Diabetic retinopathy is the leading cause of blindness among patients 20 to 70 years old in developed countries. Diabetic macular edema (DME) can develop at any stage of diabetic retinopathy and is a major cause of preventable vision loss. It is also a public health concern, given the increasing prevalence of diabetes.1–3 A recent pooled individual participant meta-analysis estimated that there are 21 million people with DME worldwide with an overall prevalence of 6.81 % among individuals with diabetes.4 The prevalence is higher in those with type 1 than with type 2 diabetes.
The pathogenesis of DME involves overlapping and inter-related pathways initiated by hyperglycaemia. These are responsible not only for vascular events, but also in continued tissue insult that result in chronic DME. Angiogenesis, inflammation and oxidative stress lead to hyperpermeability, disruption of vascular endothelial cell junctions and leukostasis.5 Diabetes generally becomes more inflammatory ith duration, and there is growing evidence that the levels of inflammatory cytokines increases with duration of DME. Retinal hypoxia has been implicated in DME pathogenesis and stimulates vascular endothelial growth factor (VEGF) transcription.5–11 VEGF increases retinal vascular permeability, causes breakdown of the blood–retina barrier and results in retinal edema.12 It is up-regulated in diabetic retinopathy, making it an important therapeutic target in DME. However the products of other hypoxia-inducible genes, such as placental growth factor13 and hepatocyte growth factor,12–14 also induces the influx of leukocytes into the retina which can cause vascular leakage, hypoxia or ischaemia.
Laser photocoagulation, which is the current standard of care, results in slow improvement in a minority of patients. Furthermore, some patients suffer permanent visual loss even after intensive treatment.15,16 Visions worsen in approximately 20 % of laser-treated patients after two years,17 following ranibizumab combined with laser treatment, 30 % show a halving of their visual angle.18 The control of systemic metabolic factors can minimise visual loss. In patients unresponsive to standard laser techniques, pharmacological treatment may be beneficial in addition to improving control of blood pressure and blood sugar. The aim of this article is to review the current pharmacological treatment options for DME, particularly the use of intravitreal implants.
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