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Results for “Retinal Neovascularization”

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At least 1,513 records · Page 84Linked to original sources
PubMed1997

[Retinal involvement in drepanocytosis in Togo. Correlation between age, genotype and retinopathy].

PURPOSE: To evaluate different retinal complications, study correlation with age and links with genotypic forms in Togolese sickle cell patients. MATERIAL AND METHOD: Patients were recruited between 1994 and 1996 at the hospital, genotypic diagnosis by electrophoresis, systematic angiofluorography were performed and laser photocoagulation of retinal neovascularisation if needed. RESULTS: A total number of 190 patients were recruited, 84 (44.21%) had retinopathy, while 106 (55.79%) were normal. The SC form was most affected with 50 patients (26.3%), followed by the SS group in 11.05% (21 patients), and AS trait, 2.65% (5 patients). Patients most affected by proliferative retinopathy were aged 35-44 years (n = 30; 15%), 25-34 years in 23.8% and 15-24 years in 20.6%. CONCLUSION: Young Togolese sickle cell patients aged 35 to 44 year-old and the SC forms appear to have a relative high risk of proliferative retinopathy in this study.

Adolescent↗
PubMed1998

[Ultrasound biomicroscopic findings of anterior hyaloidal fibrovascular proliferation].

We performed ultrasound biomicroscopy (UBM) on 5 eyes with anterior hyaloidal fibrovascular proliferation (AHFVP), which had developed after vitrectomy for proliferative diabetic retinopathy. AHFVP was observed as a thick membrane or a mass image which extended from the vitreous base to the pars plicata, and was apparently differentiated from the anterior vitreous membrane and cilliary body. UBM showed proliferative stalks extending from sclerotomy sites toward the anterior vitreous membrane. These UBM images indicated that AHFVP originated from sclerotomy sites. UBM also enabled us to detect traction detachment of the peripheral retina associated with AHFVP, which could not be observed by conventional B-mode echography. Thus UBM is useful in establishing a diagnosis of AHFVP, and this technique is valuable to determine the indication and the timing of surgical treatment for AHFVP.

Adult↗
PubMedDate not supplied

[A pathohistological study of newly formed subpigment epithelial tissue in patients with senile macular dystrophy].

Efficacy and possibility of direct operations on the macular area of the retina in humid (exudative) maculopathies (senile maculodystrophy) is validated theoretically, morphologically, and clinically. A hypothesis on the mechanism of exudative process development in the macular area in degenerative diseases is formulated on the basis of pathohistological analysis of removed subpigmental material. Indications for such operations are defined.

Aged↗
PubMed1986

An unusual presentation of branch retinal artery obstruction in association with ocular neovascularization.

A 61-year-old woman presented with a superior papillary branch artery obstruction occurring secondary to an intra-arterial embolus. Thirteen months later she developed neovascularization of the optic disc and retina in the same eye. Although the situation is unusual, this case suggests that retinal branch artery obstruction may rarely predispose to ocular neovascularization.

Carotid Arteries↗
PubMed2002

Indocyanine green angiographic interpretation of reticular dystrophy of the retinal pigment epithelium complicated by choroidal neovascularization.

A 37-year-old woman presented with flashes in her left eye and bilateral visual distortion. Fundal examination revealed a reticular 'fishnet' pattern of retinal pigmentation in both eyes consistent with reticular dystrophy of the retinal pigment epithelium. In the left eye there was a small haemorrhage and a shallow serous macular detachment. Fluorescein angiography demonstrated subfoveal choroidal neovascularization. Indocyanine green angiography (ICG) revealed more extensive involvement than fluorescein angiography, with small areas of intense hyperfluorescence amongst reticular areas of hypofluorescence. These changes, as interpreted in light of the known histopathological localization of ICG, are consistent with varying stages of dysfunction of the retinal pigment epithelium in this disease.

Adult↗
PubMed1995

Hypoxia-induced expression of vascular endothelial growth factor by retinal cells is a common factor in neovascularizing ocular diseases.

BACKGROUND: It is generally assumed that unwarranted, excessive neovascularization of the retina and iris is a direct response to a hypoxic retinal environment. Prompted by our previous findings that the potent angiogenic factor, vascular endothelial growth factor (VEGF), is hypoxia-inducible, we used in situ hybridization techniques to examine the thesis that VEGF functions as the link between retinal ischemia and a pathologic, intraocular, angiogenic response. EXPERIMENTAL DESIGN: To gain molecular access to human material representing progressive stages of angiogenic eye diseases, in situ hybridization analysis was carried out on sections of whole globes enucleated at the time of ongoing neovascularization. This methodology identified cells that have up-regulated VEGF expression during natural progression of the indicated diseases. A rabbit model was also used to determine whether experimentally induced retinal ischemia leads to up-regulation of VEGF expression. RESULTS: Proliferation of vascular elements in proliferative diabetic retinopathy and neovascularization of the retina and/or iris secondary to central retinal vein occlusion, retinal detachment, and intraocular tumors were always accompanied by induction of retinal VEGF expression. Furthermore, in each case, expression of VEGF was induced only in a particular layer of the retina (either the outer nuclear layer, the inner nuclear layer, or the ganglion cell layer), matching the zones affected by impaired perfusion. In a rabbit model simulating retinal vein occlusion, elevated levels of VEGF mRNA were detected within a few days of experimental induction of retinal ischemia, exclusively in the ischemic region. CONCLUSIONS: VEGF may be one of the long anticipated factors linking retinal ischemia and intraocular angiogenesis. Irrespective of the cause of retinal ischemia, sustained overproduction of VEGF by ischemic retinal cells may promote retinal and iris neovascularization in a number of neovascular eye diseases.

Animals↗
PubMed2002

Retinal pigment epithelium translocation after choroidal neovascular membrane removal in age-related macular degeneration.

PURPOSE: To test the feasibility of a new surgical technique and to assess visual function over the translocated retinal pigment epithelium (RPE) cells in patients operated on for subfoveal choroidal neovascularization (CNV) secondary to age-related macular degeneration (ARMD). DESIGN: Retrospective, noncomparative, interventional case series. PARTICIPANTS: Nine patients with previously untreated exudative ARMD underwent surgical excision of the subfoveal CNV with RPE translocation and were observed for 12 to 32 months. METHODS: The surgery consisted of a standard three-port pars plana vitrectomy, excision of the CNV, and RPE translocation. Pre- and postoperative ocular examination included best-corrected visual acuity measurement, fundus color stereo photography, and fundus fluorescein angiography. Optical coherence tomography and confocal laser scanning ophthalmoscopy (cLSO) were performed after surgery. A crossfixation target and a single-point flashing light were projected on different areas of the posterior pole using a cLSO. Photopic 10 to 2 perimetry, photopic fine matrix mapping, and cLSO microperimetry were also performed after surgery in six patients. MAIN OUTCOME MEASURES: Optical coherence tomography cross-sectional scans and cLSO RPE autofluorescence were recorded to detect the presence of viable translocated RPE. Visual acuity, fixation, photopic 10 to 2 perimetry, photopic fine matrix mapping, and cLSO microperimetry were used to test central visual function. RESULTS: Retinal pigment epithelium was translocated successfully at the time of CNV removal from the edge of the RPE defect to a subfoveal location in seven of nine patients. One patient experienced proliferative vitreoretinopathy, but significant hemorrhage was not a feature. Optical coherence tomography showed the translocated RPE as an area of increased optical reflectivity with optical shadowing external to it. Confocal laser scanning ophthalmoscopy showed autofluorescence of the translocated RPE. The crossfixation target was seen when projected on the translocated RPE. During eccentric fixation, the patients could see a flashing point-target projected on the translocated RPE. Photopic 10 to 2 perimetry, photopic fine-matrix mapping, and cLSO microperimetry showed the presence of central visual function. CONCLUSIONS: The authors propose that translocation of RPE at the time of CNV removal, from the edge of the RPE defect to a subfoveal location, may have a role in the surgical management of ARMD.

Aged↗
PubMed1990

[The role of retinal pigment epithelium in the early stage of development of subretinal neovascularization].

In order to evaluate the role of retinal pigment epithelium (RPE) in the early stage of experimental subretinal neovascularization, we severely damaged RPE cells before the development of subretinal neovascularization. Three adult rhesus monkeys were used in this study. One mol/l l-ornithine hydrochloride saline solution was injected intravitreously at 2 weeks before intense krypton laser photocoagulation on the retina at the posterior pole, and clinical and histopathological course were studied at 1 to 28 days after photocoagulation. As a result, no evidence of new vessel formation could be observed clinically throughout the entire course. Histopathologically, at 3 days after photocoagulation, slight proliferation of RPE cells was identified by electron microscopy at the margin of the laser lesions, and budding of vascular endothelial cells derived from choroidal microvessels was observed in the choroid. However, no newly-formed vessels extended into the subretinal space at 7 days or more after photocoagulation. These results confirmed our hypothesis that proliferated RPE cells had inductive effect on the growth of endothelial cells in the early stage of development of subretinal neovascularization.

Animals↗
PubMed1988

Posterior tractional retinal breaks complicating branch retinal vein occlusion.

A total of 358 patients with branch retinal vein occlusion (BRVO) were reviewed to examine the relationship between branch retinal vein occlusion with neovascularization elsewhere (NVE), vitreous hemorrhage, and posterior tractional retinal breaks. Twenty-eight of 358 (7.8%) BRVO patients had vitreous hemorrhage. In this group of 28 patients, 24 of the 28 (85.7%) had NVE. Of the 24 BRVO patients with vitreous hemorrhage and NVE, six (21.4%) were found to have posterior tractional retinal breaks adjacent to avulsed neovascular tissue. These data indicate a strong association between BRVO patients with vitreous hemorrhage and posterior tractional retinal breaks due to avulsion of neovascular tissue.

Aged↗
PubMed1994

A primary role for RPE transplants in the inhibition and regression of neovascularization in the RCS rat.

PURPOSE: Healthy retinal pigment epithelial (RPE) cell transplants in retinas of postnatal day 27 Royal College of Surgeons (RCS) rat are capable of preventing photoreceptor cell degeneration, inhibiting the degeneration of the retinal vascular bed and the subsequent neovascularization of the RPE that occurs in retinas injected with saline. In the present study, the authors have tested the hypothesis that RPE transplants might also prevent vascularization of the RPE layer in RCS retinas when photoreceptor cells either had just degenerated or, at 3 months, disappeared. METHOD: Retinas of 3- and 6 month-old RCS rats were injected with either healthy neonatal RPE cells or vehicle and were examined at 6 and 8 months, respectively. These retinas were studied using horseradish peroxidase visualization of the vasculature in retinal wholemount preparations and by light microscopy. RESULTS: The number of neovascular profiles in wholemount preparations of RCS retinas that had received healthy RPE transplants at 3 months and were analyzed at 6 months were significantly decreased when compared to sham-injected retinas of age-matched RCS rats, 2.09 +/- 0.94 and 15.28 +/- 1.34 profiles per mm2, respectively (P < 0.001). In addition, when comparing retinas transplanted or sham injected at 6 months and examined at 8 months, significantly fewer neovascular profiles were found in the transplant group, 9.32 +/- 1.02 and 15.42 +/- 0.84 profiles per mm2, respectively (P < 0.002). CONCLUSION: These data provide still further evidence for the role of healthy RPE in maintaining the homeostasis of the normal retinal vasculature in the retina of the RCS rat. The relationships between the RPE and the retinal vasculature are important when considering that alterations in the vascularization of the retina play a major role in some of the most sight-debilitating diseases, such as the wet form of age-related macular degeneration and proliferative diabetic retinopathy.

Animals↗
PubMed1990

Argon laser panretinal photocoagulation in ischemic central retinal vein occlusion. A 10-year prospective study.

We conducted a prospective, planned study of argon laser panretinal photocoagulation (PRP) in ischemic central retinal vein occlusion (CRVO) over a 10-year period in 123 eyes. On comparing the lasered eyes versus the nonlasered eyes, there was no statistically significant difference between the two groups in the incidence of development of angle neovascularization (NV), neovascular glaucoma (NVG), retinal and/or optic disc NV, or vitreous hemorrhage, or in visual acuity. Our study, however, did show a statistically significant (P = 0.04) difference in the incidence of iris NV between the two groups, with iris NV less prevalent in the laser group than in the nonlaser group, but only when the PRP was performed within 90 days after the onset of CRVO. The other parameter which showed a statistically significant difference between the two groups was the peripheral visual fields-the laser group suffered a significantly (P less than or equal to 0.03) greater loss than the non-laser group. We discuss the implications of these findings in light of the natural history of ischemic CRVO and of ocular NV. Since the original rationale for advocating PRP in ischemic CRVO was the proven beneficial effect of PRP on ocular NV in proliferative diabetic retinopathy, we also discuss the disparities in the disease process between ischemic CRVO and proliferative diabetic retinopathy and in their responses to PRP.

Aged↗
PubMed2002

Massive vascular endothelium growth factor (VEGF) expression in Eales' disease.

BACKGROUND: Eales' disease is an idiopathic retinal vasculitic and vaso-occlusive process complicated by extensive retinal neovascularisation and vitreous hemorrhages. The great propensity to produce retinal neovessels is one of the particular aspects of the disease that deserves to be further investigated. We report a case of Eales' disease having evolved over more than three decades, with a typical clinical presentation in one eye, while the other eye had to be enucleated because of a terminal neovascular glaucoma, thus allowing pathological examination. METHODS: The functional right eye was treated by vitrectomy, cerclage, cryocoagulation and endolaser. The non-functional phthitic left eye was enucleated and submitted for histopathological and immunohistochemical examination using antibodies against vascular endothelial growth factor, T-cells, B-cells and Müller cells. RESULTS: Evolution was favourable in the operated right eye, following management of the inflammatory reaction. The histopathological examination of the left eye revealed an occlusion of the anterior chamber angle by rubeosis iridis, tractional retinal detachments, pre-, intra- and sub-retinal neovascular membranes, and vitrous hemorrhages. Diffuse positive anti-VEGF immunostaining was found at the level of the retinal neovascular membranes. The retina exhibited prominent Müller cell immunostaining, indicating extensive gliosis, and predominantly B cell infiltrates were found in the eye. CONCLUSION: The present study indicates a close relationship between the prominent neovascular proliferation in Eales' disease and the intense expression of VEGF. The increased expression of VEGF, when compared to other conditions inducing neovascularisation, might explain the severity of neovascular growth and the propensity of repeated vitrous hemorrhages in Eales' disease.

Aged↗
PubMedDate not supplied

Retinal endothelial angiogenic activity: effects of hypoxia and glial (Müller) cells.

OBJECTIVE: To explore the impact of retinal glial (Müller) cells on survival and neovascularization-related activities of cultured retinal endothelial cells under normoxic and hypoxic conditions. METHODS: Bovine retinal endothelial cells (BRECs) were cultured under normoxia or hypoxia (0.5% O2) either alone, together with the human Müller cell line MIO-M1, or in normoxia- or hypoxia-conditioned media of MIO-M1 cells. Cell number, proliferation, apoptotic cell death, and migration of BRECs were determined. RESULTS: Exposure of BRECs to hypoxia for 24 h decreased the number of adherent cells and the proliferation rate, but increased apoptosis and cell migration. Increased apoptosis and decreased proliferation of the BRECs occurred also in the presence of conditioned media of MIO-M1 cells. Under normoxic conditions, co-culture with MIO-M1 cells resulted in increased proliferation, but decreased apoptosis and migration rates of BRECs. Under hypoxic conditions, the Müller cells released elevated amounts of VEGF but their presence decreased proliferation, apoptosis and the migration rates of BRECs. CONCLUSIONS: Hypoxia inhibits the proliferation of retinal endothelial cells. Müller cells release soluble mediators that enhance this hypoxia-mediated effect but, under certain conditions (i.e., in co-culture), may protect retinal endothelial cells from apoptosis, thus supporting their survival. Altogether the findings indicate that the key signal necessary to trigger retinal endothelial proliferation under hypoxia remains to be determined.

Animals↗
PubMed1987

Subretinal neovascular membranes associated with choroidal nonperfusion and retinal ischemia.

This is the first well-documented case of co-existent underlying choroidal nonperfusion in an eye with a subretinal neovascular membrane that was subsequently treated with krypton red laser photocoagulation by the senior author (LEM). The possible role of chronic macular ischemia secondary to choroidal circulatory impairment is discussed in relationship to other well-established risk factors. Perhaps treatment to improve macular oxygenation would be a reasonable alternative to eradication of the neovascularization by direct laser photocoagulation.

Aged↗
PubMed1997

Optic nerve neovascularization in incontinentia pigmenti.

PURPOSE: To describe the presence of optic disk neovascularization in a child with incontinentia pigmenti. METHODS: A 6-month-old infant with incontinentia pigmenti developed optic disk neovascularization in addition to vascular abnormalities in the peripheral retina. Panretinal photocoagulation was performed. RESULT: The optic disk neovascularization regressed after panretinal photocoagulation. CONCLUSIONS: Optic disk neovascularization is another notable retinal manifestation of incontinentia pigmenti. When optic disk neovascularization is detected, retinal ablation should be considered as treatment.

Female↗