%0 Journal Article
%T Inflammation in Retinal Vein Occlusion
%A Avnish Deobhakta
%A Louis K. Chang
%J International Journal of Inflammation
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/438412
%X Retinal vein occlusion is a common, vision-threatening vascular disorder. The role of inflammation in the pathogenesis and clinical consequences of retinal vein occlusion is a topic of growing interest. It has long been recognized that systemic inflammatory disorders, such as autoimmune disease, are a significant risk factor for this condition. A number of more recent laboratory and clinical studies have begun to elucidate the role inflammation may play in the molecular pathways responsible for the vision-impairing consequences of retinal vein occlusion, such as macular edema. This improved understanding of the role of inflammation in retinal vein occlusion has allowed the development of new treatments for the disorder, with additional therapeutic targets and strategies to be identified as our understanding of the topic increases. 1. Introduction Retinal vein occlusions (RVOs) are the second most common visually disabling disease affecting the retina, after diabetic retinopathy [1]. Obstruction of retinal venous flow leads to damage of the vasculature, hemorrhage, and tissue ischemia [2]. Occlusions affecting the central retinal vein, or central retinal vein occlusion (CRVO), affect the entire retina, while those affecting lesser tributaries of the venous circulation, the so-called branch retinal vein occlusion (BRVO), affect a portion of the retina. Despite the fact that the disease entity has been known to exist for over 100 years, current treatment options often still leave patients with clinically problematic visual disturbances and overall increased morbidity. RVO generally affects patients in middle age and the elderly population [2], and several studies have identified systemic risk factors, such as hypertension, diabetes, systemic vascular disease, glaucoma, and hypercoagulable states [3, 4]. Although proliferative vascular changes can cause significant morbidity (particularly due to subsequent vitreous hemorrhage and neovascular glaucoma), the main reason for decreased visual acuity in both CRVO and BRVO is macular edema [5]. As a result, elucidation of the causes of, as well as treatment for, macular edema has been at the center of large-scale studies on patients with RVO. While the causes for RVO are multifactorial, with local and systemic factors being identified as etiologic, most of the literature generally implicates vascular and inflammatory mediators as being particularly salient [6¨C8]. Prior to the advent of intravitreal drug delivery, treatment for macular edema for CRVO and BRVO was observation and grid laser photocoagulation,
%U http://www.hindawi.com/journals/iji/2013/438412/