Thelansis

 Diabetic macular edema (DME) is primarily driven by chronic hyperglycemia, leading to increased vascular endothelial growth factor (VEGF) expression. This up-regulation results in heightened vascular permeability and elevated angiogenesis. While the fundamental pathophysiology of DME revolves around VEGF, emerging evidence suggests that inflammatory mediators also play a role, significantly contributing to the vascular permeability and edema observed in DME. The predominant cause of vision impairment in Diabetic Retinopathy (DR) is DME, which can manifest at any DR stage and is characterized by edema and retinal thickening, potentially accompanied by hard exudates. As the initial stages of DME are often asymptomatic, individuals with diabetes may be unaware of developing complications. Symptoms vary depending on the edema's location within the retina; non-center-involved macular edema typically lacks noticeable symptoms. However, when the edema reaches the central macula, patients

In DME, chronic hyperglycemia causes an up-regulation of vascular endothelial growth factor (VEGF), thus increasing vascular permeability and angiogenesis. While the underlying pathophysiology of DME is VEGF mediated, there is a growing body of evidence suggesting that inflammatory mediators are also partly responsible and that those mediators contribute substantially to the vascular permeability and edema present in DME. The most common cause of vision loss from DR is DME, which can occur at any stage of DR and is characterized by edema and retinal thickening, which may also include hard exudates. As the earliest stages of DME are usually asymptomatic, individuals with DM are often unaware they have developed such complications. Symptoms are somewhat dependent on the location of the edema within the retina; non–center-involved macular edema is rarely symptomatic. However, once the edema spreads to encompass the central macula, patients generally experience progressive vision loss from