%0 Journal Article
%T Nonsteroidal Anti-Inflammatory Drugs for Retinal Disease
%A Scott D. Schoenberger
%A Stephen J. Kim
%J International Journal of Inflammation
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/281981
%X Nonsteroidal anti-inflammatory drugs (NSAIDs) are used extensively in ophthalmology for pain and photophobia after photorefractive surgery and to reduce miosis, inflammation, and cystoid macular edema following cataract surgery. In recent years, the US Food and Drug Administration has approved new topical NSAIDs and previously approved NSAIDs have been reformulated. These changes may allow for greater drug penetration into the retina and thereby offer additional therapeutic advantages. For example, therapeutic effects on diabetic retinopathy and age-related macular degeneration may now be achievable. We provide an updated review on the scientific rationale and clinical use of NSAIDs for retinal disease. 1. Introduction Nonsteroidal anti-inflammatory drugs (NSAIDs) are one of the most commonly prescribed classes of medications and are routinely employed for their analgesic, antipyretic, and anti-inflammatory properties. NSAIDs are potent inhibitors of cyclooxygenase (COX) enzymes and thereby the synthesis of pro-inflammatory prostaglandins (PGs). In ophthalmology, topical NSAIDs are used to stabilize pupillary dilation during intraocular surgery and to treat allergic conjunctivitis and postoperative inflammmation, pain and cystoid macular edema (CME) [1]. The therapeutic efficacy of topical NSAIDs for these aforementioned conditions has been well established [1, 2]. There is also increasing evidence that PGs play a role in the pathogenesis of diabetic retinopathy and age-related macular degeneration (AMD) and recent years have seen more studies examining the therapeutic role of NSAIDs for these disorders [1]. The intent of this paper is to focus on the potential application of NSAIDs to treat retinal disease. 2. Nonsteroidal Anti-Inflammatory Drugs NSAIDs are a class of medications that lack a steroid nucleus and inhibit COX enzymes [1]. COX enzymes catalyze the production of five classes of PGs: PGE2, PGD2, PGF2¦Á, PGI2, and Thromboxane A2. Two main isoforms of COX, COX-1 and COX-2, exist [3], and a third (COX-3) remains largely uncharacterized [4]. COX-1 contributes to normal physiological processes and is expressed in the gastrointestinal tract, kidneys, platelets, and vascular endothelium [1]. COX-2 is an inducible enzyme that is upregulated during pain, fever, and inflammatory responses, but is also expressed in some systems under normal conditions. COX-2 is the predominate isoform in retinal pigment epithelium (RPE) cells and is up-regulated in the presence of proinflammatory cytokines [5]. COX-2 has an important role in angiogenesis and has been
%U http://www.hindawi.com/journals/iji/2013/281981/