Infantile choroidal neovascularization associated with choroidal coloboma.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
AIMS: To determine whether pigment epithelium derived factor (PEDF), a protein that inhibits angiogenesis, is expressed in human choroidal neovascular membranes (CNVMs) and in tissues from an eye with polypoidal choroidal vasculopathy (PCV). In addition, to compare the expression of PEDF with that of vascular endothelial growth factor (VEGF), a known stimulator of angiogenesis, in these tissues. METHODS: CNVMs, associated with age related macular degeneration (AMD), angioid streaks, and PCV, were obtained during surgery. The expression of PEDF and VEGF in the excised subretinal fibrovascular membranes was determined by immunohistochemistry. RESULTS: PEDF and VEGF were strongly expressed in the vascular endothelial cells and retinal pigment epithelial (RPE) cells in the CNVMs where numerous new vessels were prominent (clinically active CNVMs). On the other hand, immunoreactivity for PEDF and VEGF was weak in the new vessels where fibrosis was prominent (clinically quiescent CNVMs). However, the RPE cells were still positive for PEDF and VEGF. The specimens from the eye with PCV also showed strong expression of PEDF and VEGF in the vascular endothelial cells and the RPE cells. CONCLUSION: Because PEDF is an inhibitor of ocular angiogenesis and an inhibitor of ocular cell proliferation, our results suggest that PEDF along with VEGF may modulate the formation of subfoveal fibrovascular membranes.
Senile macular choroidal degeneration (SMCD) is responsible for the majority of cases of new central vision loss in the over-fifty population. It is also the single largest cause of legal blindness in the United States. Choroidal neovascular membranes are frequently associated with SMCD and initiate a disciform process that may lead to profound central vision loss. Clinically, it is very difficult to visualize actual new vessel membranes without the aid of rapid sequence fluorescein angiography; various clinical signs, however, are indicative of their presence. Recognition of choroidal neovascular membranes is important; certain membranes lend themselves to photocoagulation by the retinal specialist. This treatment may be successful in preventing further severe and permanent visual loss in some individuals. The purpose of this paper is to discuss the mechanisms of disciform macular degeneration, as well as the clinical signs important to the recognition of choroidal neovascular membranes.
PURPOSE: Evaluation of a large series of choroidal nevi inducing the formation of a neovascular membrane in order to more clearly define the clinical presentation and to evaluate the efficacy of various treatment options. METHOD: Retrospective study of 22 clinical cases. RESULTS: All nevi were situated in the posterior choroid. They had a mean diameter of 3.8 mm and a mean thickness of 1.4 mm. Neovascular membranes were classic in all cases, extrafoveal in 13 cases (59%), and subfoveal in 9 cases (41%). A serous retinal detachment was present in every case, hemorrhages were present in 13 cases (59%), and lipid deposits were present in 16 cases (73%). All extrafoveal neovascular membranes were successfully treated by thermal laser photocoagulation. Initial visual acuity was 0.1 in three cases, 0.2-0.4 in five cases, 0.5-0.8 in four cases, and 1.0 or more in two cases. Final visual acuity was 0.1 in one case, 0.2-0.4 in one case, 0.5-0.8 in four cases, and 1.0 or more in seven cases. Five subfoveal neovascular membranes were treated either by thermal laser, photodynamic therapy, or irradiation. No treatment was applied in four cases and in one of these cases, spontaneous resolution of the neovascular membrane was observed. No growth of the pigmented tumor was observed with a mean follow-up of 4.8 years. CONCLUSIONS: Proliferation of a neovascular membrane on the surface of a pigmented choroidal tumor is a rare complication and is considered to be a relative indicator of a benign nature of the lesion. In the authors' experience, neovascular membranes are extrafoveal in more than half of cases and are accessible to laser photocoagulation. In contrast, the various modalities used to treat subfoveal neovascular membrane were ineffective and functional prognosis was unfavorable in these cases.
PURPOSE: To evaluate the visual benefit of photodynamic therapy (PDT) with verteporfin in patients with choroidal neovascularization (CNV) secondary to multifocal choroiditis and panuveitis over a longer follow-up period. METHODS: A total of 14 eyes of 12 patients (mean age 34 years) with a classic subfoveal CNV (13/14) or juxtafoveal CNV (1/14) were treated with PDT. Visual outcome was assessed by best-corrected visual acuity (VA). Morphologic characteristics of CNVs such as localization, size, and activity were monitored by fluorescein angiography. RESULTS: Patients were followed for 3 to 45 months (mean 23 months). During this period, one to six PDTs (mean 2.4) were performed. At the time of the first PDT no acute inflammation was seen in the affected eyes. Improved or stabilized visual function (VA loss < or = 2 lines in the Early Treatment Diabetic Retinopathy Study chart) was observed in 71.4% of the eyes. A total of 78% of the eyes showed an inactive scar in the area of CNV after PDT. Treatment failure after PDT occurred due to uninfluenced CNV growth. No further complications were observed. CONCLUSIONS: PDT in subfoveal or juxtafoveal classic CNV secondary to multifocal choroiditis and panuveitis stabilized or improved VA in the majority of patients over a longer follow-up period. No risk factor for failed VA rehabilitation could be defined.
PURPOSE: To determine whether choroidal neovascularization excision causes mechanical damage to the neurosensory retina, retinal pigment epithelium, or choriocapillaris. METHODS: Prospectively, 18 eyes of 18 consecutive patients who underwent choroidal neovascularization excision were observed. Preoperatively and postoperatively, the integrity of the choriocapillaris circulation in the pathway of choroidal neovascularization extraction was studied by fluorescein and indocyanine green angiography. Using static scanning laser ophthalmoscope microperimetry, the presence of iatrogenic scotomas that developed postoperatively in the pathway of choroidal neovascularization extraction was also investigated. RESULTS: Postoperatively, a choriocapillaris defect was detected in 17 (94.4%) of 18 cases. In 15 cases (83.3%), the choriocapillaris defect had a clear relationship to the pathway of choroidal neovascularization extraction. Postoperatively, a scotoma was present in 16 (88.9%) of 18 cases. In 14 cases (77.8%), the location of the scotoma had a clear relationship to the pathway of choroidal neovascularization extraction. CONCLUSION: Surgical excision of choroidal neovascularization leads to severe damage of the choroid and retina in the pathway of the extracted choroidal neovascularization. The injury involves the neurosensory retina, retinal pigment epithelium, and choriocapillaris.
OBJECTIVE: To determine predictors of choroidal neovascularization (CNV) and visual outcome after traumatic choroidal rupture. METHODS: A retrospective review of patients with traumatic choroidal rupture diagnosed in the Retina Service, Massachusetts Eye and Ear Infirmary, Boston, between January 1993 and August 2001 was performed. Parametric and nonparametric statistical methods were used to evaluate visual prognosis, CNV, and retinal detachment after traumatic choroidal rupture. RESULTS: One hundred eleven cases were identified and reviewed. Visual acuity (VA) changes were recorded in all of the cases. Thirty-eight (34%) of the 111 patients recovered driving vision (VA > or =20/40). Rupture location was recorded in 107 cases. Recovery of driving vision was seen in 20 (59%) of 34 eyes with peripheral choroidal ruptures, 17 (22%) of 73 eyes with macular choroidal ruptures, 38 (38%) of 99 eyes without CNV, 1 (8%) of 12 eyes with CNV, 38 (40%) of 96 eyes without retinal detachment, and 1 (7%) of 15 eyes with retinal detachment. Older age and location of rupture within the arcades were positively associated with CNV formation (P = .04 and .03, respectively). Foveal location of rupture, multiple ruptures, and poor baseline VA were associated with failure to recover driving vision in univariate regression analyses. In multivariate analysis, rupture location and baseline VA were independently associated with visual outcome. Of 12 patients diagnosed with CNV, 5 were not treated, 4 were treated with argon laser photocoagulation, 1 was treated with surgery, 1 was treated with argon laser photocoagulation followed by surgery, and 1 was treated with verteporfin photodynamic therapy. CONCLUSIONS: Most patients with traumatic choroidal rupture do not achieve final VA of 20/40 or better. Poor visual outcome was most highly associated with a macular rupture and baseline VA of less than 20/40. The formation of CNV was most strongly associated with older age and macular choroidal rupture.
PURPOSE: To study the long-term effects of photodynamic therapy (PDT), using liposomal benzoporphyrin derivative (BPD) or Verteporfin, on experimental choroidal neovascularization (CNV) and on normal retina and choroid (with no CNV) in the cynomolgus monkey eye. METHODS: Photodynamic therapy was performed in 8 cynomolgus monkey eyes with experimental CNV induced by laser injury. The effect of PDT on normal retina and choroid (with no CNV) was studied in 9 monkey eyes. Liposomal BPD was administered intravenously (0.375 mg/kg) either as a bolus, as a slow infusion over 32 minutes, or as a fast infusion over 10 minutes. Photodynamic therapy was performed using light at a wavelength of 689 or 692 nm, with an irradiance of 600 mW/cm2 and fluence of 150 J/cm2. Follow-up studies, including fundus photography and FA, were performed at 24 hours after PDT and then weekly. Indocyanine green and BPD angiography were performed in selected cases. Tissues were examined with light and electron microscopy at the end of follow-up. RESULTS: Twenty-three of the 32 areas of CNV treated with PDT showed absence of angiographic leakage at 24 hours. Twenty-eight areas of CNV were followed for 4 weeks; 22 of 28 showed absence of angiographic leakage at 2 weeks; and 20 of 28 at 4 weeks of follow-up. Forty spots on the normal retina and choroid were treated with PDT and were followed for 4 to 7 weeks. These spots showed pigment-laden cells in the outer retina, variably pigmented retinal pigment epithelium (RPE) in the treated area, intact neurosensory retina, and reperfusion of the choriocapillaris. CONCLUSIONS: Photodynamic therapy leads to absence of angiographic leakage for at least 4 weeks in experimental CNV in the monkey model. In the normal monkey eye the RPE and choriocapillaris show generalized recovery with preservation of the neurosensory retina 7 weeks after PDT.
Choroidal neovascularization in children is uncommon and mostly associated with inflammation, infectious diseases or trauma. The clinical and histological findings of a choroidal neovascular membrane that developed in a 9-year-old boy after traumatic choroidal rupture are reported.
OBJECTIVE: To evaluate choroidal osteoma for tumor growth, tumor decalcification, related choroidal neovascularization, visual acuity loss, and poor visual acuity. DESIGN: Retrospective nonrandomized single-center case series. SETTING: Ocular Oncology Service at Wills Eye Hospital, Thomas Jefferson University, Philadelphia, Pa. PARTICIPANTS: There were 74 eyes of 61 patients with choroidal osteoma evaluated between January 1, 1977, and January 1, 2003. MAIN OUTCOME MEASURES: The 5 outcome measures included tumor growth, tumor decalcification, related choroidal neovascularization, visual acuity loss of 3 or more Snellen lines, and poor visual acuity of 20/200 or worse. RESULTS: At 5 and 10 years, Kaplan-Meier analysis revealed tumor growth in 22% and 51% of eyes, tumor decalcification in 28% and 46% of eyes, choroidal neovascularization in 31% and 31% of eyes, visual acuity loss in 26% and 45% of eyes, and poor visual acuity in 45% and 56% of eyes, respectively. The clinical factor predictive of tumor growth was absent overlying retinal pigment epithelial alterations. The factor predictive of decalcification was irregular tumor surface. Of the 15 tumors that showed partial decalcification at the first visit, there was no further tumor growth in any case. Of the remaining 12 tumors that later developed decalcification, tumor growth, if it occurred, was along the margin opposite the decalcification. No tumor showed growth in the region of decalcification. Factors predictive of choroidal neovascularization included irregular tumor surface and subretinal hemorrhage. In 6 eyes that had both choroidal neovascularization and tumor decalcification, the neovascularization was detected prior to or at the same time as the decalcification. The factor predictive of visual acuity loss was presence of subretinal fluid whereas the factors predictive of poor visual acuity included symptoms and tumor decalcification. A comparison of eyes with subfoveal vs extrafoveal choroidal osteoma showed poor visual acuity in 15 (34%) of 44 eyes and 3 (10%) of 30 eyes, respectively. Eyes with decalcified choroidal osteomas manifested poor visual acuity in 13 (48%) of 27 eyes whereas those with nondecalcified tumors showed poor visual acuity in 5 (11%) of 47 eyes. CONCLUSIONS: Choroidal osteoma showed evidence of growth in 51% of eyes and decalcification in nearly 50% of eyes by 10 years. Tumors with any degree of decalcification at the initial visit showed no further growth. Overall, poor visual acuity of 20/200 or worse was found in 56% of eyes by 10 years, and decalcified subfoveal choroidal osteomas displayed a particularly poor visual prognosis.
PURPOSE: To describe the clinical, angiographic and optical coherence tomography (OCT) findings of patients with choroidal neovascularization (CNV) associated with retinal pigment epithelial detachment (PED) who were treated by neovascular ingrowth site photothrombosis. METHODS: Interventional case reports. After identification of the CNV feeder vessels, two patients had focal photothrombosis of the neovascular ingrowth site using continuous 810-nm laser application after intravenous indocyanine green (ICG) injection and were prospectively followed with fluorescein and ICG angiography as well as OCT. RESULTS: Both patients presented an increase of 3 or more ETDRS lines in visual acuity by 12 months of follow-up. Fluorescein and ICG angiography demonstrated reduced lesion perfusion and regression of the PEDs; accordingly, OCT disclosed decrease in retinal thickness and elevation caused by rapid fluid resolution. There were no significant complications related to the procedure. CONCLUSION: Photothrombosis using 810-nm light to direct laser energy continuously at the neovascular ingrowth site after intravenous ICG infusion is effective in restoring macular architecture and improving vision in patients with CNV complicated by PEDs by means of substantial decrease in the lesion perfusion and resolution of exudative manifestations.
Surgical management of choroidal neovascularization may offer patients with subretinal membranes another therapeutic option. Current techniques allow extraction of subretinal membranes, but not all patients have favorable clinical outcomes with such an approach. This article reviews the current state of subretinal surgery and attempts to summarize those characteristics that may predict good surgical results. Vitreoretinal surgical techniques for the management of subretinal membranes are reasonably well established. Certain characteristics of choroidal neovascularization have been identified that may suggest favorable surgical outcomes; however, no randomized prospective data are yet available to show the role of these procedures. The National Institutes of Health-sponsored Submacular Surgery Trials are designed to determine whether surgery or observation is better for eyes with subfoveal choroidal neovascularization in presumed ocular histoplasmosis syndrome or age-related macular degeneration and in eyes with age-related macular degeneration-associated hematomas.
PURPOSE: To examine a series of choroidal melanoma specimens to determine the frequency of overlying choroidal neovascularization (CNV) and to ascertain whether CNV over choroidal malignant melanoma is associated with any particular histological tumour characteristics. METHODS: We carried out a retrospective histological analysis of globes containing choroidal melanomas for evidence of choroidal neovascular membranes. RESULTS: Microscopic evidence of choroidal neovascular membranes was evident in 6% of cases. Choroidal neovascularization was not associated with any particular histological tumour characteristic. CONCLUSION: Choroidal neovascularization over choroidal malignant melanoma is not an infrequent occurrence and possibly appears as frequently as CNV over choroidal naevi. The presence of a choroidal neovascular membrane over a pigmented fundal lesion should not be taken as reassurance that the lesion is benign.
Choroidal neovascularization in rat eyes was induced by krypton laser photocoagulation. Lesions were studied weekly by ophthalmoscopy, fundus photography, and fluorescein angiography. Morphologic correlation was provided by serial sectioning of lesions for light and transmission electron microscopy. In addition, vascular casts were prepared for scanning electron microscopy. Choroidal neovascularization occurred in 25 (60%) of 42 lesions, as evidenced by growth of capillaries through breaks in Bruch's membrane. In addition, 24 (28%) of 86 lesions studied by fluorescein angiography demonstrated leakage. This study provides the most complete angiographic, histologic, and ultrastructural documentation of experimental choroidal neovascularization in the rat. This model may be useful for in vivo studies of choroidal angiogenesis and its modulation via drug therapy.
BACKGROUND: Retinal pigment epithelial cells (RPE cells) and choroidal endothelial cells (CECs) are important cell types in the process of choroidal neovascularization in exudative age-related macular degeneration (AMD). In this study, we evaluated the antiproliferative and antimigratory abilities of carboxyamido-triazole (CAI), a drug modulating calcium-dependent signal transduction on RPE cells and CECs. METHODS: Human fetal RPE cells and bovine CECs were exposed to CAI in a concentration range of 0.1 to 10 microM. Cell proliferation was stimulated with 10% serum or 10 ng/ml bFGF. The effect of CAIs on cell proliferation was estimated. Furthermore, we evaluated CAI's effects on CEC and RPE cell migration induced by fibronectin. RESULTS: CAI had a stronger inhibitory effect on serum-induced CEC proliferation than on RPE cell proliferation. A much stronger effect was seen on the proliferation of bFGF-stimulated RPE cells and CECs. Furthermore, the fibronectin-stimulated migration of RPE cells and CECs was inhibited by CAI. In this assay, a stronger inhibitory effect was seen on RPE cells than on CECs. CONCLUSION; CAI inhibits important substeps of choroidal neovascularization on RPR cells and CECs. Therefore, CAI may be of value for the treatment of choroidal neovascularization in exudative AMD.
PURPOSE: Choroidal neovascularization (CNV) is one of the most frequent causes of severe and progressive vision loss. Prior studies have shown that bone marrow-derived cells (BMCs) play an important role in CNV, indicating that BMCs can be a potential target for inhibiting the development of CNV. It could be helpful for our understanding of CNV to study the dynamic conduct of BMCs in the CNV microenvironment. METHODS: Green fluorescent protein (gfp) chimeric mice were developed by transplanting bone marrow cells from gfp+/+ transgenic mice to adult C57BL/6J mice. The chimeric mice underwent laser rupture of Bruch's membrane to induce CNV and were killed at 1, 2, 3, and 4 weeks after laser injury. The eyes were enucleated and processed for immunofluorescence to detect markers for vascular smooth muscle cells (alpha smooth muscle actin, alpha SMA), endothelial cells (CD31), or macrophages (F4/80) on gfp+ cells. All sections were qualitatively and quantitatively assessed by confocal microscopy. RESULTS: Large number of gfp-labeled cells appeared in the lesions and integrated into CNV. Gfp+ cells, which were immunoreactive for alpha SMA, CD31, or F4/80, can be detected through the whole study. The constituent ratio of those three cell-types in total gfp+ cells in CNV altered as CNV developed. The maximal ratios of CD31-labeled cells and F4/80-labeled cells presented at 2 week, while the ratio of alpha SMA-labeled cells upgraded continuously. CONCLUSIONS: BMCs underwent a serial of changes in position and expression during the progression of CNV. Those changes may result from the interaction between BMCs and the CNV microenvironment.
We produced choroidal neovascularization in the rhesus monkey by diminishing the blood supply to the inner retina and producing defects in Bruch's membrane by photocoagulation. The neovascular fronds which developed either infiltrated the subretinal space or proliferated through necrotic and gliotic retina into the vitreous cavity. Sequential electron microscopic sections of neovascular fronds in the subretinal space demonstrated that the advancing capillary sprouts were composed of primitive endothelial tubes surrounded by pericytes and enmeshed in a loose basement-membrane-like substance. More mature capillaris and displayed endothelial fenestrations and endothelial-pericyte membranous contacts. Large neovascular fronds developed major feeding vessels that closely resembled normal small choroidal arteries and veins. Retinal pigment epithelial cells in various guises were in constant association with proliferating neovascular networks.