application after intravenous indocyanine green (ICG) injection and were prospectively followed with fluorescein and ICG angiography as well as OCT. RESULTS: Both patients presented an increase of 3 or more ETDRS lines in visual acuity by 12 months of follow-up. Fluorescein and ICG angiography demonstrated reduced lesion perfusion and regression of the PEDs; accordingly, OCT disclosed decrease in retinal thickness and elevation caused by rapid fluid resolution. There were no significant complications related to the procedure. CONCLUSION: Photothrombosis using 810-nm light to direct laser energy continuously at the neovascular ingrowth site after intravenous ICG infusion is effective in restoring macular architecture and improving vision in patients with CNV complicated by PEDs by means of substantial decrease in the lesion perfusion and resolution of exudative manifestations.

Aged↗
PubMed2002

Regulation of angiogenesis in diabetic retinopathy: possible balance between vascular endothelial growth factor and endostatin.

OBJECTIVE: To investigate the mechanisms of regulation between vascular endothelial growth factor (VEGF) as a stimulator and endostatin as an inhibitor of angiogenesis in diabetic retinopathy (DR). METHODS: One hundred fifty-nine eyes of 120 diabetic patients were studied. Concentrations of VEGF and endostatin in vitreous fluid and aqueous humor, obtained from the eyes during ocular surgery, were measured by enzyme-linked immunosorbent assay. The severity of DR was quantified according to the Early Treatment Diabetic Retinopathy Study retinopathy severity scale; fundus findings, including soft exudates, intraretinal microvascular abnormalities, venous abnormalities, new vessels elsewhere, new vessels on the disc, vitreous hemorrhage, and retinal detachment, were graded and evaluated. Concentrations of VEGF and endostatin in plasma were also measured by enzyme-linked immunosorbent assay. MAIN OUTCOME MEASURES: Concentrations of VEGF and endostatin in vitreous fluid and plasma. The correlations among the clinical records and the levels of VEGF and endostatin were analyzed statistically. RESULTS: The concentrations of VEGF in aqueous humor and vitreous fluid were significantly correlated with the severity of DR (rho = 0.447, P<.001 and rho = 0.363, P =.007, respectively). The concentrations of endostatin in aqueous humor and vitreous fluid were also significantly correlated with the severity of DR (rho = 0.302, P<.001 and rho = 0.344, P =.009, respectively). The slope of the regression line between the VEGF and endostatin concentrations in vitreous fluid differed significantly between active DR and quiescent DR (P =.04). The concentrations of VEGF and endostatin in the eyes were not correlated with those in the plasma. CONCLUSIONS: These results show that both VEGF and endostatin are correlated with angiogenesis in DR. Our study suggests that the regulation mechanism between VEGF and endostatin is associated with the activity of DR and may be a good candidate to develop useful therapeutic agents for proliferative DR.

Adult↗
PubMed1995

Diabeteslike proliferative retinal changes in galactose-fed dogs.

OBJECTIVE: To determine whether diabeteslike lesions associated with the proliferative stage of diabetic retinopathy develop in galactose-fed dogs, since studies designed to define the complex biochemical effects of prolonged hyperglycemia on retinal vessels have been hampered by the lack of an animal model that mirrors both the early and advanced stages of diabetic retinopathy. METHODS: Eyes from 9-month-old male beagles fed a daily diet containing either 30% nonnutrient filler (control diet) or 30% galactose (galactose diet) for up to 84 months were enucleated and histologically examined. RESULTS: Retinal vessel changes associated with the proliferative stage were observed in two of nine galactose-fed dogs while the remainder demonstrated retinal changes that included the appearance of microaneurysms, acellular capillary beds associated with areas of nonperfusion, and intraretinal microvascular abnormalities. Proliferative changes were evidenced by the formation of preretinal fibrous membranes and the appearance of fibrovascular membranes on the retinal surface and on the posterior hyaloid membrane. No retinal lesions were observed in similar dogs fed a control diet for up to 84 months. CONCLUSION: The galactose-fed dog appears to be the first animal model that can develop diabeteslike retinal vessel changes associated with both the early and advanced stages of retinopathy, including the proliferative stage.

Animals↗
PubMed2005

Pigment epithelium-derived factor induces the production of chemokines by rat microglia.

Many studies have shown that pigment epithelium-derived factor (PEDF) has neurotrophic effects on retinal cells and hippocampal, spinal cord, and cerebellar granule cell neurons, but much less work has examined the effects of PEDF on glia. In this study, we show that PEDF changes microglial morphology within 1 h of exposure, to a more deactivated form, while having no effect on the expression of such activation markers as OX-42 and ED-1. In contrast, urea activates acid phosphatase, and PEDF blocks that activation. PEDF also activates NFkappaB, accompanied by the induction of mRNAs and proteins for the chemokines macrophage inflammatory protein-1alpha (MIP-1alpha, MIP-2, and MIP-3alpha. All the chemokines stimulate acid phosphatase activity, and high doses of MIP-2 and MIP-3alpha), alter the morphology of the microglia at 1 h after treatment. These results suggest that the use of PEDF for clinical treatments, such as for retinal neovascularization, brain injury, or ischemia, should be undertaken with caution because of the possibility of induction of inflammation caused by microglial or other immune cell migration in response to the chemokines induced by PEDF.

Acid Phosphatase↗
PubMed1993

Characterisation of the neovascularisation process in diabetic retinopathy by means of fractal geometry: diagnostic implications.

The neovascularisation formation and regression process of the peripheral retina in diabetic retinopathy was studied by means of fractal analysis. The fractal dimension of the local retinal vessel pattern was calculated to be significantly lower before formation of relevant neovascularisations than 2.5 years later, after formation of strong preretinal neovascularisations. Another year later the new vessels had regressed partially and the fractal dimension was again significantly reduced. This behaviour is almost independent of the representation of the vessel thickness during calculation. Since the retinal vasculature is a fractal, the fractal dimension appears as the "natural" measure of proliferative retinal vessel changes. It is demonstrated that the fractal dimension can be applied to characterise proliferative diabetic retinopathy. These features offer the possibility for computer-driven ("automated") quantitative characterisation of the treatment effect in proliferative diabetic retinopathy and possibly automated detection of proliferative diabetic retinopathy in the future. The limitations of the method are discussed.

Diabetic Retinopathy↗
PubMed2005

Retinal neovascularisation without ischaemia in the spontaneously diabetic Torii rat.

AIMS/HYPOTHESIS: The spontaneously diabetic Torii (SDT) rat has recently been established as a model of type 2 human diabetes mellitus. Male SDT rats develop severe diabetic ocular complications. This study investigated the nature of the ocular complications in this model and addressed the question of whether the SDT rat is a good model of human proliferative diabetic retinopathy. METHODS: Male SDT rats aged 50 weeks were studied for a period of 8 months. Under deep anaesthesia, one eye of each animal was enucleated following perfusion with fluorescein dextran and a retinal flat mount was prepared to study vascular structure. The other eye was enucleated and investigated histologically by haematoxylin-eosin and azan staining and by immunohistochemistry using antibodies against vascular endothelium (Griffonia simplicifolia isolectin B4 antibody) and vascular endothelial growth factor (VEGF). RESULTS: From the vascular structure study, 17 of 32 rats (53%) showed proliferative retinopathy without vascular non-perfusion. The histological study revealed traction retinal folds in rats with proliferative retinopathy. Azan staining showed some proliferative matrix in rats with normal retinal structure and those with proliferative retinopathy compared with normoglycaemic controls. Staining with Griffonia simplicifolia isolectin B4 antibody showed no specific vascular changes in any of the rats, while VEGF staining revealed higher immunoreactivity in the retina of rats with normal retinal structure and those with proliferative retinopathy, but only low immunoreactivity in the control animals. CONCLUSIONS/INTERPRETATION: There appear to be differences between the SDT rat model of diabetic retinopathy and human proliferative diabetic retinopathy, as the SDT rat develops retinal neovascularisation without retinal ischaemia. This very unique display of ocular neovascularisation may be caused by increased expression of VEGF.

Animals↗