Differentiating Steroid Delivery Systems for Macular Edema*

Steroids can intervene with many of the processes that lead to macular edema (ME). Steroids are potent anti-inflammatory agents, but they also have anti-vascular endothelial growth factor activity. Triamcinolone acetonide is probably the most commonly used steroid for ME, but it may not be the ideal formulation for ME. This article discusses several new steroid delivery systems: the fluocinolone acetonide implants and dexamethasone intravitreal implant. Drug-delivery systems under investigation have 2 fundamental approaches and philosophies: longer-acting reservoir implants with good long-term control of disease but with potential for drug or suppressive side effects, and shorter-acting, biodegradable inserts that potentially expose the eye to less drug or suppressive side effects but may not control disease as well. Sustained-release ocular implants lead to drug concentration gradients in eye tissues in which drug concentration is highest near the implant. Models of drug gradients based on implant location suggest that the implant can be shifted further into the eye, perhaps partitioning the drug better in the posterior segment and minimizing the anterior segment exposure. (Adv Stud Ophthalmol. 2010;7(2):35-41) Macular edema (ME) results from a complex pathway of events, originating from vascular disease (diabetes or central/branch retinal vein occlusion) or as primary inflammatory disease (uveitis). ME due to vascular disease is strongly associated with vascular endothelial growth factor (VEGF) levels, whereas ME due to uveitis is due primarily to inflammatory mediators, such as interleukin-1 and tumor necrosis factor-α. Steroids can intervene with many of the processes in both pathways that lead to ME. Steroids are potent anti-inflammatory agents, but they also have anti-VEGF activity.