Macular Degeneration: Rodrigues EB

Furlani BA, Meyer CH, Rodrigues EB, Maia M, Farah ME, Penha FM, Holz FG. · Federal University of Sao Paulo, Vision Institute, Department of Ophthalmology, Sao Paulo, Brazil. · Expert Opin Emerg Drugs. · Pubmed #17979601 No free full text.

Abstract: Diabetic macular edema (DME) is the most frequent cause of severe vision impairment in patients with non-proliferative diabetic retinopathy. Even though patients should achieve optimal glycemic control, normalization of blood pressure and serum lipids, as well as improvement of cardiac and renal status, these measures alone will not prevent every patient from developing visual loss caused by DME. The goal of local treatment for DME is vision improvement, usually achieved after reducing leakage on fluorescein angiography (FA) and retinal thickness on optical coherence tomography (OCT). Laser photocoagulation is still the standard treatment for clinically significant DME. However, laser photocoagulation rarely provides major visual improvement, especially in patients with diffuse DME. Thus, a therapeutic intervention that restores visual acuity impaired by DME more often remains a significant unmet medical need. This review aims to present the most important emerging drug technologies for therapy of DME at present, including corticosteroids, vascular endothelial growth factor inhibitors, protein kinase C inhibitors, small interfering RNA, hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors and non-hormonal anti-inflammatory agents. Recent progress in this field suggests that local management of DME may change rapidly in the near future. Novel emerging drugs should enable better anatomical and functional outcomes for therapy of this sight-threatening disease.

Rodrigues EB. · Retina Department, Ophthalmology Service, Hospital Regional São José, Instituto de Olhos Florianópolis/Centro Oftalmológico, Florianópolis, Brazil. · Ophthalmologica. · Pubmed #17440275 No free full text.

Abstract: PURPOSE: To summarize the current information regarding the role of immune and inflammatory response in the pathogenesis of dry age-related macular degeneration (ARMD). METHODS: A Pubmed search was conducted of the period January 1999 to 2005. Relevant information in the literature on the role of inflammation in early dry ARMD was reviewed. RESULTS: Some important evidence for inflammation in early ARMD consists in the isolation of immunoglobulins, complement proteins, cytokines and activated microglia, in retinal pigment epithelium (RPE) cells and drusen. Pivotal mechanisms in early ARMD include the accumulation of debris and proteins along the RPE surface, followed by immune-complex deposition and complement activation. In contrast, the role of other plasma enzymes such as kallikrein-kinin-bradykinin, the Hageman factor, peptides and coagulation proteins in drusen formation and ARMD has yet to be determined. CONCLUSION: A clear role for inflammatory mediators and cells has been established in recent years. Future studies should elucidate further mechanisms in ARMD development.

Rodrigues EB, Rossi EE, Grumann Junior A, Meyer CH, Ho AC. · Departamento de Retina, Serviço de Oftalmologia, Hospital Regional São José, Instituto de Olhos Florianópolis - Centro Oftalmológico - Florianópolis (SC) - Brasil. · Arq Bras Oftalmol. · Pubmed #17187150 links to  free full text

Abstract: Age-related macular degeneration (ARMD) remains a leading cause of blindness in the western world. Several clinical forms of the disease are recognized, whereas choroidal neovascularization (CNV) represents an important manifestation suitable for treatment. The treatment of CNV has been a major focus of research in the past decades, and the first evidence-based established therapy was laser photocoagulation, which reduces the risk of visual loss in extrafoveal lesions. In the late 90's photodynamic therapy has been established as an efficient method for the treatment of predominantly classic and occult CNV. Additional therapies such as macular translocation, submacular surgery, and indocyanine-mediated prothrombosis are currently under investigation in large-scale clinical trials. Molecular biology has recently provided a better comprehension of the pathogenesis of ARMD, and vascular endothelial growth factor (VEGF) was recognized as key mediator in the angiogenesis of CNV-formation. Therefore, the pharmacological approach rose as a key research area to treat CNV. The first FDA-approved agent for CNV-therapy is aptamer pegaptanib sodium (Macugen), which inactivates the key angiogenic isoform VEGF165. Additional VEGF-blockers such as ranibizumab RhuFab V2 (Lucentis) and bevacizumab (Avastin) are under evaluation in major clinical studies. Impressive results of intravitreal bevacizumab were released recently. Moreover, the steroid-derived anecortave acetate as well as the corticosteroid triamcinolone acetate have been proposed as methods for treatment of wet-ARMD. This paper presents the rationale and principles of the pharmacologic antiangiogenic therapy for CNV in ARMD.

Schmidt JC, Rodrigues EB, Meyer CH, Kroll P. · Zentrum für Augenheilkunde, Philipps-Universität Marburg, Marburg, Deutschland. · Ophthalmologica. · Pubmed #14573972 No free full text.

Abstract: BACKGROUND: Age-related macular degeneration (AMD) is a frequent cause of an irreversible loss of the ability to read. The non-exudative form of AMD has not been therapeutically approached in the past in contrast to the exudative form with choroidal neovascularizations (CNVs). Parafoveal laser coagulation can be applied, and in cases of subfoveal location a pars plana vitrectomy with subretinal resection of the CNV is possible. MATERIAL AND METHODS: Since 1995, we have operated 46 eyes of 45 patients with CNV developing from AMD. Patient ages ranged from 63 to 85 years (mean 71.8 years). Pre- and postoperatively we performed vision tests, fluorescence angiographies with sodium fluorescein and indocyanine green. Follow-up times ranged from 3 to 28 months (mean 12.3 months). RESULTS: Pre-operative vision was 0.10 (range: hand movements to 0.4). Postoperative vision at the end of the follow-up period was 0.12 (range: hand movements to 0.4). Vision at the end of the follow-up was lower in 41%, unchanged in 20% and improved in 39%. In 43 eyes, a non-exudative form of AMD developed. Two eyes had a recurrent CNV, which was removed successfully with a second pars plana vitrectomy. Three patients developed a retinal detachment, which was successfully treated by pars plana vitrectomy, encircling buckle and gas tamponade. CONCLUSIONS: We still have to wait for the results of the photodynamic study trials and a randomized study of macular dislocation. Subretinal removal of the CNV by pars plana vitrectomy allows a stabilization of the visual function in most of our cases of AMD. This method inhibits the development of large pseudotumour-like scars. Postoperatively remaining pigment epithelial defects with choroidal atrophies however limit a visual rehabilitation so that reading vision can only be achieved in cases with good pre-operative vision. Long-term results of photodynamic therapy are still lacking and have to show its effectiveness over greater time spans.