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At least 505 records · Page 28Linked to original sources

Vitreous Hemorrhage complicating laser-induced chorioretinal anastomosis for central retinal vein occlusion.

PURPOSE: To report a severe complication of laser chorioretinal anastomosis for central retinal vein occlusion. METHOD: Case report. RESULTS: In the right eye of a 62-year-old woman with nonischemic central retinal vein occlusion, retinal neovascularization at the laser chorioretinal anastomosis site caused dense secondary vitreous hemorrhage. Vitreous hemorrhage prevented laser panretinal photocoagulation for subsequent iris neovascularization, necessitating vitrectomy surgery to clear the hemorrhage and allow the treatment. CONCLUSION: Laser chorioretinal anastomosis can result in severe vitreous hemorrhage and complicate efforts to manage later sequelae of central retinal vein occlusion.

Anastomosis, Surgical↗

Scanning electron microscopy of the ocular vasculature in retinopathy of prematurity.

Clinicoanatomopathologic correlations in a case of the retinopathy of prematurity are reported. A premature infant delivered at 28 weeks of gestation (weight, 900 g) was hospitalized for a number of health problems, including bronchopulmonary dysplasia and respiratory distress syndrome. Ophthalmic examination, at the age of 5 months, disclosed stage 1B retinopathy of prematurity. The patient died at the age of 161 days; both eyes were taken for scanning electron microscopy and histopathologic studies. Scanning electron microscopy findings included absence of retinal capillaries, anterior uveal neovascularization originating from the venous side, and a coincidental typical coloboma of the optic nerve and choriocapillaris. Histopathologic findings confirmed iris stromal neovascularization, showed retinal neovascularization with proliferation into the vitreous and avascular areas between the midperiphery and ora serrata.

Blood Vessels↗

Atypical retinitis proliferans, retinal telangiectasis, and vitreous hemorrhage in a patient with tuberous sclerosis.

This report describes an unusual case of recurrent vitreous hemorrhage and atypical retinal neovascularization in a patient with tuberous sclerosis. During three years of observation, the patient also developed retinal telangiectasis with macular edema and lipid exudation. Although the patient did not have an obvious astrocytic hamartoma, a diffuse, flat retinal hamartoma within the nerve fiber layer was suspected.

Adult↗

An eye on insulin.

Diabetic retinopathy, the most frequent complication of diabetes and leading cause of vision loss, involves vascular and neural damage in the retina. Insulin and IGF-1 signaling are now shown to contribute to retinal neovascularization, in part, by modulating the expression of various vascular mediators.

Animals↗

Retinal pigment epithelial cells release an inhibitor of neovascularization.

Human retinal pigment epithelial cells in culture were found to release a substance (or substances) that causes the regression of new blood vessels on the chick embryonic yolk sac and inhibits proliferation of fetal bovine aortic endothelial cells in vitro. Neither astrocytes nor fibroblasts, under identical test conditions, released detectable inhibitors of neovascularization or endothelial cell growth. Subconfluent and superconfluent cultures of human retinal pigment epithelial cells released higher levels of inhibitor than confluent cultures.

Angiogenesis Inhibitors↗

Incidence of radiation retinopathy after high-dosage single-fraction gamma knife radiosurgery for choroidal melanoma.

OBJECTIVE: To investigate the incidence and clinical findings of radiation retinopathy after single-fraction high-dose gamma knife radiosurgery for choroidal melanoma. DESIGN: Retrospective noncomparative interventional case series. PARTICIPANTS: Thirty-two patients with choroidal melanoma. METHODS: Review of charts, color fundus photographs, and fluorescein angiograms of 32 choroidal melanoma patients after radiosurgery. All patients were treated with the Leksell gamma knife in one fraction with a marginal dose between 40 and 80 Gy (median, 50 Gy) and were followed for at least 24 months (or until enucleation because of complications secondary to radiation). MAIN OUTCOME MEASURES: Any clinical feature of radiation retinopathy and neovascular glaucoma. RESULTS: During a mean follow-up of 38 months (range, 6-81 months) we found radiation retinopathy in 84% of our patients. The most common findings in these patients were intraretinal hemorrhages with an incidence of 70%, macular edema and capillary nonperfusion in 63%, and hard exudates in 52% of the patients. Less common were microaneurysms in 30% and retinal neovascularization in 22%. The time of onset of the various radiation-associated retinal findings ranged between 1 and 22 months. Forty-seven percent of all patients developed neovascular glaucoma. In our study there was no correlation between radiation dosage applied and clinical findings. CONCLUSIONS: Single-fraction high-dose Leksell gamma knife radiosurgery of choroidal melanomas with a median marginal dose of 50 Gy is highly associated with early radiation retinopathy and with neovascular glaucoma.

Adult↗

Importance of fluorescein angiographic study in evaluating early retinal changes in Takayasu disease.

PURPOSE: To determine the usefulness of fluorescein angiography in studying Takayasu disease. METHODS: We examined 31 eyes in 16 patients with Takayasu disease using indirect ophthalmoscopy, color photography, and fluorescein angiography. Ophthalmoscopic and fluorescein angiographic findings were compared. RESULTS: Fluorescein angiography revealed no additional retinal changes in 10 eyes that had no retinal vein dilatation as seen by indirect ophthalmoscopy. Seven (33%) of 21 eyes that had dilated retinal veins also had additional abnormal findings, such as microaneurysms, arteriovenous shunts, retinal neovascularization, and avascular areas. Some differences in grading the stages of retinopathy were noted with these newly found retinal changes, as compared with the classifications determined by ophthalmoscopy alone. CONCLUSIONS: In Takayasu disease, studying the fundus of patients with fluorescein angiography is particularly important in correctly classifying the stages of retinopathy when the retinal vein appears dilated in ophthalmoscopic observation.

Adult↗

[Long-term course of indirect traumatic ruptures of the choroid].

During the last 10 years, 46 cases of indirect choroidal tears were observed with repeated photographies and fluorescein angiographies. Patients were essentially young men with a mean age of 21.7 years. Choroidal tears were mostly single (61%), localized in the temporal part of the optic disc (63.1%), crescent shaped (77.4), and extra-foveal (96.4%). Ten of the 37 cases with a follow-up developed a neo-vascular membrane. Two of these were extra-foveal and were successfully treated with Argon Laser photocoagulation. Sub-retinal neovascular membranes as well as various other complications related to the trauma, such as macular hole, sub-retinal fibrosis and atrophic changes of the retinal pigment epithelium in the macular area, were responsible for a final visual acuity less than 0.2 in 38% of the cases. The influence of the fragility of Bruch's membrane on the number of choroidal tears was evaluated by the relation between the age of the patients and the number of tears, younger patients presenting more often single choroidal tears: the difference is nevertheless not statistically significant. A careful follow-up with repeated fluorescein angiographies is recommended for at least the 2 years following the trauma.

Adolescent↗

Dexamethasone reduces oxygen induced retinopathy in a mouse model.

Dexamethasone is widely used in the postnatal period. Its impact on retinopathy of prematurity (ROP) is extremely controversial; published studies have found a detrimental, protective, or no effect on ROP. The goal of this study was to test the hypothesis that use of dexamethasone during the injury phase (oxygen exposure) reduces the severity of oxygen-induced retinopathy (OIR) in a mouse model. C57BL6 mice pups were exposed to either room air or hyperoxia (75% FiO2) from postnatal d 7 through 12 (PN7-12) with or without dexamethasone (0.5 mg/kg/d s.c.) and killed on PN17-21. Retinopathy was assessed by a scoring system of retinal flat mount preparations and periodic acid-Schiff (PAS) staining of retinal sections. Pups exposed to dexamethasone and oxygen had a lower median retinopathy score of 5 (4, 6) [median (25th, 75th quartile)] compared with animals exposed to oxygen alone with median score of 9 (6, 10) with p < 0.001. PAS staining for extra retinal neovascularization in the dexamethasone and oxygen treated animals showed a significant reduction in number of nuclei extending beyond the inner limiting membrane when compared with oxygen exposed alone (p = 0.04). Animals treated with dexamethasone had decreased weight gain compared with control animals. Dexamethasone did not appear to affect the normal development of retinal vasculature as assessed by the scoring system when compared with control animals. Thus, dexamethasone decreases severity of OIR without having an adverse effect on normal retinal vascular development in the mouse model. We speculate that dexamethasone decreases the injury response that occurs during the hyperoxic phase, thus protecting the developing vasculature and improving the subsequent retinopathy.

Animals↗

Pigment epithelium-derived factor inhibits retinal and choroidal neovascularization.

In this study, we investigated whether overexpression of pigment epithelium-derived factor (PEDF) by gene transfer can inhibit neovascularization by testing its effect in three different models of ocular neovascularization. Intravitreous injection of an adenoviral vector encoding PEDF resulted in expression of PEDF mRNA in the eye measured by RT-PCR and increased immunohistochemical staining for PEDF protein throughout the retina. In mice with laser-induced rupture of Bruch's membrane, choroidal neovascularization was significantly reduced after intravitreous injection of PEDF vector compared to injection of null vector or no injection. Subretinal injection of the PEDF vector resulted in prominent staining for PEDF in retinal pigmented epithelial cells and strong inhibition of choroidal neovascularization. In two models of retinal neovascularization (transgenic mice with increased expression of vascular endothelial growth factor (VEGF) in photoreceptors and mice with oxygen-induced ischemic retinopathy), intravitreous injection of null vector resulted in decreased neovascularization compared to no injection, but intravitreous injection of PEDF vector resulted in further inhibition of neovascularization that was statistically significant. These data suggest that sustained increased intraocular expression of PEDF by gene therapy might provide a promising approach for treatment of ocular neovascularization.

Adenoviridae↗

Retinal phlebitis with chorioretinal emboli.

Emboli to the eye may cause retinal vascular occlusive disease with a wide range of clinicopathologic manifestations including arteriolar occlusion, retinal ischemia and infarction, and retinal neovascularization. Clinical observations of a progressive obliterative arteriolitis in patients with systemic embolic disease have led to the speculation that retinal vasculitis may be a feature of ocular embolic disease. A postmortem examination of the enucleated eyes of two elderly female patients disclosed gross and histopathologic features of retinal periphlebitis associated with many chorioretinal calcific emboli. These patients also had premortem and postmortem manifestations of systemic thromboembolic disease originating from the heart and great vessels. One patient had a progressive decrease in visual acuity, paracentral scotoma, and midperipheral perivascular sheathing. These findings suggest that ocular embolism may sometimes be a factor in the development of retinal phlebitis.

Adult↗

Identification and quantification of renin and prorenin in the bovine eye.

Angiotensin-II, the most important biologically active product of the renin-angiotensin system, has been reported to play a role in neovascularization, and prorenin has been found in the vitreous of human eyes, particularly in those affected by proliferative diabetic retinopathy, a disease characterized by neovascularization. The prorenin level in these eyes was, relative to that of plasma albumin, higher than in eyes without neovascularization. These findings suggested that an intraocular renin-angiotensin system exists, which might be involved in the development of retinal neovascularization in diabetes mellitus. In this study angiotensin-I-generating activity was measured in bovine aqueous humor and vitreous and in extracts of bovine retina, pigment epithelium-choroid, and anterior uveal tract before and after subjecting these extracts to procedures known to convert prorenin to renin. The measurements were made by incubation at 37 C with plasma from nephrectomized rats at pH ranging from 5.0-8.5. True renin in the ocular samples could be separated from nonrenin acid protease by alpha-casein-Sepharose affinity column chromatography at pH 3.5; true renin did not bind to the column, whereas acid protease did. True renin was further identified by its relatively high pH optimum (6.5-7.0) for angiotensin-I generation, its complete inhibition with specific renin antiserum, and its high affinity for specific renin inhibitors. More than 75% of angiotensin-I-generating activity of the ocular samples consisted of true renin. Approximately 90% or more of total renin (renin plus prorenin) in aqueous humor, vitreous, and ocular tissue could not be explained by trapped plasma. Total renin in aqueous humor and renin in vitreous were near the detection limit of the assay of angiotensin-I-generating activity. In vitreous prorenin comprised 99% of the total renin, in retina 81%, and in pigment epithelium-choroid and anterior uveal tract less than 50%. Prorenin in ocular fluids showed a concentration gradient, posterior vitreous greater than anterior vitreous greater than aqueous humor, suggesting that the main source of extracellular prorenin was in the posterior eye. These data support the contention of local renin and/or prorenin synthesis in the eye and are in accordance with the observations in other tissues that extrarenal synthesis of renin is often associated with the release of mainly, or exclusively, prorenin into extracellular fluid.

Angiotensin I↗

Antineovascular agents in the treatment of eye diseases.

Neovascularization is a common and potentially visually threatening complication of eye diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). An antiangiogenic therapy is aimed at inhibiting the growth of new blood vessels and should prevent onset or progression of neovascularization. Accumulated evidence indicates that growth factors, endothelial cell surface receptors, and extracellular matrix (ECM) proteins are major mediators of neovascularization and appealing targets for pharmacotherapeutical intervention. Vascular endothelial growth factor (VEGF) plays a critical role in the pathogenesis of retinal neovascularization (in linking tissue ischemia to angiogenesis), and is likely to contribute also significantly to choroidal neovascularization (CNV). Several antineovascular agents antagonize the function of VEGF, by blocking its proangiogenic activity. Indeed, VEGF targeting or disruption of VEGF signalling is the most effective strategy known so far in the pharmacological treatment of ocular neovascularization. Other compounds such as pigment epithelium-derived factor (PEDF) either aim at balancing the levels of pro-angiogenic and angiostatic molecules, target inflammation (cyclooxygenase inhibitors, steroids) or comprise modifiers of the ECM such as inhibitors of matrix metalloproteinases (MMPs) and agents that block the action of integrins. Vascular targeting agents (combretastatin) promote removal of newly formed vessels. This review provides an update on recent investigations directed at the pharmacotherapeutical management of ocular neovascular diseases, placing special emphasis on the underlying target molecules and relevant intracellular signalling pathways.

Angiogenesis Inhibitors↗

Therapeutic angiogenesis: translating experimental concepts to medically relevant goals.

Angiogenesis is central to many physiological and pathological phenomena. In physiological angiogenesis, new vessels are well shaped and their growth is finely tuned to match the metabolic needs of tributary tissues. Accordingly, neovascularization is activated by physical exercise and destabilized by non-use. In contrast, pathological blood vessels that are observed in retinal neovascularization, cancer or in ischemic tissues are leaky, irregularly shaped, and tend to form arterial-venous fistulae. A great deal of attention is focused on new approaches for medical manipulation of vascular growth. These methods are aimed at facilitating the reperfusion of ischemic tissues or eradicating pathological vasculature. In this position paper, we challenge the rationale of therapeutic angiogenesis for the cure of myocardial and peripheral ischemia. Therapeutic angiogenesis aims at combating the insufficiency of, or insensitivity to angiogenic factors in the setting of atherosclerotic-induced arterial occlusion. However, clinical evidence indicates that such a defect is not common among patients with ischemic disease, as a whole. Genetic and environmental factors could account for the great heterogeneity in the expression of the master angiogenic factors. Future improvements in the strategy would require the introduction of in vitro assays and in vivo imaging systems for assessing human angiogenesis. Finally, the promise is to find individualized angiogenesis-based therapies for a genuine cure of ischemia and prevention of organ failure.

Angiogenesis Inducing Agents↗

Foveal haemorrhages in diabetic retinopathy. Clinical characteristics and visual outcome.

BACKGROUND: Haemorrhages from retinal vessels is one of the major clinical characteristics of diabetic retinopathy. Vitreous haemorrhages from retinal neovascularizations may extend to the visual axis and disturb central vision, whereas asymptomatic intraretinal haemorrhages may develop from ruptures of smaller retinal vessels. On rare occasions, however, smaller intraretinal haemorrhages may develop in the fovea, and consequently lead to a reduction in central vision. The clinical characteristics and visual outcome of these lesions have not been described in detail. METHODS: Clinical data of 4724 diabetic patients (31.4% with type 1 diabetes and 68.6% with type 2 or other diabetes types) examined in the screening clinic for diabetic retinopathy at the Department of Ophthalmology, Arhus University Hospital, 1993-1998 were reviewed. Patients who had had a previous foveal haemorrhage were subjected to a full ophthalmological reexamination. RESULTS: Six eyes of six patients with type 1 diabetes had previously had a foveal haemorrhage. The lesion had resulted in a visual reduction of on the average 1.4 visual acuity steps (SD=0.5, range:1-2, n=5), and resolution of the lesion was accompanied by an increase in visual acuity of on the average 1.2 visual acuity steps (SD=0.4, range: 1-2, n=6). Four of the patients had progressed to proliferative diabetic retinopathy and had received pan-retinal photocoagulation. CONCLUSIONS: Foveal haemorrhages in diabetic retinopathy are accompanied by a mild and transient reduction in central vision. The lesions predominate in patients with type 1 diabetes of long duration, and may indicate that retinopathy has developed into a moderate or severe stage.

Adult↗

Treatment of retinopathy of prematurity with topical ketorolac tromethamine: a preliminary study.

BACKGROUND: Retinopathy of Prematurity (ROP) is a common retinal neovascular disorder of premature infants. It is of variable severity, usually heals with mild or no sequelae, but may progress to blindness from retinal detachments or severe retinal scar formation. This is a preliminary report of the effectiveness and safety of a new and original use of topical ketorolac in preterm newborn to prevent the progression of ROP to the more severe forms of this disease. METHODS: From January 2001 to December 2002, all fifty nine preterm newborns with birthweight less than 1250 grams or gestational age less than 30 weeks of gestational age admitted to neonatal intensive care were eligible for treatment with topical ketorolac (0.25 milligrams every 8 hours in each eye). The historical comparison group included all 53 preterm newborns, with the same inclusion criteria, admitted between January 1999 and December 2000. RESULTS: Groups were comparable in terms of weight distribution, Apgar score at 5 minutes, incidence of sepsis, intraventricular hemorrhage and necrotizing enterocolitis. The duration of oxygen therapy was significantly longer in the control group. In the ketorolac group, among 43 children that were alive at discharge, one (2.3%) developed threshold ROP and cryotherapy was necessary. In the comparison group 35 children survived, and six child (17%) needed cryotherapy (Relative Risk 0.14, 95%CI 0.00 to 0.80, p = 0.041). Adjusting by duration of oxygen therapy did not significantly change these results. Adverse effects attributable to ketorolac were not detected. CONCLUSIONS: This preliminary report suggests that ketorolac in the form of an ophthalmic solution can reduce the risk of developing severe ROP in very preterm newborns, without producing significant adverse side effects. These results, although promising, should be interpreted with caution because of the weakness of the study design. This is an inexpensive and simple intervention that might ameliorate the progression of a disease with devastating consequences for children and their families. We believe that next logical step would be to assess the effectiveness of this intervention in a randomized controlled trial of adequate sample size.

Administration, Topical↗

Factors associated with visual outcome after photocoagulation for diabetic retinopathy. Diabetic Retinopathy Study Report #13.

Six risk factors for severe visual loss despite panretinal (scatter) photocoagulation were identified by analyzing data collected during the first 5 years after randomization in the Diabetic Retinopathy Study. Proportional hazards regression revealed NVD (neovascularization on/around the optic disc) to be the most important risk factor. The risk of severe visual loss rose with increasing NVD, hemorrhages/microaneurysms, retinal elevation, proteinuria, and hyperglycemia and fell with increasing "treatment density." These results are similar to previous DRS findings on untreated eyes. The importance of "treatment density" as an independent predictor of visual outcome is a new finding and lends support to the common clinical practice of repeating photocoagulation if initial treatment does not reduce or stabilize retinal neovascularization.

Aged↗