Abstract
Diabetic macular edema (DME) is the abnormal accumulation of fluid in the subretinal or intraretinal spaces in the macula in patients with diabetic retinopathy and leads to severely impaired central vision. Technical developments in retinal imaging systems have led to many advances in the study of DME. In particular, optical coherence tomography (OCT) can provide longitudinal and microstructural analysis of the macula. A comprehensive review was provided regarding the role of inflammation using OCT-based classification of DME and current and ongoing therapeutic approaches. In this review, we first describe the pathogenesis of DME, then discuss the classification of DME based on OCT findings and the association of different types of DME with inflammation, and finally describe current and ongoing therapeutic approaches using OCT-based classification of DME. Inflammation has an important role in the pathogenesis of DME, but its role appears to differ among the DME phenotypes, as determined by OCT. It is important to determine how the different DME subtypes respond to intravitreal injections of steroids, antivascular endothelial growth factor agents, and other drugs to improve prognosis and responsiveness to treatment.
Highlights
Diabetic retinopathy (DR) is a major microvascular complication of diabetes and a leading cause of visual impairment in the working-age population [1,2,3,4]
We focus on the pathogenic effect of inflammation in Diabetic macular edema (DME) as determined by optical coherence tomography (OCT)
We first review the pathogenesis of DME and discuss the use of OCT for classification of DME and current and ongoing therapeutic approaches based on OCT classification
Summary
Diabetic retinopathy (DR) is a major microvascular complication of diabetes and a leading cause of visual impairment in the working-age population [1,2,3,4]. Hyperglycemia activates cytokines and growth factors and leads to dysfunction of vascular and neuronal cells. This increases oxidative stress and inflammation, stimulates the protein kinase C and polyol pathways, and increases the production of advanced glycation end products [5, 6]. Several studies reported significantly increased systemic and local expression of proinflammatory cytokines in the retinas of patients with DR [7,8,9] These proinflammatory molecules contribute to structural and functional abnormalities of the retina and adversely affect endothelial cells, pericytes, Müller cells, and microglial cells [10]. We first review the pathogenesis of DME and discuss the use of OCT for classification of DME and current and ongoing therapeutic approaches based on OCT classification
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