Targeting the Pathophysiology of Diabetic Macular Edema

  1. Pedro Romero-Aroca, MD, PHD
  1. From the Department of Ophthalmology, Universitat Rovira i Virgili, Reus, Spain, and the Department of Ophthalmology Service, Hospital Universtari de Sant Joan, Institut de Investigació Sanitaria Pere Virgili (IISPV), Reus, Spain.
  1. Corresponding author: Pedro Romero-Aroca, romeropere{at}gmail.com.

Diabetic macular edema (DME) is the leading cause of blindness in the diabetic population, and its prevalence is variable. The Diabetes Control and Complications Trial (DCCT) reported that 27% of type 1 diabetic patients developed macular edema within 9 years of diabetes onset (1). Other studies indicate that in type 2 diabetic patients the prevalence increases from 3% within 5 years of diagnosis to 28% after 20 years duration (2). DME tends to be a chronic disease, although spontaneous recovery is not uncommon. It is important to recognize that ∼33–35% of patients with macular edema had spontaneous resolution after 6 months if untreated. To characterize the severity of macular edema and for treatment guidelines, the term clinically significant macular edema (CSME) as an equivalent of DME, defined by the Early Treatment of Diabetic Retinopathy Study (ETDRS), is used.

DME is a complex disease of multifactorial origin. The common pathway that results in DME is disruption of the blood-retinal barrier (BRB). The mechanism of BRB breakdown is multifactorial and secondary to changes in the tight junctions, pericyte loss, endothelial cell loss, retinal vessel leukostasis, upregulation of vesicular transport, and increased permeability of the surface membranes of retinal vessels and retinal pigment epithelium cells. The disruption of the BRB leads to abnormal inflow of fluid into the neurosensory retina that can exceed the outflow and cause residual accumulation of fluid in …

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