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At least 631 records · Page 35Linked to original sources
PubMed1999

Trans-scleral diode laser photocoagulation in proliferative sickle cell retinopathy.

OBJECTIVE: To demonstrate the feasibility of trans-scleral diode laser photocoagulation for the treatment of proliferative sickle cell retinopathy. DESIGN: Interventional case report. INTERVENTION: Trans-scleral diode laser scatter photocoagulation was applied to both eyes of a 30-year-old man with hemoglobin SC disease. MAIN OUTCOME MEASURES: Regression of retinal vascular proliferation and of dye leakage on fluorescein angiography. RESULTS: After coagulation, vascular proliferation receded completely. Vitreous bleeding was absorbed. There were no side effects during follow-up (22 months). CONCLUSION: Trans-scleral diode laser photocoagulation proved to be an effective and safe treatment in a case of proliferative sickle cell retinopathy with vitreous bleeding.

Adult↗
PubMed2005

[Intravitreal injection of triamcinolone acetonide for the treatment of macular edema].

PURPOSE: To study the efficacy and safety of intravitreal injection of triamcinolone acetonide for the treatment of macular edema (ME). METHODS: Thirty-five eyes of 33 patients with ME were studied. The causes of ME included diabetes (24 eyes), postoperative ME (four eyes), intraocular inflammation (three eyes), retinal vein occlusion (three eyes), and Coats disease (one eye). All patients underwent a complete ophthalmic examination and fluorescein angiography before and after treatment. Treatment consisted of a single intravitreal injection of 2 or 4 mg of triamcinolone acetonide under subconjunctival anaesthesia. Mean follow-up time was 4 months (range, 1-10 months). RESULTS: Mean visual acuity before treatment was 20/200 (range, 20/400-20/70). Visual acuity improved by one line or more on the Snellen visual acuity chart in seven eyes (20%) and remained unchanged in nine eyes (25.7%). In the 19 remaining eyes, visual acuity improved slightly and remained less than 20/200. ME diminished or resolved completely in 32 eyes (91%). This improvement was seen in all eyes with diabetic ME, pseudophakic ME, or inflammatory ME. ME recurred in three eyes 3 months after injection of triamcinolone and in one eye 9 months after injection of triamcinolone. In one diabetic patient, retinal neovascularization associated with ME resolved as a consequence of intravitreal triamcinolone injection. Reversible ocular hypertension occurred in ten eyes (28.6%). No case of endophthalmitis was seen. CONCLUSION: Intravitreal injection of triamcinolone acetonide is an effective treatment of ME. Its best indications seem to be diabetic, pseudophakic and inflammatory ME. Randomized clinical trials are warranted to assess long-term efficacy and safety of this treatment modality of ME.

Adolescent↗
PubMed1996

Eye disease in sickling disorders.

When treating patients with sickling disorders, hematologists and oncologists should know those eye lesions that require referral to an ophthalmologist, those that should lead to referral, and those that rarely are associated with decreased vision. Hyphema in any patient whose red cells contain hemoglobin S falls into the first category. Retinal neovascularization (proliferative retinopathy) and its consequence vitreous hemorrhage fall into the second. The comma sign, angioid streaks, and abnormal color vision fall into the third category. The roles of preoperative transfusion and experimental antisickling therapy in treatment and prevention of eye lesions are incompletely defined at present.

Anemia, Sickle Cell↗
PubMed2003

Pathogenesis of retinopathy of prematurity.

Retinopathy of prematurity (ROP) is a major cause of blindness in children in developed countries. ROP, a two-phase disease, is initiated with delayed retinal vascular growth after premature birth (phase I). Insufficient vascularization of the developing retina creates hypoxia, which precipitates the release of factors stimulating new and abnormal blood vessel growth (phase II). ROP develops because of abnormalities in both oxygen-regulated and non-oxygen-regulated factors, which affect both phases of the disease. Vascular endothelial growth factor (VEGF) is an important oxygen-regulated factor that, if suppressed, inhibits normal vessel growth, but in excess, precipitates retinal neovascularization. A critical non-oxygen-regulated growth factor is insulin-like growth factor (IGF-1). Similar to VEGF, low levels of IGF-1 prevent normal vessel growth (phase I), and higher levels allow neovascularization (phase II). We found that premature infants who develop ROP have low levels of serum IGF-1 compared with age-matched infants without disease. IGF-1 is critical to normal vascular development. Low IGF-1 predicts ROP, and restoration of IGF-1 to normal levels might prevent ROP.

Child↗
PubMed1999

The a- and b-wave latencies as a prognostic indicator of neovascularisation in central retinal vein occlusion.

To evaluate the prognostic value of ERG in cases of central retinal vein occlusion (CRVO) regarding the development of neovascularisation (NV), we studied 20 patients with unilateral CRVO. Half of them were allocated in the perfused group and the other 10 finally developed NV and were allocated in the non-perfused group. Flash ERG was recorded from all patients. Our findings suggest that b-wave latency is the most reliable parameter in predicting NV, followed by the a-wave latency. The b/a wave amplitude of ERG ratio does not seem to be suitable for clinical use.

Aged↗
PubMed1998

Fluorescein angiography versus ERG for predicting the prognosis in central retinal vein occlusion.

PURPOSE: It is not easy to predict which patients with a central retinal vein occlusion will develop rubeosis and which will not. We have compared two methods for doing so, fluorescein angiography and full-field electroretinogram (ERG). Our aim was to improve our possibilities for predicting rubeosis in patients with central vein occlusion. METHODS: 32 patients with a central retinal vein occlusion with a duration of less than 14 days were included in the study. Fluorescein angiography and ERG were performed in all patients. The fluorescein angiograms were studied by two independent examiners in a masked mode. The patients were then followed for at least one year. RESULTS: Development of rubeosis in patients with central retinal vein occlusion could be predicted by fluorescein angiography in 82% of the patients and with ERG in 94% of the patients. The non-ischemic central retinal vein occlusions were identified in 62% by fluorescein angiography and in 100% with ERG. Fluorescein angiography misjudged 9 patients 28%, whereas ERG only misjudged 1 patient, 3%. CONCLUSION: ERG seems to be a better method for predicting the prognosis in central retinal vein occlusion than fluorescein angiography.

Adult↗
PubMed1989

Initial clinical experience using a diode laser in the treatment of retinal vascular disease.

A pilot study has been carried out to investigate the clinical use of an infrared diode laser in the treatment of a number of retinal vascular conditions. A hand-held device was employed initially and subsequently a further prototype was developed for use in conjunction with a standard slit lamp microscope. Thirty-three eyes in thirty patients were treated for conditions such as proliferative diabetic retinopathy, exudative retinopathy and branch and central retinal vein thrombosis. Regression of neovascularisation was observed in 13 of 16 eyes (81%) with proliferative diabetic retinopathy and in six of eight eyes (75%) with branch retinal vein occlusion. Four eyes were successfully treated for established or incipient rubeosis iridis following central vein thrombosis. Focal photocoagulation applied to five eyes for diabetic exudative maculopathy resulted in partial resorption of the exudates. These results are presented together with information on the ease of use of the laser and its reliability. The implications of the development of this instrument in the context of its place in ophthalmic therapy are discussed.

Aged↗
PubMed2004

Glial cell expression of hepatocyte growth factor in vitreoretinal proliferative disease.

The hepatocyte growth factor (HGF) has been crucially implicated in the development of proliferative retinal diseases; however, it is unclear whether retinal glial cells express or respond to HGF. Therefore, we examined the expression of HGF and of the receptor for HGF, c-Met, by immunohistochemical costaining with glial fibrillary acidic protein (GFAP) in epiretinal membranes of patients with proliferative vitreoretinopathy (PVR) and proliferative diabetic retinopathy (PDR), respectively. Furthermore, it was determined whether cells of the human retinal glial cell line, MIO-M1, secrete HGF protein, and whether HGF stimulates proliferation and chemotaxis, and secretion of the vascular endothelial growth factor (VEGF). Neuroretinas of patients with PVR express elevated mRNA level for HGF in comparison to control retinas. In epiretinal membranes of patients with PVR or PDR, immunoreactivity for HGF and for c-Met, respectively, partially colocalized with immunoreactivity for GFAP. Fetal bovine serum and basic fibroblast growth factor, but not heparin-binding epidermal or platelet-derived growth factors, evoked HGF secretion by cultured retinal glial cells. HGF displayed only a marginal effect on cell proliferation while it stimulated chemotaxis. HGF promoted the secretion of VEGF, via activation of the phosphatidylinositol-3 kinase. It is concluded that glial cells in epiretinal membranes express both HGF protein and c-Met receptors. The results suggest an autocrine/paracrine role of HGF in glial cell responses during proliferative vitreoretinal disorders as well as in retinal neovascularization, by stimulating of VEGF release.

Adolescent↗
PubMed2002

The pathogenesis of diabetic retinopathy: old concepts and new questions.

Hyperglycaemia appears to be a critical factor in the aetiology of diabetic retinopathy and initiates downstream events including: basement membrane thickening, pericyte drop out and retinal capillary non-perfusion. More recently, focus has been directed to the molecular basis of the disease process in diabetic retinopathy. Of particular importance in the development and progression of diabetic retinopathy is the role of growth factors (eg vascular endothelial growth factor, placenta growth factor and pigment epithelium-derived factor) together with specific receptors and obligate components of the signal transduction pathway needed to support them. Despite these advances there are still a number of important questions that remain to be answered before we can confidently target pathological signals. How does hyperglycaemia regulate retinal vessels? Which growth factors are most important and at what stage of retinopathy do they operate? What is the preferred point in the growth factor signalling cascade for therapeutic intervention? Answers to these questions will provide the basis for new therapeutic interventions in a debilitating ocular condition.

Diabetes Mellitus↗
PubMed2005

A VEGF/JAK2/STAT5 axis may partially mediate endothelial cell tolerance to hypoxia.

Perturbation of oxygen flow occurs in disease states such as diabetic retinopathy and cancer. To maintain oxygen homoeostasis, the mammalian microvascular endothelium undergoes a dramatic reorganization to assist in bringing oxygen and nutrients to oxygen-starved tissues. This process is termed angiogenesis and is common in certain cancers with hypoxic foci and in areas of focal ischaemia in the diabetic retina. In the present study, we report on the activation of the JAK2/STAT5 pathway (where JAK stands for Janus kinase and STAT stands for signal transduction and activator of transcription) by low oxygen in microvascular endothelial cells. This activation appears to occur downstream of VEGF (vascular endothelial growth factor), a well-known proangiogenic factor, and is related to repression of proapoptotic FAS(CD95)/FASL(CD95L). These results indicate that the JAK/STAT pathway may play a pivotal role during tumour-associated or retinal angiogenesis in which endothelial cell survival during tissue hypoxia is critical for maintaining either the growth of neoplasms or the inappropriate retinal neovascularization common in diabetic retinopathy.

Animals↗
PubMed1991

Characterization of release of basic fibroblast growth factor from bovine retinal endothelial cells in monolayer cultures.

Release of basic fibroblast growth factor (bFGF) was investigated in bovine retinal endothelial cells (BREC) maintained in monolayer culture. Confluent cells released bFGF into serum-free culture medium or medium containing 5% serum at rates of up to 105.2 and 61.3 pM/day respectively. bFGF release coincided with a decrease in monolayer cell number and increases in lactate dehydrogenase (LDH) concentration and cells and cell-debris particles in the medium, which suggested that cell damage and lysis were responsible for growth-factor release. Maximum bFGF release at 24 h (230 +/- 10 pM) occurred when the cells were treated with lipopolysaccharide (10 micrograms/ml), which also produced the greatest changes in parameters of cell damage. Sub-confluent cells showed little overt damage at 24 h, but released bFGF (78 +/- 20 pM) along with LDH, indicating that some cell lysis had occurred. Insulin-like growth factor 1 (IGF-1) was also released into serum-free culture medium at a rate of 0.34 nM/day, but not into medium containing serum or when the cells were treated with lipopolysaccharide. This implies that the mechanism of IGF-1 release is different from that of bFGF and is not related to cell damage. Culture medium conditioned by BREC stimulated the proliferation of these cells, as measured by an increase in their incorporation of [methyl-3H]thymidine from 7550 +/- 479 to 10467 +/- 924 d.p.m. These results demonstrate that bFGF is released from damaged BREC and that medium conditioned by these cells can stimulate retinal-endothelial-cell proliferation. This strengthens the case for an involvement of this growth factor in retinal neovascularization.

Animals↗
PubMed2002

Retinal manifestations of ophthalmic artery hypoperfusion.

Ophthalmic artery hypoperfusion is a relatively uncommon clinical entity. This study illustrates the posterior segment findings of ophthalmic artery hypoperfusion in a series of nine patients. Colour photographs and relevant fluorescein angiograms highlighting the findings are shown. The retinal manifestations of ophthalmic artery hypoperfusion in this series of patients include midperipheral haemorrhages, dilated retinal veins, optic disk collaterals, optic disk neo-vascularization, cotton wool spots, grey intraretinal lesions, fundus pallor, optic disk swelling and choroidal infarcts. Recognition of the ophthalmic changes in this condition may lead to detection of carotid artery disease, the surgical and medical treatment of which has important bearing on patient management.

Aged↗
PubMed1998

Role of vascular endothelial growth factor in the response to vessel injury.

In the post-embryonic life, physiological angiogenesis is tightly controlled. Angiogenesis also occurs in pathological circumstances such as tumor vessel proliferation, retinal neovascularization and ischemia. The development of collateral circulation is not only not deleterious, but life saving. Other cases such as neoplastic neovascularization are the basis of the continuous growth of tumors and metastases, and therefore constitute a target of therapeutical efforts. Among a list of molecules able to control angiogenesis, we emphasize the pivotal role of vascular endothelial growth factor (VEGF). VEGF is a potent mitogen for endothelial cells, but is devoid of mitogenic activity for other cell types. VEGF is a polypeptide with four main different isoforms that are remarkably different in terms of solubility and affinity for matrix proteins. VEGF interacts with two endothelial cell-specific tyrosine kinase receptors. The main interest of its study lies in VEGF's role in pathological angiogenic processes, where an increase in the VEGF mRNA expression has been consistently observed. An interesting example is the up-regulation of VEGF's and VEGF receptors' mRNA in a considerable number of human tumors and retina, where they have a critical role in the development of neovascularization. In recent work in our laboratory, we have found further potential interactions of VEGF with pathophysiological mechanisms, namely, the increase in VEGF gene expression under exposure to reactive oxygen species and the positive interaction between VEGF and erythropoietin. VEGF has outstanding possibilities for therapeutic applications aimed at inhibiting or favoring the development of new vessels.

Endothelial Growth Factors↗
PubMed2000

[Retinal vasculopathy associated with Berger's IgA nephropathy].

AIM: Ophthalmological complications associated with Berger's IgA nephropathy comprise scleritis, episcleritis, keratoconjunctivitis as well as anterior uveitis. We present a new association of IgA nephropathy with a retinal vasculopathy. METHODS: Presentation of two clinical cases. RESULTS: Two patients presented with hematuria and epistaxis associated with a retinal vasculopathy characterised by teleangiectasies, capillary occlusion with retinal hemorrhages, neovascularisations and macular edema with decreased visual acuity. Fluorescein angiography showed zones of non-perfusion as well as vasculitic changes. A general medical exam revealed a normal arterial pressure but a slightly elevated creatinine. Immunological investigations for the presence of antibodies showed no positive results. Renal biopsy demonstrated mesangial proliferations with diffuse deposits of IgA. Over the course of a 2 year follow-up some of the retinal changes regressed under treatment with cortisone and visual acuity returned to normal. The teleangiectasies showed no progression. CONCLUSION: Berger's IgA nephropathy can be associated with a retinal vasculopathy which may be due to local deposition of IgA immune complexes in the retinal vessels.

Adult↗
PubMed2001

New concepts in pathogenesis and treatment of diabetic retinopathy.

Retinal neovascularization is a major feature of proliferative diabetic retinopathy, which represents a major public health problem, being responsible for more irreversible blindness in persons of middle and older age than any other pathology. The societal burden of ocular neovascularization has prompted extensive research into its mechanisms. The aim of this review will be to briefly summarize the current knowledge regarding the clinical and laboratory findings of diabetic retinopathy. From an investigational view, studies of ocular neovascularization provide important informations, often permitting real-time, serial observations of neovascularization in vivo. This allows investigators to analyse the relevance of specific pathogenic concepts regarding the mechanisms of angiogenesis in vivo. This review will additionally describe current concepts regarding the pathogenesis and treatment of diabetic retinopathy.

Animals↗