Ranibizumab in the Treatment of Chronic Central Serous Chorio Retinopathy

Introduction: Central serous chorio-retinopathy is self-limited in the majority of patients, who usually retain excellent vision. However, those who do not resolve spontaneously may develop permanent visual impairment because of pigment epithelial and photoreceptor damage. Most clinicians prefer to observe these patients for three months before considering any treatment options because most cases recover spontaneously. Infrequently, neurosensory retinal detachment persists and leads to RPE and photoreceptor damage. This form of the disorder is called chronic central serous chorio-retinopathy (CCSC) and can result in severe effects on macular function. The pathogenesis of chronic central serous chorio-retinopathy (CCSC) remains indistinct. Vascular endothelial growth factor (VEGF) is produced by retinal and choroidal cells, increases vascular permeability and leads to edema by uncoupling the endothelial cell to cell junctions. For this reason, anti-VEGF agents are used therapeutically to reduce or reverse the choroidal leakage in acute CSC. Intravitreal bevacizumab a humanized monoclonal VEGF antibody was reported to be associated with favorable outcomes without adverse events in patients with acute CSC. Ranibizumab is another anti-VEGF agent which has potentially better retinal penetration than bevacizumab because of its smaller molecular size and higher binding affinity for VEGF. Ranibizumab is a recombinant humanized antibody fragment that blocks vascular endothelial growth factor (VEGF). It is injected intravitreally as a treatment for exudative age-related macular degeneration, diabetic macular edema, and macular edema secondary to central and branch retinal vein occlusion.