Theodossiadis, “Regression of sight-threatening macular edema in type 2 diabetes following treatment with the anti-tumor necrosis factor monoclonal antibody infliximab

D iabetic retinopathy and diabeticmacular edema (DME) are leadingcauses of blindness in an increasing number of patients with diabetes (1). Re-duction of visual aquity in DME results from accumulation of fluid produced from a rupture of the blood-retinal barrier into the inner nuclear layer of the retina (1,2). Although the etiology of DME is unclear, an altered local expression of the pleiotropic cytokine tumor necrosis fac-tor (TNF) may play an important patho-genetic role (2–5). Standard treatment of clinically significant DME consisting of la-ser photocoagulation reduces the risk of vision loss in 60 % of cases, but recur-rences are common, even among those patients who achieve an initial response (1). Various pharmacological therapies are currently under study, including inta-vitreal triamcinolone injections (6) or high doses of nonsteroidal anti-inflammatory agents that lower retinal expression of TNF (7). The monoclonal anti-TNF antibody Infliximab neutralizes TNF actions and has been used for inflammatory arthritic conditions and Crohn’s disease since 1998 with a favorable safety profile (8). Because of the limitations of current treat-ments for DME, and based on our recent findings indicating that Infliximab is an effective therapy for cystoid macular edema associated with uveitis (9–11), we decided to give Infliximab for sight-threatening refractory DME