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Results for “Retinal Neovascularization”

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At least 307 records · Page 17Linked to original sources
PubMed2006

Intravitreal bevacizumab (Avastin) treatment of proliferative diabetic retinopathy complicated by vitreous hemorrhage.

PURPOSE: To report the short-term anatomic and visual acuity response after intravitreal injection of bevacizumab (Avastin, Genentech) in patients with proliferative diabetic retinopathy complicated by vitreous hemorrhage. METHODS: Two patients with vitreous hemorrhage due to proliferative diabetic retinopathy were treated with at least one intravitreal injection of bevacizumab 1.25 mg in 0.05 mL. The patients underwent Snellen visual acuity testing, ophthalmoscopic examination, and fluorescein angiography at baseline and follow-up visits. RESULTS: Both patients had proliferative diabetic retinopathy with vitreous hemorrhage extensive enough to preclude panretinal photocoagulation. Following intravitreal injection of bevacizumab both patients experienced improvement in visual acuity starting within the first week. At 1 month of follow-up one patient had 2 lines of improvement in visual acuity and the other 5 lines. Each patient had regression of retinal neovascularization at 1 month of follow-up. Repeat injection was given to one patient at the 1-month follow-up because of slight leakage from neovascularization on the nerve, and to the other patient at 3 months because the retinal neovascularization showed early signs of reperfusion. The vitreous hemorrhage in each patient showed partial resolution at 1 week and nearly complete regression at 1 month. No adverse events were observed in either patient. CONCLUSIONS: Initial treatment results of patients with vitreous hemorrhage and proliferative diabetic retinopathy did not reveal any short-term safety concerns. Intravitreal bevacizumab resulted in marked regression of neovascularization and rapid resolution of vitreous hemorrhage. The favorable short-term results suggest further study is needed in a larger group of patients.

Adult↗
PubMed1989

Rhegmatogenous retinal detachment associated with branch vein occlusion.

Proposed mechanisms for rhegmatogenous retinal detachment after branch retinal vein occlusion (BRVO) include hole development from preexisting retinal cysts and vitreoretinal traction secondary to retinal neovascularization. Damage caused by choriocapillary obstruction may also occur in some of the retinal breaks. Vitreoretinal traction without associated retinal neovascularization has not been previously emphasized as a pathogenetic mechanism. We document both iatrogenic and idiopathic vitreoretinal traction as causes of rhegmatogenous retinal detachment in ischemic retina after BRVO. A literature review of the role of retinal traction with and without associated neovascularization in the development of retinal tears after BRVO is included.

Aged↗
PubMed1987

Anterior hyaloidal fibrovascular proliferation after diabetic vitrectomy.

Vitrectomy was performed to treat 74 consecutive eyes for complications of diabetic retinopathy. Eight (13%) of 61 eyes followed up for an average of 12 months developed anterior hyaloidal fibrovascular proliferation. This was the most common postoperative complication, whose features included recurrent hemorrhages into the vitreous cavity or anterior vitreous, or both; vessels or fibrovascular tissue on the posterior lens capsule; anterior extraretinal vascularization extending toward the lens on the anterior hyaloid; traction detachment of the peripheral retina or ciliary body; and hypotony. Patients who developed this complication tended to be young males with severe retinal neovascularization and extensive retinal ischemia; traction retinal detachment as an indication for surgery; placement of a scleral buckle; postoperative rubeosis iridis, recurrent vitreous hemorrhages, and retinal detachment; and multiple surgeries. Four eyes progressed to atrophia bulbi. Early recognition followed by additional surgery in two patients and extensive additional photocoagulation in two other patients was successful in preserving good visual function.

Adult↗
PubMed1980

Talc retinopathy.

Twenty-three patients had bilateral intraretinal talc microemboli, which were seen on ophthalmoscopic examination. Twelve of these patients had additional retinal vascular or choroidal abnormalities in the posterior pole that were confirmed by fluorescein angiography. Six patients had peripheral retinal neovascularization associated with peripheral retinal vascular nonperfusion. Of these six patients, three had associated vitreous hemorrhage, and two had optic disk neovascularization and traction retinal detachment. The progressive fundus changes seen in talc retinopathy were documented by fluorescein angiography and compared to those seen in sickle-cell retinopathy. One eye in one patient was treated by argon laser photocoagulation for proliferative retinopathy, and three eyes in two patients with vitreous hemorrhage were treated by pars plana vitrectomy.

Adult↗
PubMed2002

A long-term follow-up of Eales' disease.

PURPOSE: To provide long-term follow-up information on Eales' patients. METHODS: Eales' patients, who had been examined at varying periods between the years 1970 and 1991 with a minimum five-year follow-up, were included in the study. RESULTS: A total of 130 patients were followed up for a minimum of five and a maximum of 26.5 years. The retinal lesions found during the first examination included vascular sheathing, disc and/or retinal neovascularization, vitreous hemorrhage, branch retinal vein occlusion, retinitis proliferans, and retinal detachment. Visual acuity improved in 37 (20%) of the 185 treated eyes, was maintained in 79 (43%), and worsened in 69 (37%). The complications were tractional detachment, cataract, rubeosis iridis, neovascular glaucoma, and phthisis bulbi. CONCLUSION: The most important elements in dealing with Eales' disease are periodic follow-up, a good and adequate laser treatment, pars plana vitrectomy combined with procedures for nonclearing vitreous hemorrhage, and retinal vasoproliferative changes to stabilize the retinal lesions and maintain functional levels of vision.

Adolescent↗
PubMedDate not supplied

Peripheral proliferative retinopathies.

Peripheral retinal neovascularization (i.e., new vessel growth peripheral to the major vascular arcades) may be secondary to a wide variety of ocular and systemic diseases. Vascular and inflammatory diseases in particular may cause peripheral neovascularization. Following a brief review of ocular angiogenesis, the various clinical entities that can cause peripheral retinal neovascularization are described. The diagnostic workup of a patient with peripheral proliferative retinopathy is outlined and techniques of treatment of the neovascularization (including feeder vessel technique, cryopexy, and panretinal photocoagulation) are discussed.

Adult↗
PubMed2002

Antiangiogenic effects of somatostatin analogues.

Inhibition of angiogenesis has become a target for antineoplastic therapy and for treatment of retinal neovascularization. The presence of somatostatin receptors on tumour cells and on the proliferating vascular endothelium has led to several in vitro and in vivo studies to investigate the antiproliferative and antiangiogenic effects of somatostatin analogues. Currently available data suggest that somatostatin analogues might inhibit angiogenesis directly through somatostatin receptors present on endothelial cells and also indirectly through the inhibition of growth factor secretion such as IGF-I and vascular endothelial growth factor (VEGF) and reducing monocyte chemotaxis. However, beneficial effects on inhibition of neovascularization have been questioned by some studies. More work is therefore required to firmly establish the role of somatostatin analogues as potential antiangiogenic therapy. The currently available somatostatin analogues have high affinity for somatostatin receptor subtype 2 (sst2) and, to a lesser extent, sst5 and sst3. However, because vascular endothelial cells express several types of somatostatin receptors, it will be important to investigate somatostatin analogues with different receptor subtype affinities, which might increase the spectrum of available therapy for tumours.

Angiogenesis Inhibitors↗
PubMed1996

Involvement of integrins alpha v beta 3 and alpha v beta 5 in ocular neovascular diseases.

Angiogenesis underlies the majority of eye diseases that result in catastrophic loss of vision. Recent evidence has implicated the integrins alpha v beta 3 and alpha v beta 5 in the angiogenic process. We examined the expression of alpha v beta 3 and alpha v beta 5 in neovascular ocular tissue from patients with subretinal neovascularization from age-related macular degeneration or the presumed ocular histoplasmosis syndrome or retinal neovascularization from proliferative diabetic retinopathy (PDR). Only alpha v beta 3 was observed on blood vessels in ocular tissues with active neovascularization from patients with age-related macular degeneration or presumed ocular histoplasmosis, whereas both alpha v beta 3 and alpha v beta 5 were present on vascular cells in tissues from patients with PDR. Since we observed both integrins on vascular cells from tissues of patients with retinal neovascularization from PDR, we examined the effects of a systemically administered cyclic peptide antagonist of alpha v beta 3 and alpha v beta 5 on retinal angiogenesis in a murine model. This antagonist specifically blocked new blood vessel formation with no effect on established vessels. These results not only reinforce the concept that retinal and subretinal neovascular diseases are distinct pathological processes, but that antagonists of alpha v beta 3 and/or alpha v beta 5 may be effective in treating individuals with blinding eye disease associated with angiogenesis.

Animals↗
PubMed2006

Inhibitive effect of genistein on interleukin-8 expression in cultured human retinal pigment epithelial cells.

Recent studies showed that interleukin-8 (IL-8) played an important role in retinal neovascularization. In this study, the effects of genistein on the expression of IL-8 in the arising retinal pigment epithelia-19 cells were studied. The levels of IL-8 protein expression in supernatants were punctually detected by ELISA. When the cells were treated with hypoxia (5% CO2, 95% N2), IL-8 secretion increased from 0.29 +/- 0.04 to 2.59 +/- 0.42 ng/ml. To study calcium-dependent IL-8 expression, cells were treated with KCl at 25 mM, norepinephrine (NE) at 10 nM, and glutamate (Glu) at 1 microM for 8 h. As a result, the levels of IL-8 protein in supernatants were significantly increased compared with that in the controls. When the cells are treated with genistein (50, 100, 200 microM) for 30 min before hypoxia or stimulations by KCl, NE, and Glu, the elevated expression of IL-8 protein was all suppressed in a concentration-dependent manner. These results suggested that suppression of IL-8 expression in retinal pigment epithelial cells might partly account for the inhibitive effect of genistein on retinal neovascularization.

Cell Hypoxia↗
PubMed1999

Tranilast inhibits protein kinase C-dependent signalling pathway linked to angiogenic activities and gene expression of retinal microcapillary endothelial cells.

1. Tranilast, first developed as an anti-allergic drug, has been reported to inhibit vascular endothelial growth factor (VEGF)-induced angiogenesis and vasopermeability. To further clarify the inhibitory mechanism, we investigated the effects of tranilast on VEGF binding and subsequent intracellular signalling pathway linked to angiogenic activities and gene expression of bovine retinal microcapillary endothelial cells. 2. Tranilast significantly (P<0.01) inhibited VEGF, basic fibroblast growth factor (bFGF), and hypoxia conditioned media-induced BREC proliferation in a dose dependent manner with IC50's of 22, 82 and 10 microM, respectively. 3. VEGF-induced migration was also inhibited by tranilast in a dose dependent manner, with IC50 of 18 microM, and complete inhibition was observed at 300 microM (P<0.01). Tranilast suppressed VEGF-induced tube formation in a dose dependent manner with maximum (46%) inhibition observed at 300 microM (P<0.05). 4. Tranilast inhibited phorbol myristate acetate (PMA)-dependent stimulation of [3H]-thymidine incorporation and VEGF- and PMA-induced gene expression of integrin alpha v and c-fos in BREC. 5. Tranilast suppressed VEGF- and PMA-stimulated PKC activity in BREC. 6. Tranilast did not affect VEGF binding or VEGF-induced phosphorylation of tyrosine residues of VEGF receptor- and phospholipase Cgamma and their associated proteins. 7. These data suggest that tranilast might prove an effective inhibitor to prevent retinal neovascularization in ischaemic retinal diseases, and that its inhibitory effect might be through suppression of PKC-dependent signal transduction in BREC.

Animals↗
PubMed1994

The photodynamic occlusion of choroidal vessels using benzoporphyrin derivative.

We used benzoporphyrin derivative-monoacid (BPD-MA), a new photosensitizing agent, in photodynamic therapy (PDT) to occlude choroidal vessels in the rabbit. Using BPD-MA, seven dutch-belted rabbit eyes were photodynamically treated to achieve acute choroidal vessel closure. Fundoscopy, fluorescein angiography (FA), and histology were performed 1 hour, 1 day, 3 days, 7 days, 14 days, 21 days, and 28 days after PDT. On FA, PDT-treated spots remained nonperfused until day 3 when gradual reperfusion from the periphery began to appear. By day 28 the area of PDT appeared completely reperfused. Histology of lesions showed acute damage to choroidal vascular endothelial cells and retinal pigment epithelial (RPE) cells. Over subsequent days, recovery of RPE cells and regeneration of large choroidal vascular endothelial cells occurred. In addition, retinal degeneration occurred gradually over the 28 days of follow-up. Since current argon laser therapy of retinal neovascularization causes immediate retinal damage, the ability to occlude choroidal vessels without inducing acute thermal damage holds promise for treating clinical pathologic conditions that feature abnormal neovascularization, such as age-related macular degeneration and diabetic retinopathy.

Animals↗
PubMed1988

Sarcoidosis and peripheral neovascularization.

Twenty-eight patients with sarcoidosis were examined. Four of the patients had a history of uveitis. Retinal periphlebitis was noted in one case, and peripheral retinal neovascularization was found in two non-sickle cell black patients. Vitreous hemorrhage developed in one of the patients with neovascularization, prior to laser treatment and this patient eventually required vitreous surgery. The other patient was treated with prophylactic laser. Peripheral retinal neovascularization may be a noteworthy finding that will be found in larger numbers with attention to the retinal periphery in cases of sarcoidosis.

Adult↗
PubMed1982

Ocular neovascularization with retinal vascular occlusion. I. Association with experimental retinal vein occlusion.

Experimental occlusion of both major temporal retinal veins simultaneously (in six eyes of cynomolgus monkeys) and of the central retinal vein (in one rhesus monkey) produced a fall in intraocular pressure (hypotensive effect) and neovascularization (NV) of the iris and, less frequently, of the optic disc (vasogenic effect). The retinal changes (severity and extent of retinopathy, retinal capillary leakage, and onset and extent of retinal capillary obliteration) were correlated with the pattern of ocular NV and hypotony. No direct correlation was seen between the retinal capillary obliteration and the hypotensive or vasogenic effect. However, a correlation was found between the retinal vascular leakage and the development of ocular NV and hypotony. The pathogeneses of ocular NV and hypotony in retinal vein occlusion are discussed in light of the findings of this study.

Animals↗
PubMed1988

Optic disk neovascularization and retinal vessel diameter in diabetic retinopathy.

We measured retinal vessel diameter before and after panretinal photocoagulation in 59 eyes with diabetic retinopathy and moderate to severe optic disk neovascularization. Treatment significantly reduced mean arteriolar and venular diameter. The diameter of the retinal arterioles after treatment correlated significantly with the amount of regression in disk neovascularization. Eyes with large diameter vessels after treatment usually had little or no regression of proliferative retinopathy, whereas regression was more frequently seen in eyes with smaller diameter vessels after treatment.

Arterioles↗
PubMed2002

Matrix metalloproteinase-9-dependent exposure of a cryptic migratory control site in collagen is required before retinal angiogenesis.

Retinal neovascularization is a leading cause of human blindness. However, little is known concerning the molecular mechanisms controlling retinal neovascularization in vivo. Here we provide evidence that exposure of a collagen type IV cryptic epitope detected by monoclonal antibody (mAb) HUIV26, delineates sites of vascular bud formation and represents one of the earliest structural remodeling events required before vessel out-growth. Exposure of these cryptic sites was inhibited in matrix metalloproteinase (MMP)-9-deficient but not MMP-2-deficient mice implicating MMP-9 in their exposure. Retinal endothelial cell interactions with the HUIV26 epitopes induced endothelial cell migration, which was blocked by mAb HUIV26. Importantly, subcutaneous administration of mAb HUIV26 potently inhibited retinal angiogenesis in vivo. Taken together, these findings suggest a novel mechanism in which MMP-9 facilitates exposure of HUIV26 cryptic sites, thereby promoting retinal endothelial cell migration and neovascularization in vivo.

Animals↗
PubMed1999

Human diabetic neovascular membranes contain high levels of urokinase and metalloproteinase enzymes.

PURPOSE: Retinal neovascularization is one of the leading causes of blindness. A crucial event in this process is the remodeling and penetration of the capillary basement membrane by migrating endothelial cells. This process requires proteolysis of basement membrane components by a variety of proteinases. The objective of the present study was to determine the expression of proteinases in human retinal tissues showing active neovascularization. METHODS: Epiretinal neovascular membranes surgically removed from patients with proliferative diabetic retinopathy were analyzed by zymography, and the types and amounts of proteinases present in the tissues were determined. Retinas from nondiabetic donor eyes served as control specimens. RESULTS: Both the high- (54 kDa) and low- (33 kDa) molecular-weight forms of urokinase were present at significantly higher levels in neovascular membranes than in normal retinas. The pro forms of the matrix metalloproteinases (MMP) MMP-2 and MMP-9 were significantly elevated in the neovascular membranes in comparison with levels in normal retinas. In addition, the active forms of these enzymes were present in the membranes, whereas there was no detectable level of the active forms in normal retinas. CONCLUSIONS: Human diabetic neovascular membranes contain high levels of urokinase and MMP. The increased activity of proteinases in the final common pathway of retinal neovascularization indicates that inhibition of these enzymes may be a useful therapeutic target as an alternative approach in the management of proliferative retinopathies.

Aged↗
PubMed2005

Antibody against junctional adhesion molecule-C inhibits angiogenesis and tumor growth.

The junctional adhesion molecule-C (JAM-C) was recently described as an adhesion molecule localized at interendothelial contacts and involved in leukocyte transendothelial migration. The protein JAM-C interacts with polarity complex molecules and regulates the activity of the small GTPase Cdc42. The angiogenesis process involves rearrangement of endothelial junctions and implicates modulation of cell polarity. We tested whether JAM-C plays a role in angiogenesis using tumor grafts and hypoxia-induced retinal neovascularization. Treatment with a monoclonal antibody directed against JAM-C reduces tumor growth and infiltration of macrophages into tumors. The antibody decreases angiogenesis in the model of hypoxia-induced retinal neovascularization in vivo and vessel outgrowth from aortic rings in vitro. Importantly, the antibody does not induce pathologic side effects in vivo. These findings show for the first time a role for JAM-C in angiogenesis and define JAM-C as a valuable target for antitumor therapies.

Angiogenesis Inhibitors↗