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PubMed2001

[Retinal thrombosis in young patients. Immunological and clinical aspects].

OBJECTIVES: To ascertain preexisting medical conditions, clinical evolution of retinopathy, and associated immunological disorders in a series of young patients suffering from retinal thrombosis, and to determine the prevalence of antiphospholipid antibodies. METHODS: Twenty two patients younger than 50 years, who had presented an acute retinal thrombotic episode, were studied prospectively with a general physical, ophthalmoscopic and immunological examination, placing special emphasis on the detection of antiphospholipid antibodies (anticardiolipin antibodies and lupus anticoagulant). RESULTS: No baseline disease stood out significantly over the others, and the most frequent risk factor found was systemic arterial hypertension (5/22%). No associated risk factor was found in nine cases (41%), and more than two factors were found in six cases (27%). Most of the vascular occlusions affected the venous vessels (18/81%), and five of them were associated with vasculitis. The ophthalmologic follow-up showed a rapid evolution to retinal neovascularization in 11 cases. Our data show many immunologically altered values, there being nine cases (41%) of the series with more than four parameters altered. The antiphospholipid assay showed a high prevalence of anticardiolipin antibodies (5/23%), and two patients were diagnosed of primary antiphospholipid syndrome. The lupus anticoagulant was negative in all patients. CONCLUSIONS: The high prevalence of anticardiolipin antibodies and immunologic abnormalities found in the retinal thrombosis younger patients leads us to recommend the systematic immunological study in these subjects. It has relevant diagnostic and therapeutic implications in a population with no evident associated risk factors and a greater severity of retinopathy.

Adult↗
PubMed1997

Upregulation of vascular endothelial growth factor in ischemic and non-ischemic human and experimental retinal disease.

Vascular endothelial growth factor (VEGF) is induced by hypoxia and it has been implicated in the development of iris and retinal neovascularization (NV) in ischemic retinopathies in which it has been suggested that Muller cells are responsible for increased VEGF production. VEGF, however, is also known to be a potent mediator of vascular permeability in other tissues and may perform this function in retina. Immunohistochemical staining for VEGF was performed on a variety of human and experimental ischemic and non-ischemic ocular disorders in which blood retinal barrier (BRB) breakdown is known to occur to determine if there is an upregulation of VEGF in these conditions. We found increased VEGF immunoreactivity in ganglion cells of rats with oxygen-induced ischemic retinopathy and in ganglion cells, the inner plexiform layer, and some cells in the inner nuclear layer of rats with experimental autoimmune uveoretinitis (EAU), in which there was no identifiable ischemia or NV. In rats with EAU, VEGF staining intensity increased from 8 to 11 days after immunization, coincident with BRB failure. These results were confirmed using two distinct anti-VEGF antibodies and by immunoblot and the immunohistochemical staining was eliminated by pre-incubating the antibodies with VEGF peptide. VEGF staining was also increased in the retina and iris of patients with ischemic retinopathies, such as diabetic retinopathy and retinal vascular occlusive disease, and in patients with disorders in which retinal ischemia does not play a major role, such as aphakic/ pseudophakic cystoid macular edema, retinoblastoma, ocular inflammatory disease or infection, and choroidal melanoma. VEGF was primarily localized within retinal neurons and retinal pigmented epithelial cells in these cases. In addition or in association with its role of inducing NV, VEGF may contribute to BRB breakdown in a variety of ocular disorders and blockage of VEGF signaling may help to reduce some types of macular edema.

Animals↗
PubMed1989

Fenestrated subendothelial basement membranes in human retinal capillaries.

A correlated TEM and SEM study of human retinal capillaries and their associated basement membranes (BMs) was carried out. Control tissues show that these vessels are comprised of a continuous layer of endothelial cells separated from overlying intramural pericytes by a discontinuous subendothelial BM (EBM) which accommodates endothelial cell-pericyte (periendothelial) junctions. Three types of junctions exist, including: (1) "peg-and-socket" arrangements where cytoplasmic processes of the two cell layers interdigitate; (2) adhering plaques similar to desmosomes; and (3) cell/cell contacts where adjacent cell membranes appear to fuse or remain separated by a approximately 2 nm space. Following detergent solubilization, acellular retinal capillaries maintain their cylindrical histoarchitectures and all BM components are imaged by TEM and SEM. Topographical (SEM) studies of cryofractured samples show EBM surfaces with numerous (approximately 1.5/microns 2) oval fenestrations (100-450 nm diameter) that correlate well with EBM discontinuities occupied by periendothelial junctions in control tissues. It seems possible that these structures may play an important role in diabetic retinal neovascularization where pericytes are known to degenerate selectively. In this condition, preformed EBM deficiencies could facilitate endothelial cell migration and sprout formation, leading ultimately to the sequelae of proliferative diabetic retinopathy.

Basement Membrane↗
PubMed1993

[Laser photocoagulation treatment of small malignant choroidal melanomas].

8 cases of malignant choroidal melanoma were treated with argon and krypton laser photocoagulation of average 11 sessions and followed up an average 56 months. Clinical complete regression was observed in 5 cases (62.5%), in whom the tumors measured from 1.0mm x 1.2mm x 1.5mm to 6.0mm x 4.5mm x 2.5mm. The other 3 cases (37.5%) recurred, in whom the tumors measured from 4.0mm x 2.0mm x 3.5mm to 11.5mm x 12.5mm x 3.5mm. The complications of treatment included branch retinal vein occlusion, retinal neovascularization, vitreous hemorrhage, macular edema and optic atrophy. These results suggested that laser photocoagulation was useful in the treatment of small malignant choroidal melanomas.

Adult↗
PubMed1981

The effect of human intraocular fluid on vascular endothelial cell migration.

Several recent studies have demonstrated that vascular endothelial cell migration is an essential element of new blood vessel formation. We have recently developed an in vitro assay to study the effect of various substances on vascular endothelial cell migration. We now report the use of this assay to study the effect of human intraocular fluid on endothelial cell migration. We have found a good correlation between the presence of progressive retinal neovascularization in an eye and the ability of vitreous cavity fluid from that eye (obtained at the time of vitrectomy) to stimulate vascular endothelial cell migration in vitro.

Blood Vessels↗
PubMed1994

Vasculotropin-VEGF stimulates retinal capillary endothelial cells through an autocrine pathway.

PURPOSE: To determine whether bovine retinal endothelial cells (BRECs) bind, synthesize, and respond to vasculotropin-vascular endothelial growth factor (VAS-VEGF). METHODS: Cultured BRECs were tested for their ability to bind 125I VAS-VEGF and their response to the growth and migration-promoting effect of VAS-VEGF. Total RNAs extracted from BRECs were reverse transcribed and amplified by polymerase chain reaction using VAS-VEGF primers. The translation was assessed by a Western blot analysis and a radioreceptor assay in the BREC-conditioned medium. Neutralization with anti-VAS-VEGF antibodies ascertained the autocrine role of VAS-VEGF. RESULTS: BRECs bind VAS-VEGF on two high-affinity binding sites (apparent Kd of 2 and 56 pM) and can proliferate and migrate upon the addition of recombinant VAS-VEGF. Furthermore, BRECs synthesize and secrete into their own culture medium a mitogen related to VAS-VEGF as far as two factors are concerned: chromatographic behavior on heparin-affinity columns, and cross-reactivity with recombinant VAS-VEGF to the binding to its receptors or antibodies. Neutralization of the purified conditioned medium with anti-VAS-VEGF antibodies revealed that VAS-VEGF can act on BRECs through an autocrine pathway. CONCLUSIONS: This is the first description of an autocrine regulation of endothelial cell growth by VAS-VEGF that could be involved in the pathogenesis of retinal neovascularization.

Animals↗
PubMed2000

Prevalence of ocular hemorrhage in patients receiving warfarin therapy.

BACKGROUND: Warfarin, the drug most commonly used for outpatient anticoagulation therapy, has bleeding as its main side effect. The objective of this study was to determine the prevalence of ocular hemorrhage in patients receiving warfarin and to compare it to the prevalence in the general population. METHODS: Patients receiving warfarin therapy who were attending the anticoagulation clinic at a tertiary care hospital in Montreal between October and December 1996 received a flyer inviting them to have their eyes examined to look for "ocular bleeding." Consenting patients were examined for subconjunctival hemorrhage, gross hyphema, and vitreous and retinal hemorrhages through external ocular examination and funduscopic examination with the pupils dilated using direct and indirect ophthalmoscopy. RESULTS: Of the 1225 patients seen at the clinic 126 (10%) agreed to participate. Four patients (3%) were found to have intraretinal hemorrhage at the time of examination. All hemorrhages were visually insignificant. INTERPRETATION: The risk of retinal hemorrhage in patients without preexisting ocular disease, such as retinal neovascularization or choroidal vasculopathy, who are receiving warfarin therapy is so small that it should not deter physicians from prescribing this drug when indicated.

Adult↗
PubMed1998

[Acute retinal necrosis syndrome. Argon laser coagulation for prevention of rhegmatogenic retinal detachment].

BACKGROUND: ARN syndrome follows severeintraocular infection by herpes viruses and primarily affects the peripheral retina. Following scar formation, despite antiviral treatment, rhegmatogenous retinal detachment occurs very often. Prophylactic argon laser photocoagulation has therefore been proposed. We report our experience. PATIENTS: We treated five patients presenting clinically with advanced unilateral ARN with acyclovir. All eyes received a prophylactic confluent double row of argon laser treatment (500 microns, 0.2 s, gray-white lesions) central to the affected area as soon as was possible, depending on the vitreous clouding. Four patients were treated with Aspirin. RESULTS: One of the five patients had a peripheral rhegmatogenous retinal detachment that was limited by the argon laser row. Another patient had a tractional detachment needing vitreoretinal surgery. Two eyes developed vitreal hemorrhage of unknown origin. CONCLUSION: A lower rate of rhegmatogenous retinal detachments than expected occurred post-laser treatment. Vitreal hemorrhage was more frequent than previously reported. The bleeding probably originated from anterior retinal neovascularization and may have been enhanced by Aspirin treatment. We recommend early prophylactic argon laser photocoagulation in all ARN patients in agreement with the results of previous studies.

Acyclovir↗
PubMed2005

Vascular endothelial growth factor and diabetic retinopathy: role of oxidative stress.

Retinal neovascularization and macular edema are central features of diabetic retinopathy, a major cause of blindness in working age adults. The currently established treatment for diabetic retinopathy targets the vascular pathology by laser photocoagulation. This approach is associated with significant adverse effects due the destruction of neural tissue and is not always effective. Characterization of the molecular and cellular processes involved in vascular growth and hyperpermeability has led to the recognition that the angiogenic growth factor and vascular permeability factor VEGF (vascular endothelial growth factor) play a pivotal role in the retinal microvascular complications of diabetes. Thus, VEGF represents an important target for therapeutic intervention in diabetic retinopathy. Agents that directly inhibit the actions of VEGF and its receptors show considerable promise, but have not proven to be completely effective in blocking pathological angiogenesis. Therefore, a better understanding of the molecular events that control VEGF expression and mediate its downstream actions is important to define more precise therapeutic targets for intervention in diabetic retinopathy. This review highlights the current understanding of the process by which VEGF gene expression is regulated and how VEGF's biological effects are altered during diabetes. In particular, cellular and molecular alterations seen in diabetic models are considered in the context of high glucose-mediated oxidative stress effects on VEGF expression and action. Potential therapeutic strategies for preventing VEGF overexpression or blocking its pathological actions in the diabetic retina are considered.

Adrenal Cortex Hormones↗
PubMed1976

[Diabetic retinopathy: documentation, evaluation of its course and possibilities of treatment by photocoagulation].

Optimal documentation of retinal lesions by panorama fundus photographs is required for evaluation of the course of diabetic retinopathy (DR). The data are prepared for automatic storage and computation. The natural course of DR is occasionally characterized by remarkable spontaneous remissions. Therefore, unilateral treatment is needed to evaluate the efficacy of photocoagulation. The following preliminary results on 215 patients treated unilaterally with Xenon photocoagulation, and followed up for 6 months to 6 years, were statistically significant: marked decrease of intra- and epiretinal vessel new formations, prophylaxis of retinal neovascularization and vitreous hemorrhages, preservation of the macula and retention of visual acuity in diabetics below 60 years of age. The unpredictable rate of progression of DR in individual cases is responsible for occasional failures of photocoagulation.

Adult↗
PubMed2005

[Variations in intraocular pressure (IOP) and necessity for paracentesis following intravitreal triamcinolone injection].

BACKGROUND: Intravitreal triamcinolone injection (IVT) has become a treatment option for macular edema of heterogeneous etiology and neovascular retinal diseases including AMD. Besides the risk for a steroid-induced secondary open-angle glaucoma, the acute rise in intravitreal volume induces IOP elevations immediately after injection. To decrease the intravitreal volume a paracentesis is advocated by many surgeons. The aim of this study was to determine variations in IOP at different time points immediately after IVT in order to assess the necessity for routine paracentesis. METHODS: The IOP was recorded by Goldmann applanation tonometry preoperatively, 10 minutes, 1, 3 and 24 hours after intravitreal injection of 0.1 mL (4 mg) triamcinolone. A consecutive series of 32 eyes of 32 patients with diabetic macular edema, diffuse edema after central vein occlusion or occult subfoveal choroidal neovascularization due to age-related macular degeneration was included. Statistical analysis was performed with ANOVA test and Bonferroni correction. RESULTS: Compared to baseline (15.24 +/- 0.52 mm Hg) IOP was significantly elevated 10 min postoperatively (22.28 +/- 1.4 mmHg; p < 0.05). One hour after injection IOP decreased to 15.58 +/- 0.69 mmHg (p < 0.05). Three and 24 h after injection mean IOP was not significantly different from preoperative baseline levels. Immediately after IVT light perception was tested and retinal perfusion was evaluated by indirect ophthalmoscopy. In none of the patients was a paracentesis necessary. CONCLUSION: Intravitreal injection of 0.1 mL triamcinolone led to a moderate transient rise in IOP. Based on these results, a routinely performed paracentesis immediately before or after IVT is not required. As paracentesis bears an additional risk including endophthalmitis it should only be considered if functional testing following injection indicates a relevant impairment of retinal perfusion.

Aged↗
PubMed1976

Argon laser photocoagulation in ocular histoplasmosis syndrome.

Argon laser photocoagulation was performed on 30 patients with ocular histoplasmosis syndrome involving the macula. Selection of patients for photocoagulation was dependent upon locating the sub-retinal neovascularization (SRNV) at least one vein-width removed from the capillary-free zone of the fovea on fluorescein angiography. Of the 30 treated patients, 27 maintained or improved visual acuity an average of 1 1/2 years following photocoagulation.

Adult↗
PubMed1993

MHC class II antigen expression by ocular cells in proliferative diabetic retinopathy.

An immunohistological study was performed on ciliary biopsies of the pars plana obtained surgically in 10 patients suffering from diabetic retinopathy and on 15 surgical specimens of pre-retinal neovascularized membranes. Using immunofluorescence and immunoperoxidase procedures, linear deposits of IgG, IgA and complement components were found in the 8 pars plana from patients with proliferative diabetic retinopathy, at the basal pole of the pigment epithelial cells and within the stroma. In contrast, these deposits were absent from normal pars plana and from the cases of background retinopathy. Moreover, pigment and non-pigment epithelial cells were found to express HLA DR and DQ determinants, in six of the eight patients with proliferative retinopathy. Immunohistological examination of pre-retinal membranes showed deposition of immunoglobulins and complement components within the connective stroma and along the new blood vessels. Endothelial cells of the newly formed vascular walls strongly expressed class II antigens on their membrane, as well as scattered stromal cells. As neither pigment epithelial cells nor retinal vascular endothelial cells normally express class II determinants, our results suggest the involvement of immunological phenomena in intraocular proliferative diseases and eventual interactions between the immune system and peptide growth factors. However, whether or not this immune reaction plays a role in the initiation or extension of intra-ocular proliferation remains to be determined.

Adult↗
PubMed1987

Inherited retinal venous beading.

Four generations of a family with an unusual pattern of ocular vascular abnormalities were studied. Two male and three female members in two affected generations demonstrated prominent retinal venous segmental beading. Various individuals demonstrated areas of focal retinal infarction, surface retinal neovascularization, vitreous hemorrhage, microaneurysm formation, altered vascular permeability with lipid exudation, and focal edema. Several members demonstrated abnormalities of distribution of arterioles and venules. Saccular aneurysmal changes were present in conjunctival vessels. Renal disease was present in two affected individuals in the fourth and fifth decades, respectively.

Adolescent↗
PubMed1980

Treatment of intraocular proliferation with intravitreal injection of triamcinolone acetonide.

We studied the inhibitory effect of triamcinolone acetonide on experimental intraocular proliferation. Autotransplantation of fibroblasts from rabbit rump skin into the vitreous cavity resulted in intravitreal strand formation and traction retinal detachment in 36 of 43 eyes (84%) over a period of three months. A single intravitreal injection of 1 mg of triamcinolone acetonide inhibited fibroblast growth and significantly reduced the number of retinal detachments in 15 of 44 eyes (34%). Retinal neovascularization caused by fibrous strands coming into contact with vacularized retina was also reduced by triamcinolone acetonide (31 of 43 control eyes [72%] vs eight of 44 treated eyes [18%]). Intravitreal corticosteroid therapy may be an important adjunct to the therapy of perforating injuries and massive periretinal proliferation.

Animals↗
PubMed1997

Combined subretinal and sub-retinal pigment epithelium neovascular membranes in age-related macular degeneration: a clinicopathologic study of six cases.

BACKGROUND AND OBJECTIVE: Subfoveal neovascular membranes are usually located either in the subsensory retinal space or below the retinal pigment epithelium (RPE). This article describes the clinical and histopathologic features of subfoveal membranes with both subretinal and sub-RPE components (combined membranes). PATIENTS AND METHODS: Six surgically excised subfoveal neovascular membranes from six patients were examined histopathologically. Preoperative and postoperative clinical information was obtained from each patient. RESULTS: Clinically, the combined membranes had no special characteristic features. The most common fluorescein angiographic finding postoperatively was a window defect of the RPE. Visual acuity improved in three patients and became worse in the other three patients. CONCLUSIONS: All patients with combined subfoveal neovascular membranes had age-related macular degeneration. In this disease, a single subfoveal membrane may extend into both the subretinal and the sub-RPE spaces. Patients may benefit from surgical removal of the membrane.

Aged↗
PubMed1976

Occlusive retinal vascular disease and deafness.

An 8-year-old white girl with a history of vertigo, nausea, and vomiting developed a progressive hearing loss, bilateral retinal arteriolar narrowing in each eye, vasoproliferation, and subsequent intravitreal hemorrhage. An attempt at peripheral retinal ablation with cryotherapy in the left eye resulted in retinal detachment. Spontaneous retinal detachment occurred in the right eye and was successfully repaired. Repeated intermittent hemorrhages occurred despite intraocular diathermy. Three years after onset, visual acuity was R.E.: 6/21 (20/66) and L.E.: light perception. She remains totally deaf. A 20-year-old white woman developed severe bilateral sensorineural hearing loss with poorly functioning labyrinths, followed by midperipheral retinal arteriolar occlusions and vasoproliferation on the optic nerve head. Progressive retinal neovascularization was followed by rubeosis iridis and repeated episodes of intravitreal bleeding. Six years after onset, visula acuity was R.E.: hand motions, and L.E.: 6/3 (20/100). She remains totally deaf. Both patients were of normal gestation, development, and mentality, without evidence of other systemic disease. The cause of this disease was not found.

Adult↗
PubMed2003

Antiphospholipid antibody syndrome in a six-year-old female patient.

PURPOSE: To report the first instance of primary antiphospholipid antibody (APA) syndrome in an otherwise healthy 6-year-old female patient with retinal venous thromboses. DESIGN: Observational case report. METHODS: A 6-year-old girl with poor vision in the left eye and preretinal hemorrhage underwent testing for infectious, autoimmune and embolic disease, diabetes, and hypertension. Testing for factor V Leiden and prothrombin G20210A mutations, homocysteine, anticardiolipin antibodies (ACAs), lupus anticoagulant, and functional assays for protein S, protein C, and antithrombin III were performed to detect a hypercoagulable state. No IRB approval was necessary. RESULTS: Only a positive lupus anticoagulant and moderately elevated ACA IgG were found. The ACA IgG was moderately elevated on repeat testing 18 months later. Laser to nonperfused retina caused some regression of retinal neovascularization. Aspirin was recommended to reduce the risk of future thromboses. CONCLUSIONS: Although uncommon, retinovascular thrombosis in children can occur in APA syndrome. Testing for ACA and lupus anticoagulant should be considered.

Anti-Inflammatory Agents, Non-Steroidal↗