Cases reported "Diabetic Retinopathy"

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1/33. Peripheral choriovitreal neovascularization in proliferative diabetic retinopathy: histopathologic and ultrastructural study.

    We describe the histopathologic and ultrastructural evidence of choriovitreal neovascularization in the peripheral fundus of a non-vitrectomized eye with proliferative diabetic retinopathy (PDR). One eye with PDR was surgically enucleated because of neovascular glaucoma and studied with light and electron microscopy. The eye had neovascular membranes at the ora serrata of the peripheral fundus. The newly formed vessels originated from the choroid, passed through Bruch's membrane and the retina, and extended into the vitreous. These vessels had either developing or mature characteristics. The endothelial cells of the developing vessels contained a bulky cytoplasm with many intracytoplasmic filaments, ribosomes and rough endoplasmic reticulum. Budding endothelial cells were frequently found in the developing vessels. The endothelial cells of the mature vessels had attenuated cytoplasm and fenestrations with diaphragms. These observations suggest that choriovitreal neovascularization in the peripheral fundus is one of the features of PDR.
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2/33. Reduced expression of the adherens junction protein cadherin-5 in a diabetic retina.

    PURPOSE: Transvascular leakage occurs in diabetic retinopathy. The tight junction proteins occludin and zonula occludens-1 (ZO-1) and adherens junction protein cadherin-5 are critical to the maintenance of endothelial barrier. We report a comparison of junction protein expression in the normal and diabetic retina. METHOD: Case report. Postmortem retinal cryosections were prepared from the left eye of a 73-year-old woman with diabetic retinopathy. Cryosections were immunostained for cadherin-5, occludin, and ZO-1 and compared with retinal cryosections from the right eye of a 72-year-old man with no progression of retinal disease. RESULTS: Immunofluorescence showed positive retinal vessel staining for occludin and ZO-1 in both eyes and cadherin-5 in the normal eye but reduced cadherin-5 staining in the retinal vessels of the diabetic eye. CONCLUSION: Increases in transvascular leakage observed in diabetic retinal vasculature may be associated with reduction in the expression of the critical adherens junction protein, cadherin-5.
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3/33. Documented acquired asteroid hyalosis in a case of early diagnosed diabetes mellitus.

    BACKGROUND: There have been many reports in the literature of the possible linkage of asteroid hyalosis (AH) to diabetes mellitus (DM). The controversy regarding an association between AH and DM has been one of the longest disputes in the ophthalmic literature. Here we present a case in which AH developed in a patient followed for 9 years after being diagnosed with DM. CASE REPORT: The patient had been examined on nine occasions (since his initial visit in June 1989) and asteroid hyalosis was not discovered until July 1996, when he came in with newly diagnosed diabetes mellitus. This suggests there may well be an association of asteroid hyalosis and diabetes mellitus. DISCUSSION: The patient in this case had a number of risk factors for the development of this ocular condition. He had a long history of systemic arterial hypertension, which has been reported to be linked to the formation of AH. He also had a chronic case of cystoid macular edema, which indicated a vascular compromise to the retinal vessels in the posterior pole, and this leakage may be responsible for serous constituents leaking into the vitreous, which may have caused AH. CONCLUSIONS: This may be the first time in the reported literature that AH was found to occur in a previously normal-appearing vitreous, which was documented over a 9-year period. We would suggest that asteroid hyalosis may be secondary to some form of vasculopathy in many incidences and that diabetes mellitus is one of the conditions that may be associated with the formation of AH.
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4/33. Retinal neovascular markers in retinopathy of prematurity: aetiological implications.

    AIM: (1) To determine if expression of the blood-tissue barrier associated glucose transporter GLUT1 is preserved by the neovasculature of retinopathy of prematurity (ROP), in contrast with the reported loss of GLUT1 expression in preretinal vessels of proliferative diabetic retinopathy. (2) To compare the vascular immunophenotype of ROP to juvenile haemangioma, another perinatal neovascular disorder that has recently been shown to express placental type vascular antigens, including GLUT1 and Lewis Y antigen. methods: A retrospective case report was carried out. Immunoreactivities for GLUT1 and Lewis Y antigen were assessed in a human eye with stage 3 ROP and compared with those in a control (paediatric) eye. The presence or absence of endothelial GLUT1 and Lewis Y immunoreactivity was determined in preretinal and intraretinal vessels. RESULTS: Immunoreactivity was positive for GLUT1 and negative for Lewis Y in the intraretinal and preretinal neovasculature of the ROP affected eye and in the normal retinal vessels of the control eye. CONCLUSIONS: Retention of immunoreactivity for GLUT1 distinguishes ROP from proliferative diabetic retinopathy. Furthermore, absence of Lewis Y antigen co-expression distinguishes ROP from juvenile haemangioma, a perinatal form of GLUT1 positive neovascularisation that has recently been linked to placental vasculature.
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5/33. Pseudodoubling of the optic disc: a colour Doppler imaging study.

    Pseudodoubling of the optic disc is a rare clinical presentation. In these cases it is necessary to exclude retinal coloboma or atrophy following vascular or infectious diseases. We present a case of pseudodoubling of the optic disc in a woman with type 2 diabetes and arterial hypertension. Ophthalmoscopic examination of the fundus showed a disc-like lesion in the right eye and a diabetic retinopathy in the left eye. The lesion was evaluated with fluorescein angiography, neuroradiological and colour Doppler imaging investigations. Colour Doppler imaging confirmed the angiographic findings of anomalous vascularisation of the pseudopapilla and provides an analysis of the choroidal vessel anastomosis between the optic disc and the retinal lesion, revealing that the pseudodoubling in this patient was the result of a chorioretinal coloboma.
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6/33. Intravitreal triamcinolone acetonide for florid proliferative diabetic retinopathy.

    BACKGROUND: The spectrum of ocular indications in which intravitreal injections of triamcinolone acetonide may be therapeutically useful has recently been expanding. methods: Prospective clinical interventional case study in a young adult male with florid proliferative diabetic retinopathy (FPDR). RESULTS: A greater reduction of retinal thickening and fluorescein leakage from retinal new vessels was observed in the right eye after intravitreal injection of triamcinolone followed by scatter panretinal photocoagulation (PKP) than in the left eye treated only by laser. CONCLUSION: Intravitreal injection of triamcinolone acetonide may be a useful adjunct to scatter panretinal photocoagulation for FPDR.
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7/33. Spontaneous regression of neovascularization at the disc in diabetic retinopathy.

    Neovascularization at the disc (NVD) is the most serious complication in diabetic retinopathy, and leads to vitreous hemorrhage and tractional retinal detachment. We report two cases of spontaneous regression of NVD in proliferative diabetic retinopathy. Two men (31 and 46 years old) with diabetes had NVD in both eyes. They were treated with panretinal photocoagulation on the left eye first, but their right eyes went untreated, because they did not revisit our clinic for several months. Fortunately, on revisit, their neovascularization had disappeared a few months later in both eyes, including their untreated right eyes. We could not find any specific causes for the spontaneous regression of the new vessels.
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8/33. Progression of diabetic retinopathy during improved metabolic control may be treated with reduced insulin dosage and/or somatostatin analogue administration -- a case report.

    It is well known that intensified insulin treatment of poorly controlled type 1 diabetic patients may worsen an existing diabetic retinopathy (DR). This observation has been explained by an insulin-induced stimulation of the GH/IGF-I axis. Here, we report on three cases, where the progression of DR during intensified metabolic control was treated with manipulation of insulin therapy and/or by administration of octreotide. serum concentrations of IGF-I, IGFBP-3, insulin, cystatin c, creatinine, endogenous creatinine clearance and HbA1c-levels were assessed by routine laboratory methods; serum IGF-I bioactivity was estimated by a highly specific kinase receptor activation assay. visual acuity and retinopathy stage was assessed by established clinical methods including fluorescein angiography. After glycaemic control was improved by intensified insulin therapy, serum IGF-I levels acutely increased. Subsequently, DR progressed to an advanced stage ("florid retinopathy"), with macular edema, and proliferation of new vessels (in two cases). Immediate reduction of insulin dosage and administration of octreotide lowered serum total IGF-I levels (and IGF-I bioactivity as measured in one patient). Subsequently, macular edema resolved partly, and visual acuity improved, allowing laser photocoagulation to be performed. In conclusion, in poorly controlled type 1 diabetic patients, intensified insulin therapy is able to cause florid DR with acute macular edema. These sight-threatening changes may improve by short-term reduction of insulin dosage or by administration of octreotide, and we speculate that this may be related to down-regulation of (serum) IGF-I.
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9/33. hypertension, the endothelial cell, and the vascular complications of diabetes mellitus.

    hypertension is a major factor that contributes to the development of the vascular complications of diabetes mellitus, which primarily include atherosclerosis, nephropathy, and retinopathy. The mechanism of the pathophysiological effects of hypertension lies at the cellular level in the blood vessel wall, which intimately involves the function and interaction of the endothelial and vascular smooth muscle cells. Both hypertension and diabetes mellitus alter endothelial cell structure and function. In large and medium size vessels and in the kidney, endothelial dysfunction leads to enhanced growth and vasoconstriction of vascular smooth muscle cells and mesangial cells, respectively. These changes in the cells of smooth muscle lineage play a key role in the development of both atherosclerosis and glomerulosclerosis. In diabetic retinopathy, damage and altered growth of retinal capillary endothelial cells is the major pathophysiological insult leading to proliferative lesions of the retina. Thus, the endothelium emerges as a key target organ of damage in diabetes mellitus; this damage is enhanced in the presence of hypertension. An overall approach to the understanding and treatment of diabetes mellitus and its complications will be to elucidate the mechanisms of vascular disease and endothelial cell dysfunction that occur in the setting of hypertension and diabetes.
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10/33. Intravitreal bevacizumab (Avastin) in the treatment of proliferative diabetic retinopathy.

    PURPOSE: To report the biologic effect of intravitreal bevacizumab in patients with retinal and iris neovascularization secondary to diabetes mellitus. DESIGN: Interventional, consecutive, retrospective, case series. PARTICIPANTS: Forty-five eyes of 32 patients with retinal and/or iris neovascularization secondary to diabetes mellitus. methods: patients received intravitreal bevacizumab (6.2 microg-1.25 mg). Ophthalmic evaluations included nonstandardized Snellen visual acuity (VA), complete ophthalmic examination, fluorescein angiography, and optical coherence tomography. MAIN OUTCOME MEASURES: Change in fluorescein angiographic leakage of the proliferative diabetic retinopathy (PDR). Secondary outcomes included changes in Snellen VA. RESULTS: No significant ocular or systemic adverse events were observed. All patients with neovascularization demonstrated by fluorescein angiography (44/44 eyes) had complete (or at least partial) reduction in leakage of the neovascularization within 1 week after the injection. Complete resolution of angiographic leakage of neovascularization of the disc was noted in 19 of 26 (73%) eyes, and leakage of iris neovascularization completely resolved in 9 of 11 (82%) eyes. The leakage was noted to diminish as early as 24 hours after injection. In addition to the reduction in angiographic leakage, the neovascularization clinically appeared to involute in many patients with a reduction in the caliber or presence of perfused blood vessels. In 2 cases, a subtle decrease in leakage of retinal or iris neovascularization in the fellow uninjected eye was noted, raising the possibility that therapeutic systemic levels were achieved after intravitreal injection. recurrence of fluorescein leakage varied. Recurrent leakage was seen as early as 2 weeks in one case, whereas in other cases, no recurrent leakage was noted at last follow-up of 11 weeks. CONCLUSIONS: Short-term results suggest that intravitreal bevacizumab is well tolerated and associated with a rapid regression of retinal and iris neovascularization secondary to PDR. A consistent biologic effect was noted, even with the lowest dose (6.2 microg) tested, supporting proof of concept. The observation of a possible therapeutic effect in the fellow eye raises concern that systemic side effects are possible in patients undergoing treatment with intravitreal bevacizumab (1.25 mg), and lower doses may achieve a therapeutic result with less risk of systemic side effects. Further study is indicated.
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