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PubMed1997

Neuroprotective therapy for argon-laser induced retinal injury.

Laser photocoagulation treatment of the central retina is often complicated by an immediate side effect of visual impairment, caused by the unavoidable laser-induced destruction of the normal tissue lying adjacent to the lesion and not affected directly by the laser beam. Furthermore, accidental laser injuries are at present untreatable. A neuroprotective therapy for salvaging the normal tissue might enhance the benefit obtained from treatment and allow safe perifoveal photocoagulation. We have developed a rat model for studying the efficacy of putative neuroprotective compounds in ameliorating laser-induced retinal damage. Four compounds were evaluated: the corticosteroid methylprednisolone, the glutamate-receptor blocker MK-801, the anti-oxidant enzyme superoxide dismutase, and the calcium-overload antagonist flunarizine. The study was carried out in two steps: in the first, the histopathological development of retinal laser injuries was studied. Argon laser lesions were inflicted in the retinas of 18 pigmented rats. The animals were killed after 3, 20 or 60 days and their retinal lesions were evaluated under the light microscope. The laser injury mainly involved the outer layers of the retina, where it destroyed significant numbers of photoreceptor cells. Over time, evidence of two major histopathological processes was observed: traction of adjacent normal retinal cells into the central area of the lesion forming an internal retinal bulging, and a retinal pigmented epithelial proliferative reaction associated with subretinal neovascularization and invasion of the retinal lesion site by phagocytes. The neuroprotective effects of each of the four compounds were verified in a second step of the study. For each drug tested, 12 rats were irradiated with argon laser inflictions: six of them received the tested agent while the other six were treated with the corresponding vehicle. Twenty days after laser exposure, the rats were killed and their lesions were subjected to image-analysis morphometry. The extent of retinal destruction was assessed by measuring the lesion diameter and the amount of photoreceptor cell loss in the outer nuclear layer. Methylprednisolone and MK-801 were shown to ameliorate laser-induced retinal damage, whereas both superoxide dismutase and flunarizine were ineffective. Furthermore, MK-801 diminished the proliferative reaction of the retinal pigment epithelial cells. On the basis of our results we suggest that the pigmented rat model is suitable for studying and screening various compounds for their neuroprotective efficacy in treating retinal laser injury. We further suggest that glutamate might play a key role in mediating retinal injury induced by laser irradiation.

Animals↗
PubMed2002

Optic disc swelling in an adolescent with insulin dependent diabetes mellitus.

A 14-year-old Ukrainian girl with uncontrolled insulin dependent diabetes developed bilateral optic disc swelling when diabetic treatment was instituted. There was no retinal ischaemia. The disc swelling resolved completely over 8 months without specific ocular therapy. Disc swelling in juvenile diabetics must be differentiated from disc neovascularization. These patients may develop retinal ischaemia and neovascularization after the disc changes resolve.

Adolescent↗
PubMed2004

Iron chelation abrogates excessive formation of hydroxyl radicals and lipid peroxidation products in monocytes of patients with Eales' disease: direct evidence using electron spin resonance spectroscopy.

PURPOSE: Eales' disease (ED) is an idiopathic retinal vasculitis condition, which affects the retina of young adult males. Retinal changes include perivasculitis, non-perfusion and neovascularization. Disruption of blood-retinal barrier (BRB) is the common feature in intra-ocular inflammatory diseases. Disruption of BRB results in vascular hyper permeability and infiltration of circulating leukocytes into the retinal parenchyma. Monocyte (MC) activation results in oxidant thrust and subsequent tissue damage. This has been reported in various intra-ocular inflammatory diseases such as uveitis and Behcet's disease. However, there are no such reports available in ED. Hence in the present study we have investigated the role of MC activation and hydroxyl radicals (OH) production and its possible involvement in promoting the development of retinal vasculitis in patients with ED. METHODS: Twelve patients with ED and twelve healthy volunteers were recruited for the study. MC was separated from their peripheral blood. MC from patients with ED and control subjects was stimulated with phorbol-12-myristate-acetate (PMA) and OH generated was analyzed using an electron spin resonance spectrometer (ESR). Superoxide dismutase (SOD), thiobarbituric acid reactive substances (TBARS), and iron content was determined in MC to assess the oxidant thrust and antioxidant defense. RESULTS: OH generation was elevated in MC from patients with ED, which coincided with diminished SOD activity and elevated levels of iron and TBARS, when compared with healthy control subjects. OH generation was abrogated when MC from ED were co-incubated with PMA and iron chelators such as diethylenetriaminepentacetic acid (DTPA) and desferrioxamine. Iron chelation also inhibited TBARS accumulation restored SOD activity in MC of patients with ED. CONCLUSIONS: For the first time we have demonstrated the production of OH generation in MC of patients with ED using ESR. Further we have shown the beneficial effect of iron chelation in mitigating free radical mediated changes in cellular metabolism. Based on our findings, we provide further evidence for the role of oxidant thrust in promoting retinal tissue damage in patients with ED.

Adult↗
PubMed1985

Intraocular ossification.

Intraocular ossification was investigated in a series of 20 eyes. Only 12 eyes were phthisical. The etiological factors were trauma, inflammation, glaucoma and massive intraocular gliosis. Bone tissue was of the compact and spongy type. A correlation was found between the intraocular ossification and retinal detachment, intraocular hemorrhage, intraocular neovascularization and uveitis.

Adolescent↗
PubMed1995

[TNF-alpha level in the vitreous body. Increase in neovascular eye diseases and proliferative diabetic retinopathy].

BACKGROUND: Deficient retinal capillary perfusion results in angioneogenesis of the eye. Its extension depends on the degree of ischemia. Mild stages are restricted to the retina, while marked ischemia results in neovascularization of the iris (rubeosis iridis). The neovascularization may be induced by the release of growth factors into the vitreous. Tumor necrosis factor alpha seems to be an important angiogenetic growth factor. PATIENTS AND METHODS: The patients were divided up into three groups with different retinal stages of ischemia, as judged by the extension of new vessel formation of the eye: a control group without angioneogenesis, a diabetes group with less severe to moderate angioneogenesis of patients with proliferative diabetic retinopathy and a rubeosis group with massive angiogenesis (rubeosis iridis) resulting from different causes. TNF-alpha was determined by immunological methods. RESULTS: The TNF-alpha level of vitreous in rubeosis (25.8 pg/ml; n = 6) was 2-fold elevated compared to controls (13.1 pg/ml; n = 10; p < 0.05) and 1.4-fold elevated compared to the diabetes group (18.2 pg/ml; n = 17). The values ranged from unmeasurable values to 41.25 pg/ml. Within the rubeosis group similar changes were observed independently of the causes of ischemia. There was no correlation between TNF-alpha-levels in the diabetes group and serum creatinine. CONCLUSIONS: 1. TNF-alpha is upregulated in ischemia. 2. TNF-alpha seems to be a mediator of angiogenesis in the eye. 3. Changes in diabetes may be secondary to local ischemia rather than being specific for diabetic retinopathy.

Adult↗
PubMed2006

Hypercapnia- and trans-arachidonic acid-induced retinal microvascular degeneration: implications in the genesis of retinopathy of prematurity.

High oxygen tension is a major factor in the genesis of retinopathy of prematurity (ROP). However, clinical and experimental evidence suggests a significant role for high carbon dioxide (CO(2)) tension as well. Along these lines, although ischemia is often considered to be synonymous with an oxygen deficit, it is also associated with a concomitant local elevation of CO(2) that can lead to impaired developmental and ischemic neovascularization. The mechanisms by which hypercapnia induces retinal microvascular degeneration, a critical step which precedes the subsequent proliferative preretinal neovascularization, are not known. Nitrative stress has an important role in microvascular degeneration leading to ischemia in conditions such as ROP. Hypercapnia is a facilitator of nitration in vitro. We hereby present evidence that prolonged exposure to CO(2) impairs developmental retinal neovascularization through a mechanism involving increased endothelial nitric oxide synthase and induction of a nitrative stress; effects of hypercapnia are independent of its hyperaemic effects. Moreover, we demonstrate that an in vivo nitrative stress associated with retinal vasoobliteration results in nitration of arachidonic acids into trans-arachidonic acids (TAAs), which can act as mediators of nitrative stress by causing microvascular degeneration by inducing expression of the antiangiogenic factor thrombospondin-1. These recent findings establish a previously unexplored means by which hypercapnia hinders efficient neovascularization and provide new insight into the molecular mechanisms of nitrative stress on microvascular injury involving TAA, and suggest new therapeutic avenues in the management of nitrative stress disorders such as in ischemic retinopathies (of prematurity and of diabetes) and encephalopathies.

Animals↗
PubMed1995

The prevalence of age-related maculopathy in the Rotterdam Study.

PURPOSE: To determine the prevalence of age-related maculopathy in an elderly population in The Netherlands. METHODS: Fundus photographs of 6251 participants of the Rotterdam Study, a single-center prospective follow-up study in persons 55 to 98 years of age, were reviewed for the presence of drusen, pigmentary abnormalities, and atrophic or neovascular age-related macular degeneration. RESULTS: The prevalence of at least one drusen of 63 microns or larger increased from 40.8% in persons 55 to 64 years of age to 52.6% in those 85 years of age or older. Similarly, the prevalence of the following abnormalities increased significantly in these age categories: drusen of 125 microns or larger from 4.8% to 17.5%, retinal pigment epithelial hypopigmentations from 3.5% to 9.0%, and increased retinal pigment from 3.7% to 15.3%. Atrophic or neovascular age-related macular degeneration was present in 1.7% of the total population. Atrophic age-related macular degeneration increased from 0.1% in persons 55 to 64 years of age to 3.7% in those 85 years of age or older. Neovascular age-related macular degeneration increased from 0.1% to 7.4% in these age groups. No sex differences were observed for these lesions. CONCLUSIONS: The prevalence of atrophic or neovascular age-related macular degeneration is 1.7%. In those 55 years of age or older, the prevalence increases strongly with age and it is similar in men and women. Neovascular age-related macular degeneration was twice as common as atrophic age-related macular degeneration. These findings suggest that age-related maculopathy may be less common in this European population than in similar populations in the United States.

Aged↗
PubMed2005

An increase in superoxide dismutase ameliorates oxygen-induced retinopathy in transgenic mice.

PURPOSE: Oxygen therapy is a well-recognized risk factor for retinopathy of prematurity. We examined whether an increase in the naturally occurring enzyme copper-zinc superoxide dismutase (CuZnSOD), which controls oxygen, can reduce the severity of oxygen-induced retinopathy in a mouse model. METHODS: Seven transgenic mice overexpressing CuZnSOD and six wild-type mice were exposed to 75% oxygen from postnatal day 7 to 12. Seven transgenic mice and five mice of the wild type were kept in room air and served as controls. Fluorescein-conjugated dextran angiography of retinal vasculature was performed and flat-mounted preparations were evaluated by scoring blood vessel growth, blood vessel tuft formation, extraretinal neovascularization, degree of central constriction, and tortuosity of vessels. In addition, quantification of the number of blood vessel tufts was performed in a masked fashion with haematoxylin and eosin staining of paraffin-embedded eye sections. RESULTS: The mean retinal score+/-SD obtained by the wild-type mice was 9.4+/-2.0, whereas the transgenic mice overexpressing CuZnSOD obtained a value of 2.4+/-1.6 (P=0). The two control groups (wild type and transgenic) that were kept in room air, each obtained a score of 0. Significantly fewer extraretinal vascular tufts were seen in the transgenic mice (0.26+/-0.34) than in the wild-type mice (4.27+/-1.6) after both groups were exposed to oxygen (P<0.001). CONCLUSIONS: The results suggest that high SOD activity protects neonatal mice against oxygen-induced retinopathy, and support the assumption that oxygen radicals are a major causative factor in oxygen-induced retinopathy.

Animals↗
PubMed1999

[Vitreous hemorrhage and pre-retinal hemorrhage "without obvious point of origin" in diabetic patients. Apropos of 5 cases].

Five diabetic patients with nonproliferative retinopathy or controlled retinopathy after photocoagulation developed intravitreous or preretinal hemorrhages of unknown origin. Intravitreous hemorrhage of unknown origin is characterized by the absence of angiographic hyperfluorescence suggestive of neovascularization. Examination of the retinal periphery with a three mirror lens reveals the absence of tears and an normally appearing arteriovenous network with no sign of bleeding. The clinical cases reported here demonstrated: 1) the significance of posterior vitreous detachment in the genesis of hemorrhage, 2) the difficulty encountered in assessing the seriousness of the hemorrhage and providing optimal treatment, 3) the importance of initiating treatment early.

Adult↗
PubMedDate not supplied

Bilateral midperipheral large drusen and retinal pigment epithelial detachments associated with multifocal areas of choroidal neovascularization: a histopathologic study.

PURPOSE: The ocular histopathologic features of a patient with bilateral multiple midperipheral areas of choroidal vascularization, large drusen, and detachments of the retinal pigment epithelium (RPE) are presented. METHODS: The eyes were obtained at autopsy and fixed in 4% buffered formaldehyde. Serial sections through the macula area and inferior segments were prepared. Light as well as electron microscopy was performed. RESULTS: Microscopic examination disclosed numerous large drusen measuring up to 200 micro m in height and 280 micro m in diameter and areas of serous RPE detachments in the midperiphery of both eyes. Some of the large drusen had choroidal vascularization. Areas of sub-RPE neovascularization that measured up to 6.5 mm in diameter were present in the midperiphery of both eyes. The choroidal origin for neovascularization was evident in 10 areas. A 1-mm area of hemorrhagic detachment of the RPE contiguous with choroidal neovascularization (CNV) was present in the immediate postequatorial area temporally in the left eye. No drusen, basal deposit, or CNV was present in the macular area. CONCLUSION: Multifocal midperipheral RPE detachments and CNV can occur in the absence of significant age-related macular disease.

Choroidal Neovascularization↗
PubMed1990

Treatment of foveal pigment epithelial detachments with contiguous extrafoveal choroidal neovascular membranes.

Fourteen eyes of 14 patients who had subfoveal retinal pigment epithelial detachments and extrafoveal contiguous choroidal neovascular membranes associated with age-related macular degeneration underwent laser photo-coagulation treatment directed solely to their choroidal neovascular membrane. In eight of 14 eyes (57%), photocoagulation treatment resulted in closure of the choroidal neovascular membrane with subsequent collapse of the pigment epithelial detachment. Six of the eight eyes also had visual improvement. In six of 14 eyes (43%), the neovascular membrane eventually progressed into the fovea with resultant visual loss. The results of our study suggest that photocoagulation of extrafoveal choroidal neovascular membranes associated with foveal detachments of the retinal pigment epithelium may preserve and even improve visual function in affected patients.

Aged↗
PubMed1994

[Exudation of indocyanine green from subretinal neovascularization and its significance].

Owing to its tight binding to protein, exudation of indocyanine green from subretinal new vessels would not normally be expected, but it has been demonstrated. We investigated 102 subretinal new vessels to find out how often exudation develops and to understand the reason for it. Exudation was found in 29 (28.4%) of the cases examined; 37 (36.6%) were stained, which means that these membranes became hyperfluorescent but not lighter than other, definitively non-exuding, structures on the fundus. In 26 (25.5%) no hyperfluorescence was seen in the late phase, and in 10, or 9.8%, neovascularization remained occult. The correlation of indocyanine green exudation with retinal blood or lipid deposits was significant (r = 0.77, p = 0.0001). Histological examinations showed a correlation of lipid deposits with a severe disintegration of retinal vessels. This finding, in combination with others, indicates that the exudation of indocyanine green reflects severe destruction of vessel walls, which does not seem to occur consistently in all neovascular membranes. The exudation of indocyanine green might be of prognostic value.

Adult↗
PubMed1999

Choroidal neovascularization following macular hole surgery.

BACKGROUND: Retinal pigment epitheliopathy, a recognized finding in eyes that have undergone macular hole surgery, may limit visual outcome and predispose to the development of choroidal neovascularization (CNV). This study reports on the features and outcomes of CNV following otherwise successful surgery for idiopathic macular holes. METHODS: Case series including three eyes of two patients who developed CNV following macular hole surgery. RESULTS: Choroidal neovascularization developed 3 to 30 months after macular hole surgery. The CNV was crescent-shaped, surrounding a central area of retinal pigment epithelial mottling that corresponded to the site of the macular hole in all three cases. All neovascular membranes were adjacent to the fovea and were associated with substantial leakage of fluorescein. The macular hole remained closed in all cases. CONCLUSION: Choroidal neovascularization is a rare complication following macular hole surgery. Retinal pigment epitheliopathy and defects in the Bruch's membrane, pre-existing or secondary to surgery, may be predisposing factors.

Aged↗
PubMed1990

Pathology of experimental autoimmune uveoretinitis in mice.

The histopathology and immunopathology of murine experimental autoimmune uveoretinitis (EAU) following active immunization with the interphotoreceptor retinoid-binding protein (IRBP) were studied. The methods used included conventional light microscopy and immunoperoxidase staining. Lesions were located mainly in the uvea and the retina and were characteristically focal. The prominent histopathologic findings in the retina were vasculitis, granuloma, retinal fold, focal serous detachment, and loss of photoreceptors. Granulomas, formation of Dalen-Fuchs nodules, inflammatory cellular infiltration and increase in the thickness of the choroid and ciliary body were frequent findings. Subretinal neovascularization occurred in 10% of the experimental animals. Mild to moderate inflammation was also noted in the vitreous. The predominant infiltrating cells in the retinal and uveal granuloma and the Dalen-Fuchs nodules were macrophages. In contrast, the predominant infiltrating cell types in the vitreous were T helper/inducer lymphocytes. T suppressor/cytotoxic cells were rarely seen. Expression of Ia antigens on the ocular cells was confined to the immediate area of the inflammatory sites. The kinetics of histopathology showed two peaks at the 5th and 10th week after immunization, suggesting a relapsing course of the disease.

Animals↗
PubMed1999

Increased interleukin-6 in aqueous humor of neovascular glaucoma.

PURPOSE: To demonstrate the involvement of proinflammatory cytokines in intraocular neovascularization by detecting the presence of interleukin (IL)-6, IL-2, and tumor necrosis factor (TNF)-alpha in aqueous humor and serum of patients with neovascular glaucoma (NVG) secondary to central retinal vein occlusion (CRVO). METHODS: According to the grade of iris neovascularization (NVI), patients with CRVO were divided into three groups: CRVO without NVI, CRVO with NVI, and CRVO with regressed NVI. Healthy patients with cataract were enrolled as control subjects. Enzyme-linked immunosorbent assay was used to quantitate the concentrations of the cytokines IL-6, IL-2, and TNF-alpha in aqueous humor and serum from patients with NVG and control subjects. RESULTS: In serum, the levels of IL-6, IL-2, and TNF-alpha did not differ among groups. In aqueous humor, only IL-6 showed significant change among groups. IL-6 levels in aqueous humor of group 2, CRVO with NVI (1532.0+/-221.1 pg/ml; P < 0.001), and group 3, CRVO with regressed NVI (234+/-154.6 pg/ml; P < 0.001), were significantly higher. There was no significant difference in IL-6 levels between the control group (26.4+/-21.8 pg/ml) and group 1 (15.6+/-0.9 pg/ml). CONCLUSIONS: The inflammatory cytokine IL-6 in aqueous humor increased spatially and temporally correlated with the grade of NVI in patients of NVG secondary to CRVO. The aqueous IL-6 increased in NVI and decreased after vessels regressed. It is possible that the significantly higher level of IL-6 was due to intraocular synthesis because of the minimal change in serum. The increased level of IL-6 may have a putative role along with other angiogenic factors in angiogenesis of NVG as a possible predictor of NVI.

Aged↗
PubMed1996

Posterior segment neovascularization associated with optic nerve aplasia.

PURPOSE: To report the presence of posterior segment neovascularization in eyes with optic nerve aplasia. METHODS: Three eyes in two patients with clinical optic nerve aplasia were studied. RESULTS: Examination disclosed posterior segment neovascularization in one eye and progressive posterior segment neovascularization in two eyes. CONCLUSIONS: Posterior segment neovascularization may occur in association with optic nerve aplasia. Retinal ischemia or retinochoroidal anatomic disorganization, or both, may provide the stimulus for neovascularization in such eyes.

Coloboma↗