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      19th EURETINA Congress Keynote Lecture: Diabetic Retinopathy Today

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          In the last decades, significant changes have been taking place regarding the pathogenesis of diabetic retinopathy (DR) and the complex mechanisms that eventually lead to the various manifestations of the disease, including diabetic macular edema (DME). DR was first considered a pure microvascular disease, due to the evident capillary structural changes (microaneurysms), fluid extravasation, and lipid exudation. With the advent of fundus fluorescein angiography, the concept of ischemia and the correlation between peripheral nonperfusion and neovascularization has been introduced, which was eventually followed by the advent of new therapeutic strategies, such as peripheral photocoagulation. Nowadays, thanks to more advanced imaging techniques, namely optical coherence tomography (OCT), OCT angiography, and wide-field imaging (imaging up to 200° of the retina in a single shot), it became clear that other elements participate in the occurrence of DR and DME, including inflammation and neurodegeneration. In the future, integration of standard investigations with new diagnostic devices would allow the prompt recognition of DR even before clinical signs of the disease are ophthalmoscopically evident, and the development of personalized treatment for both retinopathy and DME will be available.

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          Most cited references 66

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          Twelve-month safety of intravitreal injections of bevacizumab (Avastin): results of the Pan-American Collaborative Retina Study Group (PACORES).

          Vascular endothelial growth factor (VEGF) plays an important role in many diseases of the posterior pole that are characterized by macular edema and/or intraocular neovascularization. Recently anti-VEGF agents such as ranibizumab and pegaptanib sodium have been shown to be beneficial in the treatment of choroidal neovascularization (CNV) secondary to age-related macular degeneration (ARMD). However in most parts of the world, both pegaptanib sodium and ranibizumab are not readily available. Bevacizumab, a humanized recombinant monoclonal IgG antibody that binds and inhibits all VEGF isoforms, has been proposed as an alternative treatment option. A total of 1,265 consecutive patients were injected with bevacizumab for diseases such as proliferative diabetic retinopathy, diabetic macular edema, retinal vein occlusions, and CNV of several etiologies including ARMD at eight Latin American institutions from 1 September 2005 to 31 January 2006. Of these 1,265, 92 were excluded because they were injected once and lost to follow-up. The remaining 1,173 patients constitute the subjects of this retrospective, multicenter, open label, uncontrolled interventional case series that reports the cumulative systemic and ocular adverse events following intravitreal bevacizumab during 12 months of follow-up. Patients were examined at baseline and then monthly. If the patients were unable to attend the 12-month visit, a telephone interview was conducted to assess for possible systemic complications. A total of 4,303 intravitreal injections of bevacizumab on 1,310 eyes was reported. All 1,173 patients were accounted for at the 12-month visit. Systemic adverse events were reported in 18 (1.5%) patients. These included seven (0.59%) cases of an acute elevation of systemic blood pressure, six (0.5%) cerebrovascular accidents, five (0.4%) myocardial infarctions, two (0.17%) iliac artery aneurysms, two (0.17%) toe amputations and five (0.4%) deaths. Ocular complications included seven (0.16%) bacterial endophthalmitis, seven (0.16%) tractional retinal detachments, four (0.09%) uveitis, and a case (0.02%) each of rhegmatogenous retinal detachment and vitreous hemorrhage. Despite the limited follow-up, repeated intravitreal injections of either 1.25 mg or 2.5 mg of bevacizumab appears to be safe and well tolerated during the 1st year.
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            A method of photographing fluorescence in circulating blood in the human retina.

             H Novotny,  D L ALVIS (1961)
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              A highly conserved vascular permeability factor secreted by a variety of human and rodent tumor cell lines.

              We have previously reported that rodent tumor cell lines secrete a potent vascular permeability factor with a molecular weight of 34,000-42,000 (Senger et al. Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid. Science (Wash. DC), 219: 983-985, 1983). This tumor-secreted vascular permeability factor (VPF) causes a rapid and completely reversible increase in microvascular permeability in the species (guinea pig or rat) from which the tumors were derived without causing mast cell degranulation or endothelial cell damage or exciting an inflammatory cell infiltrate. This VPF may be responsible, at least in part, for the increased permeability which is commonly displayed by solid and ascites tumor vessels. We have now examined 7 human tumor cell lines and have determined that 5 of them also secrete this same VPF. Antibody raised to guinea pig line 10 VPF neutralized more than 90% of the vascular permeability-increasing activity secreted by these 5 human tumor lines. Furthermore, VPFs from both guinea pig and human tumor sources bound to and were eluted similarly from immobilized heparin and comigrated identically on sodium dodecyl sulfate-polyacrylamide gels. Finally, 2 tumorigenic (in nude mice) human cell lines were found to secrete at least 14-fold more VPF than their directly matched, nontumorigenic counterparts, suggesting that elevated expression of this permeability factor may correlate with neoplastic transformation. These data suggest that a broad spectrum of tumor cells from several species, including humans, secretes a highly conserved molecule that enhances local vascular permeability and that this function may be important for tumor growth.

                Author and article information

                S. Karger AG
                May 2020
                04 February 2020
                : 243
                : 3
                : 163-171
                aSchool of Medicine, Vita-Salute San Raffaele University, Milan, Italy
                bDepartment of Ophthalmology, IRCCS San Raffaele Scientific Institute, Milan, Italy
                Author notes
                *Francesco Bandello, MD, Department of Ophthalmology, University Vita-Salute, IRCCS San Raffaele Scientific Institute, Via Olgettina 60, IT–20132 Milan (Italy), Bandello.francesco@hsr.it
                506312 Ophthalmologica 2020;243:163–171
                © 2020 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 2, Pages: 9
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