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Review
. 2021 Feb 23:2021:6654168.
doi: 10.1155/2021/6654168. eCollection 2021.

Intravitreal Therapy for Diabetic Macular Edema: An Update

Affiliations
Review

Intravitreal Therapy for Diabetic Macular Edema: An Update

Claudio Furino et al. J Ophthalmol. .

Abstract

Diabetic macular edema (DME) represents a prevalent and disabling eye condition. Despite that DME represents a sight-threatening condition, it is also among the most accessible to treatment. Many different treatment options including photocoagulation, intravitreal medical treatment (either vascular endothelial growth factor inhibitors or corticosteroids therapies), and surgical removal are currently available. Although laser has been considered as the gold standard for many years, over the past several years vascular endothelial growth factor inhibitors (anti-VEGFs) have become first-line therapy. However, many patients do not adequately respond to them. With the development of sustained-release corticosteroid devices, steroids have gained a presence in the management of the DME. We review and update the role of anti-VEGF and intravitreal sustained-release corticosteroid management of DME. According to the currently available scientific evidence, the choice of one anti-VEGF over another critically depends on the baseline best-corrected visual acuity (BCVA). While aflibercept may be the drug of choice in low baseline BCVA, the three anti-VEGFs (bevacizumab, ranibizumab, and aflibercept) provided similar functional outcomes when the baseline BCVA was higher. DEX implants are a valuable option for treating DME, although they are usually seen as a second choice, particularly in those eyes that have an insufficient response to anti-VEGF. The new evidence suggested that, in eyes that did not adequately respond to anti-VEGF, switching to a DEX implant at the time to 3 monthly anti-VEGF injections provided better functional outcomes.

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Conflict of interest statement

Dr. Claudio Furino has received a grant from Allergan during the conduct of the study. Dr. Francesco Boscia, Dr. Michele Reibaldi, and Dr. Giovanni Alessio declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1
An overview of the different pathways involved in the development of diabetic macular edema (adapted from Daruich et al. [8] and Romero-Aroca et al. [9]). LDL: low-density lipoprotein; ROS: reactive oxidative species; Oxi: oxidized; AGEs: advanced glycation end-products; PKC: protein kinase C; ICAM-1: inflammatory intercellular adhesion molecule-1; VEGF: vascular endothelial growth factor; VCAM-1: vascular cell adhesion molecule-1; PEDF: pigment epithelium-derived factor; CCL2: chemokine C-C motif ligand 2; Ang-2: angiopoietin-2; IL: interleukin; TNF: tumor necrosis factor; DME: diabetic macular edema.
Figure 2
Figure 2
Overview of the medical treatment options for diabetic macular edema (adapted from Urias et al. [15]). NSAIDS: nonsteroidal anti-inflammatory drug; VEGF: vascular endothelial growth factor; DARPin: designed ankyrin repeat protein; FGF: fibroblast growth factor beta; PDGF: platelet-derived growth factor; CCR: chemokine receptor; IGF-1: insulin-like growth factor-1; EPO: erythropoietin.

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