Diabetic retinopathy is a prototypical microvascular disorder. Hyperglycemia causes a multiple pathological changes in the retinal vasculature. It has been suggested that apoptosis of pericytes due to high glucose levels plays a key role in the development of the earliest events during diabetic retinopathy. Advancement of the disease resulted in a progressive vessel leakage leading to edematous distortion of macula and increase in hypoxia inducing development of neovascularization with sight threatening complications. Four basis hypotheses explaining the hyperglycemia harmful effects were suggested: (1) increased glucose flux through the aldose reductase pathway, (2) overproduction of advanced glycation end products, (3) activation of protein kinase C isoforms, and (4) increased glucose flux via the hexosamine pathway. It was admitted as well that apoptosis of neurons and glial cell activation occur even earlier than vascular damage. Disturbance in glial cell functions leads to increase in metabolic abnormalities such as glutamate accumulation, promotion of inflammation, and oxidative stress resulting in neuron apoptosis and deterioration of vascular disorders. Clarification of significant biochemical mechanisms involving in the development of diabetic retinopathy can help to create new effective ways in diabetic retinopathy treatment.
Part of the book: Diabetic Eye Disease
Central serous chorioretinopathy (CSC) is characterized by neurosensory retinal detachment and vision deterioration at the posterior pole mostly in working-age men. The exact molecular pathogenesis of CSC remains unclear. It is proposed that leakage into subretinal space is caused by increased permeability of choroidal vessels and outer blood-retinal barrier breakdown. The majority of CSC cases are self-limited for a few months with a good visual prognosis. However, if neuroretinal detachment persists longer than 4–6 months, the condition requires treatment because chronic disease induces progressive and irreversible photoreceptor and retinal pigment epithelium (RPE) damage leading to reduced visual acuity. Treatment of CSC aims at achieving a complete resolution of subretinal fluid, and preservation of photoreceptor and RPE. There have been a number of interventions proposed for CSC management. However, treatment of this disease is still a subject of controversy. The purpose of this chapter is to overview pathophysiological hypotheses, diagnosing, and current treatment options for CSC.
Part of the book: Macular Diseases