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Results for “Retinal Neovascularization”

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At least 19 recordsLinked to original sources
PubMed1989

Diabetes as a risk factor for retinal neovascularization in retinal vein occlusion.

We evaluated a series of patients with retinal vein occlusive disease to determine whether diabetic patients with vein occlusions developed retinal neovascularization more frequently than did nondiabetics. Retinal neovascularization occurred in 68.8% of diabetics after central retinal vein occlusion compared with 27.8% of nondiabetics. Diabetics with branch retinal vein occlusions showed no greater likelihood for subsequent retinal neovascularization than did nondiabetics.

Diabetic Retinopathy↗
PubMed1990

[Moschcowitz syndrome and retinal neovascularization with retinal detachment].

The authors examined a patient with thrombotic thrombocytopenic purpura (Moschcowitz's disease). Six months after the patient was first seen with massive bilateral vascular occlusion, she presented with advanced retinal neovascularization in both eyes and traction retinal detachment in the left eye. While traction retinal detachment is a very rare sequela of this hematologic disorder, patients with Moschocowitz's disease should be carefully examined for early signs of ocular neovascularization in order to prevent loss of residual vision.

Adult↗
PubMed1979

Infrequency of retinal neovascularization following central retinal vein occlusion.

Forty-eight patients with the clinical diagnosis of central retinal vein occlusion and ten surgically enulceated eyes with central retinal vein occlusion documented by histopathologic examination were studied and reviewed. Retinal neovascularization developed in only one of the ten eyes. Rubeosis iridis occurred in 14% (7) of the clinical cases and in all of the histopathologic cases. Ten eyes with neovascular glaucoma, enucleated following central retinal vein occlusion, showed absence of retinal endothelial cells. The absence of retinal capillary endothelial cells is significant in explaining the rare occurrence of retinal neovascularization following central retinal vein occlusion. However, the small number of cases may reflect a biased result. Further studies of more cases over a longer period are required to reach the final conclusion.

Humans↗
PubMed1979

Infrequency of retinal neovascularization following central retinal vein occlusion attributed to endothelial death.

48 patients with central retinal vein occlusion by clinical diagnosis and 10 eyes by histopathological documentation were studied and reviewed. Only 1 eye developed retinal neovascularization. Rubeosis iridis occurs in 14% of clinical cases and all of histopathologic cases. 10 long-standing neovascular glaucoma enucleated eyes following central retinal vein occlusion show absence of retinal endothelial cells. The absence of retinal capillary endothelial cells seems to be significant in explaining the rare occurrence of retinal neovascularization following central retinal vein occlusion. However, the small number sampling may reflect a biased result. Further prospective studies with more cases and time observation are required to draw the final conclusion.

Capillaries↗
PubMed1987

Retinal neovascularization after branch retinal arterial obstruction.

We examined two eyes from two noninsulin-dependent diabetic patients that developed vitreous hemorrhage secondary to retinal neovascularization after branch retinal arterial obstruction. Although there was no ophthalmoscopic evidence of diabetic retinopathy, diabetes mellitus may have predisposed the retinas to a neovascular response, which was precipitated by the arterial obstruction.

Adult↗
PubMed1986

Retinitis pigmentosa and retinal neovascularization.

Four patients with retinitis pigmentosa and either disc or peripheral retinal neovascularization with recurrent vitreous hemorrhage are described. One patient with peripheral retinal neovascularization also had rubeosis and neovascular glaucoma. The effects of relative hyperoxia on the retinal microcirculation in retinitis pigmentosa as well as intraocular inflammation may account for such changes. Laser photocoagulation appears effective in preventing vitreous hemorrhage in these patients, but systemic administration of corticosteroids did not cause the new vessels to regress.

Adult↗
PubMed1989

[Role of the vitreous in retinal neovascularization evaluated by a comparison of central retinal vein occlusion and branch retinal vein occlusion].

Thirty three patients (33 eyes) with central retinal vein occlusion (CRVO) and 80 patients (81 eyes) with branch retinal vein occlusion (BRVO) were studied in an attempt to investigate the role of the vitreous in the formation of retinal neovascularization. All these eyes had some areas of capillary nonperfusion confirmed by fluorescein angiography and no scatter photocoagulation before the first examination. The incidence of new vessels at the optic disc (NVD) in CRVO was not significantly different from that in BRVO. However, the incidence of new vessels elsewhere (NVE) in CRVO was significantly less than that in BRVO. Follow-up vitreous examination of 36 cases while they had not developed NVD and/or NVE showed a higher incidence of posterior vitreous detachment from the mid-peripheral retina (MP-PVD) in CRVO than in BRVO. On the other hand, there was no statistically significant difference in the incidence of posterior vitreous detachment from the optic disk (D-PVD) between CRVO and BRVO. The high incidence of MP-PVD in CRVO may explain the low incidence of NVE in CRVO.

Adult↗
PubMed1987

Breakdown of the blood-retinal barrier in a model of retinal neovascularization.

Breakdown in the blood-retinal barrier occurs in retinal neovascularization in a number of diseases. To study the anatomic basis of this breakdown, we examined retinal neovascularization induced by injection of 250,000 homologous fibroblasts into the vitreous cavity of pigmented rabbits. Neovascularization is evident by electron microscopy in this model 3 days after fibroblast injection. Fluorescein angiography followed by intravenous horseradish peroxidase (HRP) injection was performed prior to enucleation on 2, 3, 5, 7, and 14 days after fibroblast injection. Fluorescein leakage from retinal vessels occurs early (at day 1) and persists as the neovascularization progresses. The leakage in the early stages is concentrated near puckers from the medullary wings. In the later stages, fluorescein leakage is most prominent in the developing tips of the new vessels. Horseradish peroxidase was not observed to leak from the lumen of new vessels. "Gaps" or separations in the endothelial cell junctions were not observed in developing vessels. The breakdown of the blood-retinal barrier in this model of retinal neovascularization is therefore selective, (ie, fluorescein leaks but not HRP) and it is not due to gaps or fenestrations between endothelial cells in developing vessels.

Animals↗
PubMed1976

The role of lactic acid in retinal neovascularization.

In order to gain information on the possible role of lactate in the development of neovascularization following retinal malperfusion, the lactate content in vitreous-retina-choroid specimens of 02-treated kittens and streptozotocin-diabetic rats was determined. In both experiments there was no significant difference of lactate content between the diseased eyes and healthy controls.

Animals↗
PubMedDate not supplied

[Pathogenesis of retinal neovascularization].

Presented are the causes and actual opinions on the pathogenesis of retinal neovascularization. The ischaemic hypothesis of neovascularization is particularly discussed; it is commonly accepted to day as the most probable hypothesis.

Arteriovenous Malformations↗
PubMed1989

[Treatment of retinal neovascularization secondary to branch vein occlusion with argon laser photocoagulation].

20 cases (22 eyes) of retinal neovascularization (RNV) secondary to branch vein occlusion were treated with argon laser photocoagulation. The RNV and the area of nonperfusion in these eyes were detected by fluorescein angiography. The results showed that argon laser photo coagulation was a highly effective therapy for RNV which was refractory to treatment. Photocoagulation minimized or resolved RNV and prevented recurrent vitreous hemorrhage. The relationship of RNV with the area of nonperfusion, the selection of the direct or indirect modality, and the points of note for success and prevention of complications were discussed.

Adult↗
PubMed1977

Peripheral retinal neovascularization in sarcoidosis and sickle cell anemia.

A 30-year-old black woman with biopsy-proven sarcoidosis and sickle cell anemia had peripheral retinal neovascularization. Elevated fibrovascular proliferations and distal retinal ischemia with nonperfused ghost vessels passing through the area of neovascularization were found at the temporal periphery. No signs of intraocular inflammation were present. Both diseases occur in black patients and should always be considered in the presence of peripheral retinal neovascularization.

Adult↗
PubMed1977

Experimental retinal neovascularization induced by intravitreal tumors.

Adult rabbit retinal vessels underwent neovascularization in response to tumor implantation within the vitreous body. The neovascular response was presumably elicited by the tumor angiogenesis factor (TAF). The response of adult retinal vessels to an angiogenic stimulus raises the possibility that a similar substance may cause retinal neovascularization in humans, and that in normal conditions the vitreous may be able to suppress angiogenic activity.

Angiogenesis Inducing Agents↗
PubMed1985

Peripheral retinal neovascularization in diabetes mellitus.

The cases of seven patients with diabetes mellitus and peripheral proliferative retinopathy (retinal neovascularization at or anterior to the equator) were studied. Associated abnormalities found included systemic arterial hypertension in five, a positive fluorescent treponemal antibody titer in four, and benign monoclonal gammopathy, intravenous drug abuse and hemoglobin AS each in one patient. The presence of additional systemic diseases should be suspected in diabetic patients with predominantly peripheral proliferative retinopathy.

Adult↗
PubMed1978

A new approach to the problem of retinal neovascularization.

Tumor cells introduced into the rabbit vitreous produced a form of retinal neovascularization, but only when the tumor cells were in direct contact with the vascularized retina. This contrasted with the production of neovascularization at a distance of several millimeters in other angiogenesis models. An extract of adult rabbit vitreous was found to inhibit the growth of limbal neovascularization induced by tumors implanted in the rabbit corneal stroma. The experimental model of retrolental fibroplasia provides a bioassay to investigate further the apparent inhibitory substances in the vitreous.

Angiogenesis Inducing Agents↗
PubMed1988

Peripheral retinal neovascularization and rubeosis iridis after a bilateral circular buckling operation.

This report describes a young high-myopic patient who developed rubeosis iridis with peripheral retinal neovascularization one year after a circular buckling operation. Subsequently, vitreous bleeding and exudation led to traction retinal detachment which was treated successfully by anterior vitrectomy and cryopexy. It is suggested that this case represents a mild form of anterior-segment ischemia, combined with peripheral retinal ischemia.

Child↗
PubMed1979

Disk and peripheral retinal neovascularization secondary to talc and cornstarch emboli.

A 30-year-old man was examined because of blurred vision. The symptoms had occurred immediately after the patient had injected himself intravenously with crushed, unfiltered, methylphenidate HCl (Ritalin) tablets. Fine yellow-white crystals were scattered throughout the retin of both eyes. The crystals were presumed to be talc emboli. Disk and peripheral retinal neovascularization were present. Fluorescein angiography revealed widespread retinal capillary nonperfusion. This is the first reported case, to the best of my knowledge, of disk neovascularization occurring after intravenously injected, crushed, unfiltered, methylphenidate HCl tablets.

Adult↗