ABSTRACT
BACKGROUND AND OBJECTIVE: To evaluate the effect of intravitreal ranibizumab in patients with leaking disciform scars. PATIENTS AND METHODS: In this retrospective case series, 31 eyes received one or two ranibizumab injections for treatment of choroidal neovascularization. Visual acuity, central retinal thickness, and macular volume were measured prior to injection and at 1-month follow-up. RESULTS: After one injection (n = 31), mean optical coherence tomography (OCT) central foveal thickness decreased from 317 to 242 microm (P = .00016). Mean OCT macular volume decreased from 7.89 to 6.80 mm3 (P = .00019). After two injections (n = 12), mean OCT central foveal thickness decreased from 310 to 248 microm following the second injection (P = .04). Mean OCT macular volume decreased from 7.80 to 6.43 mm3 at 1-month follow-up after a second injection (P = .006). There was no significant change in visual acuity after injections. CONCLUSION: In the short-term, ranibizumab decreases the leakage associated with choroidal neovascularization in chronic macular degeneration.
Subject(s)
Angiogenesis Inhibitors/therapeutic use , Antibodies, Monoclonal/therapeutic use , Choroidal Neovascularization/drug therapy , Macular Degeneration/drug therapy , Aged , Aged, 80 and over , Antibodies, Monoclonal, Humanized , Choroidal Neovascularization/diagnosis , Exudates and Transudates , Female , Follow-Up Studies , Humans , Injections , Macular Degeneration/diagnosis , Male , Middle Aged , Ranibizumab , Retrospective Studies , Tomography, Optical Coherence , Treatment Outcome , Vascular Endothelial Growth Factor A/antagonists & inhibitors , Visual Acuity , Vitreous BodyABSTRACT
Both the macro- and microvascular complications adversely affect the life quality of patients with diabetes and have been the leading cause of mortality and morbidity in this population. With the advancement of technologies in biomedical research, we have gained a great deal of understanding of the mechanisms underlying these complications. While euglycemic control still remains the best strategy, it is often difficult to maintain at a level that can completely prevent the vascular complications. Therefore, it is necessary to use the processes leading to vascular dysfunction as a framework for designing novel molecular therapeutic targets. Several of the mechanisms by which diabetes induces vascular complications include increased flux through the polyol pathway, increased oxidative stress, activation of protein kinase C (PKC), vascular inflammation, and abnormal expression and actions of cytokines in the vasculature. Many of the therapies that target these pathways have proven successful in experimental models of diabetic complications. However, clinical studies using these treatments have mainly yielded inconclusive results. The pathogenesis of diabetic vascular complications and results from animal studies and key clinical studies are reviewed here.
