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Review Diabetic Macular Oedema Review of Diabetic Macular Oedema Therapy R Maria Peralta and Kevin J Blinder The Retina Institute, St Louis, MO, US W ithin the realm of diabetic retinopathy, diabetic macular oedema (DMO) is one of the most common causes of visual loss in the young adult population. In this review, we will discuss the epidemiology, pathophysiology and treatment of DMO. A brief historical view of the treatment perspective will be presented as well. We will end with a case report of the standard of care treatment of DMO. Keywords Diabetic retinopathy, diabetic macular oedema, therapy, anti-vascular endothelial growth factor (VEGF) Disclosure: R Maria Peralta has no relevant conflicts of interest to declare. Kevin J Blinder is a consultant and speaker for Regeneron Pharmaceuticals, Allergan and Bausch & Lomb. Compliance with Ethics: All procedures were followed in accordance with the responsible committee on human experimentation and with the Helsinki Declaration of 1975 and subsequent revisions, and informed consent was received from the patient involved in this case study. Authorship: All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship of this manuscript, take responsibility for the integrity of the work as a whole, and have given final approval to the version to be published. Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit. Received: 31 October 2017 Accepted: 5 December 2017 Citation: European Ophthalmic Review, 2017;11(2):108–11 Corresponding Author: Kevin J Blinder, The Retina Institute, 1600 S. Brentwood Blvd, Suite 800, St Louis, MO 63144, US. E: KJBlinder@gmail.com Support: No funding was received in the publication of this article. As our life expectancy, along with our sedentary lifestyles increase, the prevalence of diabetes mellitus increases as well. With increasing prevalence and duration of diabetes, the incidence and prevalence of diabetic retinopathy grows as well. Diabetic macular oedema (DMO) is a frequent cause of vision loss in people with diabetes and is one of the leading causes of vision loss among people with diabetic retinopathy. DMO is the retinal thickening from accumulation of intracellular or extracellular fluid caused by hyperpermeability of the inner endothelial blood-retinal barrier. The main leakage site are abnormally permeable microaneurysms, intra-retinal microvascular abnormalities (IRMA) and damaged retinal capillaries. Treatment of DMO can be complicated due to varying patient response to treatment approaches. The most novel and effective treatment presently is combination therapies with anti-vascular endothelial growth factor (VEGF) injections and corticosteroids. 1 Epidemiology Diabetic retinopathy affects approximately 93 million people worldwide, and is the leading cause of vision loss in adults aged 20–74 years. 2 Out of those 93 million, 21 million have DMO. The overall prevalence of DMO is 6.81% for DMO in people with diabetes worldwide, accounting for 12% of new cases of blindness, annually. Studies have shown that 24% of eyes with DMO will lose at least three lines of vision within 3 years. 3 The Diabetes Control and Complications Trial (DCCT) reported that 27% of patients with type 1 diabetes develop DMO within 9 years of onset. 4 Further, from 1980–2011, the prevalence of diagnosed diabetes increased 176% in the US. 5 Pathophysiology Early detection and intervention in DMO is key to reducing the risk of permanent vision loss. Therefore, understanding the pathophysiology of DMO is vital to progression in treating DMO. DMO causative factors include both inflammatory and ischaemic mechanisms. DMO is associated with hyperglycaemia as well as oxidative stress; endothelial and pericyte cells along with the associated tight junctions in the blood-retinal barriers degrade, causing blockage of capillary perfusion to retinal and neural cells. The body’s response is the release of cytokines, chemokines and other mediators such as VEFG. VEFG also increases leukocyte adhesion to capillaries, which contributes to endothelial and neuronal apoptosis. Other inflammatory mediators implicated in diabetic retinopathy and DMO development are chemokines like C-C motif chemokine ligand 2 (CCL2), integrins transmembrane receptors, insulin-like growth factor (IGF-1), platelet-derived growth factor, and basic fibroblast growth factor. The diagnosis of DMO takes into account location of retinal thickening relative to the fovea, both clinically and by optical coherence tomography (OCT) micro-anatomy. DMO is classified as centre-involving or non-centre-involving, and OCT-based classifications have been proposed that better allows extension in characterisation of volume and morphologic features. 6 However, it is important to remember that protocol A (Diabetic Retinopathy Clinical Research network [DRCR. net]) concluded that there is only “a modest correlation between OCT-measured centre point 108 TOU C H ME D ICA L ME D IA