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PubMed1998

Macular vasculopathy and its evolution in incontinentia pigmenti.

PURPOSE: To describe macular vasculopathy in incontinentia pigmenti. METHODS: Twelve baby girls with incontinentia pigmenti were evaluated under general anesthesia by fluorescein angiography of the macula. Nine eyes of nine patients had sufficient detail to allow evaluation of capillary changes. Angiography was initiated as early as three months of age, and was repeated in seven eyes at 3-12 month intervals. Changes in capillary patterns were identified. RESULTS: Irregularly enlarged or distorted foveal avascular zones were noted in all nine maculas. Sparseness of the perifoveolar capillary bed was a characteristic finding. Sequential macular angiography demonstrated nonprogressive (stable) capillary closure in two eyes; progressive closure was noted in another macula; progressive closure plus addition or reopening of macular capillaries occurred in three eyes; and central retinal artery occlusion, with cherry red spot formation, was observed in one eye at 12 days of age. In addition, progressive tractional detachment of the macula, associated with bleeding pre-retinal neovascularization, occurred in two of these eyes, and progressive macular neovascularization also occurred in one eye. CONCLUSIONS: Macular ischemia is characteristic of incontinentia pigmenti and is often progressive. It is the initiating event of a typical vasculopathy, characterized by capillary remodelling and, occasionally, by neovascularization and tractional detachment of the retina.

Disease Progression↗
PubMed1991

Retinal and vitreal neovascularization in retinopathy of prematurity. A scanning electron microscopic study in the kitten.

The angioarchitecture of vitreal and retinal neovascularizations produced experimentally in the eyes of kittens aged 2 to 9 weeks was studied with scanning electron microscopy. Various forms of new retinal and vitreal vessels were observed depending on topographic locations. Intraretinal neovascularization was observed at the retinal periphery as it grew toward the avascular zone in forms of short vascular buds, aneurysmal outgrowths, and neovascular loops. Posterior or to this frond of neovascularization, intertwining intraretinal telangiectasia was observed. At the posterior pole, capillaries with microaneurysms extended posteriorly toward the deeper layers of the retina from the vascular trunks at the nerve fiber layer. Vitreal neovascularization broke through the internal limiting membrane and exhibited aneurysmal outgrowths, clusters of glomerular swellings, and sinusoidal vascular channels. At the optic disc, vitreous neovascularization took the form of aneurysmal outgrowths and long vascular buds. Vitreal neovascularization showed different characteristics from the intraretinal neovascularization. We hypothesize that the topographic variation of the angioarchitecture of retinal and vitreal neovascularizations depends on the maturity of the vessels and might be related to the hemodynamics at each site.

Animals↗
PubMed2006

Ocular neovascularization in a patient with Fanconi anemia.

CASE REPORT: An 11-year-old girl diagnosed with Fanconi anemia was referred to us for redness and pain in her right eye. Findings in the right eye included visual acuity of counting fingers, neovascular glaucoma, vitreous hemorrhage, optic disc neovascularization, and features of peripheral ischemic retinopathy. Findings in the left eye included peripheral retinal neovascularization and areas of retinal capillary nonperfusion. COMMENTS: Patients with Fanconi anemia may develop ocular neovascularization with subsequent severe visual loss due to vitreous hemorrhage or neovascular glaucoma. Regular ophthalmic examination, including ophthalmoscopy and fluorescein angiography in selected cases, is recommended in such patients.

Child↗
PubMed1986

Presumed retinovitreal neovascularization in dystrophic retinas of spontaneously hypertensive rats.

The authors have observed abnormal blood vessels, strongly suggestive of neovascular proliferation, arising from the retinal circulation and extending through the inner limiting membrane of the retina into the vitreous in five spontaneously hypertensive (SHR) rats with severe retinal dystrophy. The animals in whom these presumptive retinovitreal new vessels occurred were all 15 mo of age or older. The new vessels frequently demonstrated thinned and, rarely, fenestrated endothelium, abnormal intracellular junctions, increased numbers of endocytic vesicles, bizarre appearing pericytes, and highly abnormal basement membranes, features that have been observed in retinovitreal new vessels in proliferative retinopathies in humans. Unlike such new vessels arising from the human retinal circulation, however, those that we observed in dystrophic rat retinas were usually surrounded by proliferating retinal pigment epithelial cells within the retinal substance. Unlike the vessels, the pigment epithelial cells did not break through the inner limiting membrane of the retina to enter the vitreous. The pigment epithelial cells that made contact with the internal limiting membrane of the retina demonstrated apical and basal plasma membrane specializations that are typical of these cells in their normal anatomical location, while pigment epithelial cells migrating in cords through the neural retina lacked such specializations. This animal model may be of great value in understanding the mechanisms of retinal neovascularization.

Animals↗
PubMed2003

The role of Fas-FasL in the development and treatment of ischemic retinopathy.

PURPOSE: Define a role for Fas-FasL in oxygen-induced retinopathy and explore the mechanism of pigment-epithelium-derived growth factor (PEDF) inhibition in this model. METHODS: Seven-day-old mice C57BL/6J (B6), FasL-defective (B6-gld), or Fas-defective (B6-lpr) mice were exposed to 75% oxygen for 5 days (postnatal day [P]7-P12) and returned to room air. On day P17, vascular architecture was assessed microscopically after perfusion with FITC-dextran, and preretinal nuclei were quantified by PAS and hematoxylin staining. In some experiments, mice were treated intraperitoneally with PEDF. Vascular architecture and preretinal nuclei counts were compared with those in PBS-treated control animals. RESULTS: Oxygen-induced retinopathy was significantly increased in FasL-defective gld mice compared with wild-type B6 animals. This was manifested by an increase in the number of microaneurysms, neovascular tufts, and preretinal nuclei. PEDF treatment prevented retinopathy in B6, B6-gld, and B6-lpr mice. CONCLUSIONS: Fas-FasL interactions regulate the extent of oxygen-induced retinal neovascularization. The inhibition of neovascularization in B6 gld, and B6-lpr mice by PEDF suggests that Fas-FasL interactions are probably not the mechanism for inhibition in this model.

Animals↗
PubMed2006

Bactericidal/permeability-increasing protein's signaling pathways and its retinal trophic and anti-angiogenic effects.

Bactericidal/permeability-increasing protein (BPI) was originally identified as a lipopolysaccharide (LPS) binding protein with gram-negative bactericidal activity in the leukocytes. In this study, we characterized the previously unknown effects of BPI in the eye and the molecular mechanisms involved in its action. BPI mRNA was detected in bovine retina; retinal pigment epithelium; and primary cultures of bovine retinal pigment epithelial cells (RPE), pericytes (RPC), and endothelial cells (REC); while BPI protein was measured in human vitreous and plasma. BPI, but not control protein thaumatin, activated extracellular regulated kinase (ERK) and AKT, and increased DNA synthesis in RPE and RPC but not in REC. A human recombinant 21 kDa modified amino-terminal fragment of BPI (rBPI21) reduced H2O2-induced apoptosis in RPE and inhibited vascular endothelial growth factor (VEGF)-stimulated ERK phosphorylation in REC when preincubated with VEGF. Intraperitoneal (i.p.)-injected rBPI21 reduced ischemia-induced retinal neovascularization and diabetes-induced retinal permeability. Since BPI has unusual dual properties of promoting RPC and RPE growth while suppressing VEGF-induced REC growth and vascular permeability, the mechanistic understanding of BPI's action may provide novel therapeutic opportunities for diabetic retinopathy and age-related macular degeneration.

Angiogenesis Inhibitors↗
PubMed2002

Preclinical and phase 1A clinical evaluation of an anti-VEGF pegylated aptamer (EYE001) for the treatment of exudative age-related macular degeneration.

BACKGROUND: Recent studies have suggested that vascular endothelial growth factor (VEGF) is an important stimulus for the growth of new blood vessels in the eye. Anti-VEGF therapy is thus a potential treatment for exudative macular degeneration and diabetic retinopathy. METHODS: Previously described animal models of vascular leakage and ocular neovascularization, including the Miles assay, the rat corneal angiogenesis model, and the mouse retinopathy of prematurity (ROP) model, were used to study this drug. After these studies, a phase IA single ascending dose study of intravitreal injections of the drug was performed in 15 patients with subfoveal choroidal neovascularization secondary to exudative age-related macular degeneration (AMD). RESULTS: The Miles assay model showed almost complete attenuation of VEGF-mediated vascular leakage following addition of EYE001, and the corneal angiogenesis model also showed a significant reduction in neovascularization with EYE001. The ROP model showed inhibition of 80% of the retinal neovascularization compared with controls (P = 0.0001). The phase IA safety study of patients with exudative AMD showed no significant safety issues related to the drug. Ophthalmic evaluation revealed that 80% of patients showed stable or improved vision 3 months after treatment and that 27% of eyes demonstrated a three-line or greater improvement in vision on the Early Treatment for Diabetic Retinopathy Study chart at this time. CONCLUSION: Anti-VEGF therapy is a promising new avenue for the treatment of neovascular diseases of the eye, including exudative macular degeneration and diabetic retinopathy. Preclinical data from studies with EYE001 support clinical evaluation of its efficacy in such diseases. This report is the first to describe administration of anti-VEGF therapy in humans for exudative macular degeneration and shows the safety of such therapy for single injections. Further clinical studies are necessary to determine the safety of multiple intravitreal injections of EYE001 and larger studies are needed to prove the efficacy of this novel, potentially therapeutic agent for neovascular AMD.

Aged↗
PubMed1985

Ocular findings in incontinentia pigmenti.

Incontinentia pigmenti is an uncommon disorder affecting females, and is associated with ocular, dental, skeletal, and central nervous system abnormalities. Ocular abnormalities are found in 35% of cases. The authors present an eight-month-old girl with neonatal history of skin bullae, who was noted to have esotropia, leukocoria, and a fixed pupil. Histologic examination of the enucleated globe reveals total retinal detachment with retinal neovascularization into the collapsed vitreous, reactive retinal gliosis, and scattered giant nodular proliferations of retinal pigment epithelium. It is suggested that the underlying defect is at the level of the retinal pigment epithelium and that the neurosensory retinal changes are secondary.

Child Development↗
PubMedDate not supplied

Clinical features and prognosis in ocular toxoplasmosis.

PURPOSE: To evaluate retrospectively the clinical characteristics, complications, and prognosis in patients with ocular toxoplasmosis. PATIENTS AND METHODS: We reviewed the records of 189 patients (243 eyes) with ocular toxoplasmosis who were examined between 1972 and 1999. Color fundus photography and, in some patients, fluorescein angiography and indocyanine green angiography were performed. There were 98 male (52%) and 91 female (48%) patients with a mean age of 22.8 +/- 8.9 years. RESULTS: Of the patients, 140 (74%) had congenital and 49 (26%) had acquired toxoplasmosis. At the initial examination, there were active lesions in 65 eyes and inactive lesions in 178 eyes. Active lesions included retinochoroiditis in 59 (91%), papillitis in 2 (3%), and neuroretinitis in 4 (6%) eyes. There was also an inactive scar in 17 eyes with active retinochoroiditis. Localisation of the active retinochoroiditis was the macula in 44 (74%), the macula and peripheral retina in 3 (5%), the peripheral retina in 9 (15%) and the peripapillary retina in 3 (5%) eyes. Optic atrophy, pigment epithelial detachment, choroidal neovascularization, lamellar macular hole, and retinal neovascularization were seen during the follow-up period. CONCLUSIONS: Ocular toxoplasmosis commonly affects the macula and seriously impairs visual acuity. The prevention of acquired and congenital infections is very important in controlling ocular toxoplasmosis. Patients should be followed to avoid late complications.

Adolescent↗
PubMed1989

Histopathology of experimental preretinal neovascularization.

Despite the morbidity resulting from abnormal retinal neovascularization, morphological events associated with its development have not been fully described. We therefore studied sequential morphologic events during preretinal neovascularization in an experimental model induced by injection of 250,000 homologous fibroblasts into the vitreous cavity of rabbits. Within 2 days following fibroblast injection, thickening of many venular and capillary endothelial cells resulted in partial obliteration of their lumina. 3H-thymidine incorporation occurred first in the nonvascular cells of the superficial medullary ray and thereafter in the preretinal vessels and extraretinal fibroblasts. Capillary budding was obvious within 3 days, with endothelial cells extending cytoplasmic processes into fragmented extracellular matrix (ECM). Endothelial cells, at the tips of budding vessels, and at more proximal sites in the parent vessel, incorporated 3H-thymidine and did not lose cell contact or migrate individually into the ECM. Lumina were present throughout the entire length of the buds and endothelial cells remained polarized. Neovascular events observed in this experimental model parallel those previously described in diabetic retinopathy and retinopathy of prematurity in humans.

Animals↗
PubMed2004

Systemic rapamycin inhibits retinal and choroidal neovascularization in mice.

PURPOSE: Rapamycin exhibits significant antitumor/antiangiogenic activity that is coupled with a decrease in vascular endothelial growth factor (VEGF) production and a reduction in the response of vascular endothelial cells to stimulation by VEGF. VEGF plays a significant role in neovascular pathologies of the eye, thus we tested the possibility of using rapamycin to inhibit retinal and choroidal neovascularization (CNV). METHODS: CNV was induced in adult mice with laser photocoagulation. Retinal neovascularization was induced using the retinopathy of prematurity (ROP) hyperoxia/hypoxia model. Experimental animals received intraperitoneal (ip) injections of rapamycin (2 mg/kg/day or 4 mg/kg/day) for 1-2 weeks. Controls were not treated or received ip injections of phosphate buffered saline (PBS). Eyes were analyzed histologically for evidence of CNV or retinal neovascularization. ROP eyes were further analyzed for changes in VEGF and VEGF receptor (Flt-1 and Flk-1) protein content following rapamycin treatment. RESULTS: Rapamycin significantly reduced the extent of neovascularization in both the CNV and the ROP model. Immunohistochemical staining of treated and untreated ROP retina did not reveal a significant reduction in levels of VEGF protein or its receptors. Immunostaining for Flt-1 increased, while no obvious changes in Flk-1 were observed. Quantitative analysis of total protein via enzyme linked immunosorbent assay (ELISA) confirmed an increase in Flt-1 and VEGF, following drug treatment, with no effect on Flk-1. CONCLUSIONS: These results suggest rapamycin may provide an effective new treatment for ocular neovascularization.

Animals↗
PubMed2006

Vitreoretinal disorders in anterior megalophthalmos.

PURPOSE: To describe vitreoretinal abnormalities in patients with anterior megalophthalmos (AM) and to report the results of vitreoretinal surgery in these cases. METHODS: In a retrospective, noncomparative case series, a diagnosis of AM was made according to the following criteria: megalocornea, iris hypoplasia, lens subluxation, cataract formation at an early age, and absence of congenital glaucoma. Vitreous biomicroscopy and funduscopy were performed in all patients. Patient records were also reviewed. RESULTS: Twenty-four patients with AM (12 male, 12 female), aged 4 months to 64 years, were included in this study. Funduscopy was possible in 46 eyes. Vitreous degeneration was the most common abnormal posterior segment finding, present in 34 eyes (73.9%). Nine eyes (19.5%) had optically empty vitreous with strands. Lattice degeneration was seen in five eyes (10.8%). Spontaneous vitreous hemorrhage occurred in three eyes, and peripheral retinal neovascularization was detected in two. Retinal detachment occurred in 18 eyes (37.5%); retinal breaks were detected in eight of these before surgery. Thirteen eyes underwent a total of 18 procedures. Retinal reattachment was finally achieved in 12 of the 13 eyes. CONCLUSIONS: Anterior megalophthalmic eyes seem to be affected by a type of vitreoretinopathy predisposing to retinal detachment. Current vitreoretinal surgical techniques usually achieve good anatomic results in these cases.

Adolescent↗
PubMed2002

Arteriovenous sheathotomy for branch retinal vein occlusion.

Branch vein occlusion is a significant cause of visual loss attributed to retinal vascular disease and is second only to diabetic retinopathy. BVO nearly always occurs at an AV crossing because of compression of the vein by the artery, resulting in hemodynamic abnormalities in the vein, including thrombus formation, reversal of flow toward the artery, and AV collateral formation. Relatively little information is available on the natural history of BVO; most of what exists is derived from clinical trials, including the BVOS. Current treatment options focus on treating sequelae of the occluded venous branch, such as macular edema, retinal neovascularization, vitreous hemorrhage, and traction retinal detachment. A novel therapeutic approach is decompression of the AV crossing, which has had promising initial results including restoration of vision and reversal of hemodynamic abnormalities. A prospective, controlled, clinical trial is being organized to determine the role of AV sheathotomy in the treatment of BVO.

Decompression, Surgical↗
PubMed2005

Association of genetic polymorphisms of vascular endothelial growth factor and risk for proliferative retinopathy of prematurity.

The intention of our retrospective study was to determine whether vascular endothelial growth factor (VEGF) genetic polymorphisms are associated with risk for proliferative retinopathy of prematurity (ROP), a condition that is characterized by abnormal retinal neovascularization and can lead to retinal detachment and result in blindness. We enrolled 86 very low birth weight infants (birth weight < or =1500 g) who had been treated with cryo/laser therapy because of the risk for proliferative ROP (treated group). Their VEGF T-460C and G+405C genotypes were determined from dried blood samples and were compared with VEGF genotypes of 115 VLBW infants who were not treated with cryo/laser therapy (untreated group). We found that the allele frequency of VEGF +405C was higher in the treated group than in the untreated group (0.30 versus 0.41; p <0.05). The likelihood of being treated for ROP was higher in heterozygous and homozygous carriers of VEGF +405C alleles [odds ratios adjusted for risk factors of ROP (95% CI): 2.00 (1.02-3.92; p=0.04) and 3.37 (1.17-9.65; p=0.007), respectively]. VEGF -460TT/+405CC haplotype was more prevalent in the treated patients than in the untreated patients (13 of 86 versus 1 of 115; p <0.001), and the association remained significant (p <0.01) even after the adjustment for risk factors of ROP (gestational age, supplemental oxygen therapy, and gender). These findings suggest that the VEGF genotype may be associated with risk for proliferative ROP in VLBW infants.

Female↗
PubMed1989

Two sisters with telangiectases [corrected], spondyloepiphyseal dysplasia, hypothyroidism, neovascularization and tractional retinal detachments: a new entity?

Two sisters had an unusual constellation of findings, including telangiectases [corrected] involving the face and limbs, unclassifiable spondyloepiphyseal dysplasia, hypothyroidism, and tractional retinal detachment preceded by retinal and iris neovascularization. To our knowledge, this combination of defects has not been previously documented in the literature.

Abnormalities, Multiple↗
PubMed2001

The balance between proteinases and inhibitors in a murine model of proliferative retinopathy.

PURPOSE: To examine the expression of matrix metalloproteinases (MMPs) and their inhibitors during the development of retinal neovascularization (NV) in a mouse model. METHODS: A well-characterized murine model of retinal NV was used to study the expression of specific MMPs (MMP-2, MMP-9, and MT1-MMP) and tissue inhibitor of metalloproteinases (TIMPs types 1, 2, and 3). NV of the retina was induced in mice by exposure to 75% O(2) from postnatal day (P)7 to P12, followed by return to room air from P12 to P17. Expression of MMP mRNA was analyzed by reverse transcription-polymerase chain reaction (RT-PCR). In addition, retinal tissue removed from control (without NV) and experimental animals (with NV) was analyzed for the expression of TIMP-1, TIMP-2, and TIMP-3 mRNA and protein using RT-PCR and Western blot analysis. RESULTS: During the angiogenic period from P13 to P17, MMP-2 and -9, and MT1-MMP message expression increased in experimental retinas compared with control samples. The TIMP-2 message and protein levels increased steadily in the retina of control animals until P17. This was in contrast to that seen in the retinas of the experimental animals in which TIMP-2 message and protein remained low and significantly less than in control samples. There were no significant changes in TIMP-3 message levels in retinal tissues, and TIMP-1 message and protein were undetectable. CONCLUSIONS: Correlation was made at the mRNA and protein levels of TIMP expression compared with that of MMPs in a murine model of retinal NV, which suggests a temporal role for MMP-2 and -9, MT1-MMP, and TIMP-2 in new vessel formation in response to hypoxic stimulation.

Animals↗