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PubMed1979

Posterior pole neovascularization in a patient with hemoglobin SC disease.

A 33-year-old black woman with hemoglobin SC disease and a history of photocoagulation for peripherally located retinal neovascularization had a neovascular frond at the temporal border of her right macula. Multiple zones of black sunburst hyperpigmentation were located nearby. Fluorescein angiography showed that the lesions were closely related to an extensive zone of avascular retina in the posterior pole. The perifoveal vasculature was uninvolved, and the patient was unaware of any visual deficit. Although sickle cell maculopathy is a well-recognized entity, there have been no published reports, to the best of our knowledge, of posterior pole neovascularization in patients with sickle cell hemoglobinopathy. The fluorescein angiographic findings in our case provide further support for the hypothesis that retinal hypoxia is an important stimulus for retinal neovascularization.

Adult↗
PubMed2006

The role of growth hormone, insulin-like growth factor and somatostatin in diabetic retinopathy.

Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are implicated in the aberrant cell growth and pathological neovascularization that characterises proliferative diabetic retinopathy. While serum levels of IGF-I are reported to be either high or low in diabetic patients, there is evidence that local tissue levels of IGF-I may be more relevant to diabetic retinal pathology. IGF-I and IGF binding proteins (IGFBP) are expressed throughout the retina in vascular, neuronal and glial cells, and are altered in response to hyperglycaemia and hypoxia. Further support for a pathological role for local IGF-I comes from studies showing IGF-I to be increased in the vitreal fluids of patients with proliferative diabetic retinopathy. IGF-I may exert its cell growth promoting properties by stimulating a number of pathways including protein-kinase B (Akt), nuclear factor kB (NF-kappaB)/AP-1 and hypoxic-inducible factor-1alpha (HIF-1alpha). In addition, other growth factors may participate in IGF-I induced cell growth including vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF) and fibroblast growth factor (FGF). The importance of the GH/IGF system in diabetic retinopathy and retinal neovascularization has been highlighted by the use of agents that inhibit the system. GH receptor antagonists, GH receptor antisense oligonucleotides, somatostatin analogues and receptor neutralising antibodies to IGF-I reduce hypoxic-induced retinal neovascularization. These approaches may also prove to have benefits for improving vascular patency and vision in patients with diabetic retinopathy.

Diabetic Retinopathy↗
PubMed2004

Pathological angiogenesis is reduced by targeting pericytes via the NG2 proteoglycan.

The NG2 proteoglycan is expressed by nascent pericytes during the early stages of angiogenesis. To investigate the functional role of NG2 in neovascularization, we have compared pathological retinal and corneal angiogenesis in wild type and NG2 null mice. During ischemic retinal neovascularization, ectopic vessels protruding into the vitreous occur twice as frequently in wild type retinas as in NG2 null retinas. In the NG2 knock-out retina, proliferation of both pericytes and endothelial cells is significantly reduced, and the pericyte:endothelial cell ratio falls to 0.24 from the wild type value of 0.86. Similarly, bFGF-induced angiogenesis is reduced more than four-fold in the NG2 null cornea compared to that seen in the wild type retina. Significantly, NG2 antibody is effective in reducing angiogenesis in the wild type cornea, suggesting that the proteoglycan can be an effective target for anti-angiogenic therapy. These experiments therefore demonstrate both the functional importance of NG2 in pericyte development and the feasibility of using pericytes as anti-angiogenic targets.

Animals↗
PubMed1999

Thermotherapy for retinoblastoma.

OBJECTIVE: To evaluate the results of thermotherapy for retinoblastoma. DESIGN: Prospective, nonrandomized analysis of the treatment method. PARTICIPANTS: A total of 188 retinoblastomas in 80 eyes of 58 patients who were treated with thermotherapy. MAIN OUTCOME MEASURES: Tumor response and ocular adverse effects. RESULTS: Of 188 retinoblastomas treated with thermotherapy, mean tumor base was 3.0 mm and tumor thickness was 2.0 mm. Complete tumor regression was achieved in 161 tumors (85.6%), and 27 tumors (14.4%) developed recurrence. Using univariate analysis, the predictors of local tumor recurrence were male sex (P = .005), no color change ("no visible take") in tumor after treatment (P = .01), increasing number of treatment sessions (P = .002), and previous use of chemoreduction (P = .02). By multivariate analysis, the most important predictors of local tumor recurrence were male sex (P = .01) and previous use of chemoreduction (P = .03), the latter likely reflecting the fact that these tumors were initially larger with more ominous findings, and required chemoreduction therapy to reduce them to a size amenable to focal treatment with thermotherapy. When evaluating thermotherapy variables as a function of tumor size, it was apparent that larger tumors (> or =3.0-mm base) required greater energy and time than did smaller tumors (<3.0-mm base). Comparison of treatment variables for larger vs smaller tumors was as follows: number of treatment sessions, 3.3 vs 2.3; spot size, 1.7 vs 1.3 mm; power, 540 vs 370 mW; treatment duration, 49 vs 14 minutes; and coupling of thermotherapy with chemotherapy, 79% vs 48% of cases (P < or =.001 for each variable). Complications of thermotherapy in the 80 eyes included focal iris atrophy in 29 eyes (36%), peripheral focal lens opacity in 19 eyes (24%), retinal traction in 4 eyes (5%), retinal vascular obstruction in 2 eyes (2%), and transient localized serous retinal detachment in 2 eyes (2%). There were no cases of corneal scarring, central lens opacity, iris or retinal neovascularization, or rhegmatogenous retinal detachment. All eyes with focal lens opacity demonstrated adjacent focal iris atrophy. By multivariate analysis, the predictors of thermotherapy-induced focal iris atrophy were increasing number of treatment sessions (P = .001) and increasing tumor base (P = .02). CONCLUSIONS: Thermotherapy is used for relatively small retinoblastomas without associated vitreous or subretinal seeds. This treatment provides satisfactory control for selected retinoblastomas, with 86% of tumors demonstrating lasting regression. Tumors that measure 3.0 mm or larger in base at the time of thermotherapy require more intense treatment than smaller tumors and are at greatest risk for ocular complications such as focal iris atrophy and focal paraxial lens opacity.

Chemotherapy, Adjuvant↗
PubMed1987

[Retinal dystrophy with Coats syndrome].

The combination of retinopathia pigmentosa and Coats syndrome is described. The clinical picture shows spotty pigmentations, retinal neovascularizations, peripheral exudative retinal detachment, defects of the retinal pigment epithelium, and changes in the macula.

Adult↗
PubMed2005

Sodium fluorescein as a retinal pH indicator?

Retinal neovascularization is a symptom associated with various diseases revealing ocular fundus manifestation. Often, these neovascularizations originate from retinal hypoxia. A concomitant phenomenon of hypoxia is acidosis. To recognise this would permit the identification and treatment of hypoxic fundus areas long before first vascular modifications are seen. Thus, the goal of this investigation was to elucidate whether sodium fluorescein could be used as a retinal pH indicator. Sodium fluorescein solution was diluted in PBS (ratio: 1:150,000). The pH was varied from 6.5 to 8.6 by supplementation of HCl or NaOH, respectively. The fluorescence was excited by a pulsed diode laser (wavelength: 446 nm, pulse width: 100 ps) and detected by time-correlated single photon counting (TCSPC) technique. A least-squares fit of the measured fluorescence decay versus time by an exponential function results in the fluorescence lifetime. Ten measurements were taken at each pH for statistical analysis. The dependence of the fluorescence lifetime on the temperature and the concentration of sodium fluorescein was investigated in the same way. The fluorescence lifetime was found to rise from 3.775 ns to 4.11 ns with increasing pH (6.5 to 8.6). However, the gradient decreases with increasing pH. We found highly significant differences (Student's t-test, P<0.0005) of the fluorescence lifetimes for pH values with a mean difference of 0.125 at pH<7.65 whereas the differences were still significant (P 7.65 and mean pH differences of 0.2. The fluorescence lifetime was independent of the temperature (22 degrees C to 37 degrees C) and the concentration of sodium fluorescein (dilution 1:150,000 to 1:2000). The fluorescence lifetime of sodium fluorescein depends on the pH but not on temperature and concentration. Thus, the discrimination of areas with retinal acidosis should be possible by combination of the TCSPC technique with scanning laser ophthalmoscopy. Further investigations have to clarify whether the accuracy of the measurement at the fundus in vivo is sufficient.

Acidosis↗
PubMed2006

Therapeutic potential of angiostatin in diabetic nephropathy.

Angiostatin is a proteolytic fragment of plasminogen and a potent angiogenic inhibitor. Previous studies have shown that angiostatin inhibits retinal neovascularization and reduces retinal vascular permeability in diabetic retinopathy. Here, it is reported for the first time that angiostatin is also implicated in diabetic nephropathy (DN). Angiostatin levels are dramatically decreased in the kidney of streptozotocin-induced diabetic rats. Consistently, diabetic kidneys also showed decreased expression and proteolytic activities of matrix metalloproteinase-2, an enzyme that releases angiostatin from plasminogen. Adenovirus-mediated delivery of angiostatin significantly alleviated albuminuria and attenuated the glomerular hypertrophy in diabetic rats. Moreover, angiostatin treatment downregulated the expression of vascular endothelial growth factor and TGF-beta1, two major pathogenic factors of DN, in diabetic kidneys. In cultured human mesangial cells, angiostatin blocked the overexpression of vascular endothelial growth factor and TGF-beta1 that were induced by high glucose while increasing the levels of pigment epithelium-derived factor, an endogenous inhibitor of DN. Moreover, angiostatin effectively inhibited the high-glucose-and TGF-beta1-induced overproduction of proinflammatory factors and extracellular matrix proteins via blockade of the Smad signaling pathway. These findings suggest that the decrease of angiostatin levels in diabetic kidney may contribute to the pathologic changes such as inflammation and fibrosis in DN. Therefore, angiostatin has therapeutic potential in DN as a result of its anti-inflammatory and antifibrosis activities.

Angiostatins↗
PubMedDate not supplied

Retinal branch vein occlusion.

Obstruction of a major temporal branch vein, or one of its macular tributaries, presents a significant threat to vision. Visual acuity may be reduced by macular edema or the consequences of retinal neovascularization, and these afflictions frequently become irreversible. Since the complicating macular edema and retinal neovascularization respond, at least in part, to argon laser therapy in some other conditions, some investigators have begun to treat branch vein occlusions with this modality. However, since the pathogenesis and natural history of the disorder have not yet been elucidated by prospective studies, it is not clear whether such treatment is indicated. Clinical and experimental studies are reviewed, and treatment rationale and techniques are discussed. The authors emphasize the need for well-controlled randomized studies to evaluate the natural history of branch vein occlusion and the efficacy of photocoagulation in its treatment.

Diagnosis, Differential↗
PubMed1989

A two-year follow-up study of serum insulinlike growth factor-I in diabetics with retinopathy.

Serum insulinlike growth factor-I (IGF-I) concentration was evaluated prospectively over two years in 35 diabetic patients with severe background or preproliferative retinopathy (group 1) and 24 diabetics with mild background retinopathy matched for age, sex, and glycemic control (group 2). In addition, 12 normal subjects were also studied to assess the variability of individual serum IGF-I levels over two years. Mean serum IGF-I (+/- SD) micrograms/l at entry, one year, and two years was not significantly different in the patient groups (157 +/- 71 v 168 +/- 77; 166 +/- 78 v 159 +/- 87; 143 +/- 58 v 159 +/- 67) or when compared with the normal subjects (181 +/- 47, 188 +/- 30; 221 +/- 56). Eight patients in the preproliferative group and none in the mild background group developed proliferative retinopathy. In this subgroup developing retinal neovascularization, serum IGF-I at the time of the first appearance of retinal new vessels was significantly higher than 3 months (1 to 4 months) before the onset of proliferation (271 +/- 94 v 196 +/- 58; P = .036). Values at the time of proliferation were not, however, significantly different from the mean serum IGF-I value of all patients in group 1 and by 4 months (3 to 6 m) had returned to their previous values. Although a transient elevation of IGF-I occurs at the time of retinal new vessel formation, the rise in serum concentration is not sufficiently great or early enough to be of clinical value as a predictor of retinal neovascularization.

Adult↗
PubMed2000

Ocular changes in heredo-oto-ophthalmo-encephalopathy.

BACKGROUND: Heredo-oto-ophthalmo-encephalopathy (HOOE) is a dominantly inherited disease characterised by gradual loss of vision from the age of 20, progressive hearing loss from the late 20s, cerebellar ataxia in the 30s, and death in dementia in the fourth or fifth decade. Currently, no detailed description has been given of the ocular changes seen in HOOE. Therefore, the ocular changes of HOOE were described on the basis of clinical and histological data from six affected family members. METHODS: Three members of the family affected by HOOE were subjected to a full ophthalmological re-examination, and postmortem examination was done on three eyes from two affected family members. RESULTS: Visual loss in HOOE was caused by posterior subcapsular cataract and retinal neovascularizations leading to vitreous haemorrhages and neovascular glaucoma. In the retina there was extensive accumulation of an amyloid material, both diffusely and in the walls of the retinal vessels. The retinal glial cells showed extensive pathological changes and retinal Müller cells were seen to occlude the lumen of retinal vessels. CONCLUSION: Heredo-oto-ophthalmo-encephalopathy is a familial amyloidosis of the central nervous system which is different from previously reported cases of amyloidosis by including cataract and retinal neovascularizations. The disease is accompanied by extensive changes in retinal glial cells that may play a part in the pathophysiology of the ocular complications of the disease.

Cerebellar Ataxia↗
PubMed1982

Ocular neovascularization with retinal vascular occlusion. II. Occurrence in central and branch retinal artery occlusion.

Sixty-one patients (64 eyes) with central retinal artery occlusion (CRAO) and 41 patients (44 eyes) with branch retinal artery occlusion (BRAO) were studied in detail clinically to find out the pathogenesis of their ocular neovascularization (NV). Ocular NV was seen in 12 eyes (11 patients) with CRAO: iris NV was seen in all 12 eyes, angle NV was seen with neovascular glaucoma (NVG) in ten of them, and no NV was seen in BRAO. Nine of ten patients with CRAO associated with NVG were old, having severe carotid artery disease (CAD) and severe generalized atherosclerotic arterial disease; in the remaining patient, NVG was caused by diabetes mellitus. Severe CAD results in chronic ocular ischemia, which, in turn, produces NV of the iris and angle and NVG; the latter, combined with poor perfusion pressure in the central retinal artery (caused by severe CAD), results in CRAO. Our study showed little evidence that CRAO, per se, is responsible for ocular NV. Various evidence in support of this hypothesis is presented. Our study also showed that the only eyes to recover good vision were those with transient CRAO for up to 11/2 hours, and no treatment helped.

Adolescent↗
PubMed1977

Evolution of neovascularization in sickle cell retinopathy. A prospective fluorescein angiographic study.

With prospective observations we have documented by fluorescein angiography the development of retinal neovascularization in the eyes of patients with sickle cell-hemoglobin C disease (hemoglobin SC). In each patient, arteriolarvenular (AV) anastomoses occurred before the development of neovascular sea fans. To our knowledge, this report constitutes the first such documentation in the literature. New sea fans from AV anastomoses appeared throughout an average interval of 18 months (range, 8 to 36 months) in approximately 21% of young adults with hemoglobin SC. Each year approximately 14% of young patients with hemoglobin SC may develop retinal neovascularization.

Adolescent↗
PubMed1985

Cases reported at the FAN club meeting, Bonn, November 1984. Case 1: A case of preretinal neovascularization after retinal artery occlusion.

A 63 year-old man presented with an occlusion of the inferior temporal artery in his right eye, followed ten days later by an obstruction of the central retinal artery. Internal carotid stenosis was diagnosed and the patient underwent carotid endarterectomy. The retinal arterial circulation was restored except in the previously occluded inferotemporal artery. Nine months after the occlusion, preretinal new vessels began to grow at the border of the ischaemic area. Possible mechanisms governing the proliferation of new vessels after retinal arterial occlusion are discussed.

Angiography↗
PubMed2001

Is one 60 degrees fundus photograph sufficient for screening of proliferative diabetic retinopathy?

OBJECTIVE: To compare one 60 degrees fundus photograph to seven field stereo fundus photographs in identifying proliferative diabetic retinopathy. RESEARCH DESIGN AND METHODS: A total of 44 eyes in 23 patients with moderate/severe nonproliferative diabetic retinopathy were included. Evaluation of each eye was based on one 60 degrees fundus photograph. Eyes were re-examined using seven field 30 degrees stereo fundus photographs according to the protocol of the Early Treatment Diabetic Retinopathy Study, and the photographs were examined independently by three ophthalmologists to identify retinal neovascular lesions. In addition, fluorescein angiography was performed in all patients to verify the presence of the lesions. RESULTS: In four eyes of three patients (11.1% of eyes) evaluated based on seven field stereo photographs, retinal neovascularization was found. This condition was not found on examination of 60 degrees fundus photographs. CONCLUSIONS: Examination of one 60 degrees fundus photograph was found to be insufficient as a screening procedure in patients with moderate/severe nonproliferative diabetic retinopathy.

Adult↗
PubMedDate not supplied

Histopathological findings in proliferative membrane from a patient with sarcoid uveitis.

BACKGROUND: Sarcoid uveitis is occasionally accompanied by proliferative changes, such as retinal neovascularization and vitreous hemorrhage. Steroid administration, retinal photocoagulation, and vitrectomy may be indicated in such proliferative cases. CASE: A 19-year-old woman presented with proliferative sarcoid uveitis accompanied by recurrent vitreous hemorrhage. OBSERVATIONS: At the initial examination, bilateral vitreous opacity, retinal exudates, mild vitreous hemorrhage, retinal vasculitis, and neovascularization of the retina and optic disc were observed. Although prednisolone was administered and panretinal photocoagulation was performed several times, recurrent vitreous hemorrhage continued. Since the vitreous hemorrhage was not absorbed, pars plana vitrectomy and lensectomy were performed. After surgery, neovascularization and intraocular inflammation decreased, and the corrected visual acuity in the right eye improved to 20/50. Histopathologic analysis of the proliferative membrane removed during surgery revealed substantial neovascularization and numerous neutrophils in the vessels. CONCLUSIONS: Based on these findings, an inflammatory reaction as well as retinal ischemia were thought to be involved in the proliferative changes in this patient.

Adult↗