Retinal neovascularization, collaterals, and vascular shunts.
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Anemia, Sickle Cell↗
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Peripheral retinal neovascularization with chronic myelogenous leukemia.
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Adult↗
Retinal neovascularization in sickle cell retinopathy.
Neovascularization of the retina occurs in several types of sickle cell hemoglobinopathies and is highly characteristic in appearance. It arises in the equatorial plane of the fundus following preliminary arteriolar occlusions and arteriolar-venular anastomoses. Neovascular sea fans arise at the interface of perfused and nonperfused portions of the retina, starting during the first decade of life and continuing for many years thereafter. Although some sea fans undergo spontaneous autoinfarction, most show progressive growth and constant intravitreal transudation of plasma components. Traction on the sea fans and the retina results in bleeding into the vitreous, retinal tears, and retinal detachment. Therapeutic intervention with a variety of coagulative techniques is feasible and is usually indicated whenever sea fans are discovered. All therapeutic modalities are capable of inducing significant complications. This is particularly true of argon laser photocoagulation when energy is concentrated into small areas (less than 200 mu) for short durations (less than 0.2 second). With appropriate precautions, photocoagulation results in a high rate of successful obliteration of neovascular tissue. Both vitrectomy and scleral buckling are valuable therapeutic procedures, but both have disproportionately high complication rates in eyes with the propensity for intravascular sickling of erythrocytes. Specific prophylactic measures are therefore indicated when these operative techniques are employed in patients with sickle cell diseases.
Adult↗
Regression of retinal neovascularization in diabetic retinopathy.
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Diabetic Retinopathy↗
[Development of blood vessels and neovascularization (retinitis proliferans) in the eyeground].
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Humans↗
Diabetic retinal neovascularization treated by photocoagulation.
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Adult↗
Eales' disease: accumulation of reactive oxygen intermediates and lipid peroxides and decrease of antioxidants causing inflammation, neovascularization and retinal damage.
PURPOSE: To measure the blood levels of oxygen and lipid-free radicals as lipid peroxidation products and of vitamins E, C and A, in order to explain intraocular inflammation, retinal neovascularization and detachment in Eales' disease. METHODS: Levels of the lipid peroxidation products produced by oxygen and lipid free radicals (estimated as thiobarbituric acid reactive substances-TBARS), vitamin E with ferric chloride, vitamin C with 2,6-dichlorophenol-indophenol and vitamin A with antimony trichloride were all evaluated in three groups of subjects between 20 and 40 years of age. Twenty three were patients with Eales' disease in the active perivasculitis stage (Group I), 19 were patients with Eales' disease in the healed-perivasculitis stage (Group II), and 46 were healthy volunteers (Group III), used as normal controls. Patients in each group were subdivided into two age groups, 20-30 and 31-40 years, each group containing both sexes. RESULTS: The results showed a 4.6- and 5.6-fold increase in the levels of TBARS in erythrocytes of patients with Eales' disease in the active perivasculitis stage (Group I) and a 2-fold increase in patients with Eales' disease in the healed perivasculitis stage (Group II), when compared to levels in the controls (Group III). On the other hand, there was a decrease of 75 and 76.2% in the levels of vitamin E in serum, 34 and 40.9% of vitamin C in plasma and 72.8 and 67% of vitamin A in serum in patients with Eales' disease in the active perivasculitis stage (Group I), as compared to the controls (Group III). Also decreases of 56 and 43.5% of vitamin E in serum, 26.8 and 12.5% of vitamin C in plasma and 50.5 and 49.4% of vitamin A in serum were found in patients with Eales' disease in the healed perivasculitis stage (Group II) as compared to the healthy controls (Group III). The two values of variations between the patients and the normal control group given above for TBARS, vitamins E,C and A are for the two age groups, 20-30 and 31-40 respectively. The differences were statistically significant (P < 0.01 to 0.001). CONCLUSIONS: Lowered levels of antioxidant vitamins E and C and consequent accumulation of oxygen and lipid free radicals, or vice versa, could explain the inflammation, neovascularization and retinal pathology in patients with Eales' disease. Also, vitamin A deficiency could aggravate retinal illness.
Adult↗
Intraocular expression of endostatin reduces VEGF-induced retinal vascular permeability, neovascularization, and retinal detachment.
Endostatin, a proteolytic fragment of collagen XVIII, is an endogenous inhibitor of tumor angiogenesis that also inhibits choroidal neovascularization. In this study, we assessed the effects of increased intraocular expression of endostatin on vascular endothelial growth factor (VEGF)-induced changes in the retina. After subretinal injection of a pair of gutless adenoviral vectors (AGV) designed to provide tamoxifen-inducible expression of endostatin, diffuse endostatin immunoreactivity was induced thoroughout the retina by administration of tamoxifen. Induction of endostatin in double transgenic mice with doxycycline-induced expression of VEGF in the retina resulted in significant suppression of leakage of intravascular [3H]mannitol into the retina. The ability of endostatin to reduce VEGF-induced retinal vascular permeability was confirmed by using [3H]mannitol leakage and two other parameters, fluorescein leakage and retinal thickness, after subretinal injection of a bovine immunodeficiency lentiviral vector coding for endostatin (BIV-vectored endostatin, or BIVendostatin). Subretinal injection of BIVendostatin resulted in more discrete, less intense staining for endostatin in the retina than that seen with the inducible AGV system, which suggested lower levels and allowed visualization of sites where endostatin was concentrated. Endostatin staining outlined retinal blood vessels, which suggested endostatin binding to a component of vessel walls. More prolonged or higher level expression of VEGF in the retina resulted in neovascularization and retinal detachment, both of which were also significantly reduced by BIVendostatin. These data suggest that endostatin may be an endogenous inhibitor of vasopermeability as well as neovascularization. In patients with diabetic retinopathy, endostatin gene transfer may provide a way to decrease the risk of three causes of visual loss: macular edema, neovascularization, and retinal detachment.
Animals↗
Histopathologic study of presumed parafoveal telangiectasis.
PURPOSE: To report the postmortem histopathologic features that closely resemble the clinical features of parafoveal telangiectasis. METHODS: Light and electron microscopy. RESULTS: Histopathologic features included macular edema; telangiectatic vessels; retinal, subretinal, and superficial retinal neovascularization; retinal pigment epithelial hyperplasia around neovascular aggregates; retinal-choroidal vascular anastomosis; and superficial pigmented cells with lipofuscin. CONCLUSION: The postmortem histopathologic findings in a 36-year-old woman with Down syndrome and other systemic conditions correlate with features noted in previous reports of presumed parafoveal telangiectasis.
Adult↗
Deficient activation and different expression of transforming growth factor-beta isoforms in active proliferative diabetic retinopathy and neovascular eye disease.
An increased expression and secretion of angiogenic growth factors was proposed to occur in proliferative diabetic retinopathy and other neovascularizing retinal diseases. However, a loss of anti-angiogenic factors also might promote retinal neovascularization. Therefore we investigated the active and latent vitreous levels of the subtypes of the endothelial anti-mitogen transforming growth factor-beta in vitreous of 58 patients. Four groups of patients were compared: Controls without retinal hypoxia, patients with quiescent and active proliferative diabetic retinopathy (PDR), and patients with severe retinal hypoxia resulting in rubeosis iridis. Whereas the amount of total TGF-beta in the four groups did not differ significantly, latent TGF-beta isoform expression showed complex alterations in ocular vitreous. Levels of active TGF-beta of patients with active PDR (79.5 +/- 28 pg/ml; n = 8) were decreased to 20% of the control levels (378 +/- 55 pg/ml; n = 12; p = 0.0005) and 25% of the mean concentration in quiescent PDR (346 +/- 64 pg/ml; n = 9; p = 0.0021). Levels in rubeosis (52 +/- 10 pg/ml; n = 10) did not differ significantly from those found in active PDR but were decreased to 15% of those in patients with quiescent PDR (p = 0.0004). Furthermore a highly significant inverse correlation between active TGF-beta and alpha2-antiplasmin, a liver produced inhibitor of the activation of TGF-beta by plasmin was noted (r = -0.59; n = 28; p = 0.001). We conclude that deficient activation of TGF-beta occurs in active proliferative diabetic retinopathy and in hypoxic angiogenesis most likely as a consequence of a blood retina barrier breakdown and influx of alpha2-antiplasmin from serum. The disinhibition of endothelial cell proliferation may be a central component in the process of neovascularization.
Aged↗
Ocular findings in homozygous sickle cell disease in Jos, Nigeria.
Ophthalmological examinations were performed in 78 homozygous sickle cell (Hb SS) patients, aged 4-42 years attending the sickle cell clinic of the Jos University Teaching Hospital, and the University Clinic, Jos, in Nigeria. Conjunctival signs present in about 77% of cases were observed in all ages and sexes. White without pressure present in 62.8% of the cases was the commonest retinal sign and in 56.3% of the cases was associated with peripheral retinal vessel disease. Salmon patches (6.4%), iridescent spots (10.3%), mottled brown areas (16.7%) and black sunbursts (7.7%) were seen as early as 10 years of age but showed an upward trend with age. Peripheral retinal vessel disease present in 52.5% of the cases was the second commonest retinal sign and with the exception of arteriolar occlusion showed no sex predilection, but an upward trend with age. Arterio-venous anastomosis (7.7%), vitreous haemorrhages and veils (3.8%) were the only severe proliferative signs noted. There were no cases of retinal neovascularization, retinal detachment or of angoid streaks, and the posterior poles were normal. Retinal signs were present as early as 8 years of age and showed an upward trend with age.
Adolescent↗
Implication of the hypoxia response element of the Vegf promoter in mouse models of retinal and choroidal neovascularization, but not retinal vascular development.
Retinal neovascularization (NV) and macular edema, resulting from blood-retinal barrier (BRB) breakdown, are major causes of visual loss in ischemic retinopathies. Choroidal NV (CNV) occurs in diseases of the retinal pigmented epithelium/Bruch's membrane complex and is another extremely prevalent cause of visual loss. We used mice in which the hypoxia response element (HRE) is deleted from the vascular endothelial growth factor (vegf) promoter (Vegf(delta/delta) mice) to explore the role of induction of VEGF through the HRE in these disease processes. Compared to wild type (Vegf+/+) mice with oxygen-induced ischemic retinopathy (OIR) in which vegf mRNA levels were increased and prominent retinal NV and BRB breakdown occurred, Vegf(delta/delta) littermates with OIR failed to increase vegf mRNA levels in the retina and had significantly less retinal NV and BRB breakdown, but showed prominent dilation of some superficial retinal vessels. Vegf(+/delta) littermates with ischemic retinopathy developed comparable retinal NV to Vegf+/+ mice, exhibited intermediate levels of BRB breakdown, and did not show vasodilation. In a mouse model of CNV, due to laser-induced rupture of Bruch's membrane, the area of CNV at Bruch's membrane rupture sites was more than tenfold greater in Vegf+/+ mice than in Vegf(delta/delta) littermates. In contrast to these dramatic differences in pathologic ocular NV, Vegf(delta/delta) mice showed subtle differences in retinal vascular development compared to Vegf+/+ mice; it was slightly delayed, but otherwise normal. These data suggest that induction of VEGF through the HRE in its promoter is critical for retinal and CNV, but not for retinal vascular development.
Animals↗
Systemically expressed soluble Tie2 inhibits intraocular neovascularization.
Retinal and choroidal neovascularization are the most frequent causes of severe and progressive vision loss. Studies have demonstrated that Tie2, an endothelial-specific receptor tyrosine kinase, plays a key role in angiogenesis. In this study, we determined whether adenovirus-mediated gene delivery of extracellular domain of the Tie2 receptor (ExTek) could inhibit experimental retinal and choroidal neovascularization. Immunofluorescence histochemistry with a monoclonal antibody to human Tie2 showed that Tie2 expression is prominent around and within the base of newly formed blood vessels of retinal and choroidal neovascular lesions. A single intramuscular injection of adenovirus expressing ExTek genes achieved plasma levels of ExTek exceeding 500 microg/ml in mice for 10 days (in neonates) and 7 days (in adults). This treatment inhibited retinal neovascularization by 47% (p < 0.05) in a murine model of ischemia-induced retinopathy. The same treatment reduced the incidence and extent of sodium fluorescein leakage from choroidal neovascular lesions by 52% (p < 0.05) and 36% (p < 0.01), respectively, in a laser-induced murine choroidal neovascularization model. The same mice showed a 45% (p < 0.001) reduction of integrated area of the choroidal neovascularization. These findings indicate that Tie2 signaling is a common component of the angiogenic pathway in both retinal and choroidal neovascularization, providing a potentially useful target in the treatment of intraocular neovascular diseases.
Adenoviridae↗
Retinal ischemia with neovascularization in cisplatin related retinal toxicity.
PURPOSE: To report a case of macular ischemia and retinal neovascularization in a patient who received cisplatin related chemotherapy. DESIGN: Interventional case report. METHODS: A patient with germ cell testicular tumor received polychemotherapy (bleomycin, etoposide, and cisplatin or BEP) for a recurrence of his tumor. Ten weeks after completion of treatment, he presented with loss of vision in his left eye. RESULTS: Fluorescein angiography revealed bilateral retinal ischemia and left retinal neovascularization. Panretinal laser photocoagulation was performed. Unfortunately, his vision did not improve. CONCLUSIONS: Like interferon, cisplatin related chemotherapy could cause considerable ocular morbidity. It can cause marked irreversible visual loss at therapeutic dose, and it is not well recognized. Retinal neovascularization related to cisplatin therapy has not been previously reported. Physicians should be aware and warn patients of the potential ophthalmic side effects of cisplatin related chemotherapy.
Adult↗
Ocular neovascularization with retinal vascular occlusion-III. Incidence of ocular neovascularization with retinal vein occlusion.
A prospective natural history study was conducted in 721 eyes with various types of retinal vein occlusion (RVO) to determine the incidence of various types of ocular neovascularization (NV) and the factors that influence the development of ocular NV. The material was 360 eyes with central retinal vein occlusion (CRVO), 97 eyes with hemi-CRVO, and 264 eyes with branch retinal vein occlusion (BRVO); these cases were further subdivided into six groups for logical data analysis: nonischemic CRVO (venous stasis retinopathy-VSR, 282 eyes), ischemic CRVO (hemorrhagic retinopathy-HR, 78 eyes), hemi-VSR (66 eyes), hemi-HR (31 eyes), major BRVO (191 eyes) and macular BRVO (73 eyes). Ocular NV attributable to RVO was seen only in HR, hemi-HR, and major BRVO. In HR the anterior segment was the major site of NV, with iris and angle NV and neovascular glaucoma (NVG), while in hemi-HR and major BRVO the retina and optic disc were the major sites of NV. The principal factor influencing the development of ocular NV in RVO seems to be the severity and extent of retinal ischemia, while duration of follow-up since onset also plays an important role in determining the incidence of ocular NV. The findings and subject of ocular NV in RVO are discussed in detail along with a review of the pertinent literature.
Adult↗
Peripheral neovascularization complicating rhegmatogenous retinal detachments of long duration.
Nine eyes in nine patients with rhegmatogenous retinal detachments of 1-18 years, duration showed clinical evidence of significant retinal neovascularization in the equatorial region. The retinal new vessels showed a sea-fan configuration. Their extent in the periphery of the fundus ranged from 10 degrees to 180 degrees. All retinal detachments were associated with round atrophic retinal holes in the equatorial region. Retinal reattachment was achieved in all eyes with scleral buckling. The retinal new vessels totally regressed within 15 days to 3 months after retinal reattachment. It is believed that the peripheral retinal new vessels were secondary to retinal hypoxia resulting from decreased retinal blood flow in the detached retina.
Adolescent↗
Lentivirus-mediated expression of angiostatin efficiently inhibits neovascularization in a murine proliferative retinopathy model.
Ischemic retinal diseases, such as diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration, are a major cause of blindness worldwide. Angiostatin is an internal peptide fragment of plasminogen that inhibits endothelial proliferation in vitro and tumor growth in vivo. We now demonstrate that HIV vector encoding angiostatin (HIV-angiostatin) can inhibit retinal neovascularization in a mouse model of proliferative retinopathy. Intravitreal injections of HIV-angiostatin led to stable expression of the angiostatin gene in retinal tissue. Retinal neovascularization was histologically quantitated by a masked protocol. Retinal neovascularization in the eye injected with HIV-angiostatin was reduced in 90% (9/10; P=0.025) of animals, compared with the eye injected with phosphate-buffered saline. Reduction of histologically evident neovascular nuclei per 6-microm section averaged 68%, with maximal inhibitory effects of 87%. Neovascularization was not reduced in the eyes injected with HIV vector encoding enhanced green fluorescent protein. This is the first report that HIV-angiostatin can reduce neovascular cell nuclei in a murine proliferative retinopathy model. These data suggest that the anti-angiogenic activity of angiostatin has therapeutic potential for the treatment of retinal neovascularization.
Angiostatins↗
Optical scattering, absorption, and polarization of healthy and neovascularized human retinal tissues.
The optical scattering, absorption, and polarization properties of human retinal tissues are investigated for a number of laser wavelengths in the visible range. The indices of refraction of these tissues are determined by applying Brewster's law. The inverse adding doubling method based on the diffusion approximation and radiative transport theory is applied to the measured values of total diffuse transmission, total diffuse reflection, and index of refraction to determine the optical absorption, scattering, and scattering anisotropy coefficients of the intact retinal tissues from healthy and diseased (neovascularized) human eyes. The polarization studies show that the retinal tissues possess significant intrinsic polarization characteristics, that are more pronounced in diseased tissues than in healthy tissues.
Absorption↗