Regression of macular edema secondary to branch retinal vein occlusion during anti-TNF-α therapy for rheumatoid arthritis

ression of macular edema secondary to branch retinal vein occlusion during anti-TNF-α therapy for rheumatoid arthritis Case report (4074) Total Article Views Authors: Shu Kachi, Kenshin Kobayashi, Hiroaki Ushida, et al Published Date June 2010 Volume 2010:4 Pages 667 - 670 DOI: http://dx.doi.org/10.2147/OPTH.S10532 Shu Kachi, Kenshin Kobayashi, Hiroaki Ushida, Yasuki Ito, Mineo Kondo, HirokoTerasaki Department of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya, Japan Abstract: A patient with macular edema secondary to a branch retinal vein occlusion (BRVO) was treated with intravenous injections of infliximab, an antitumor necrosis factor (TNF)-α antibody, for her rheumatoid arthritis (RA). Before the injection, the thickness of the right fovea, determined by optical coherent tomography, was 629 μm and the best-corrected visual acuity (BCVA) was 20/50. After eight injections of infliximab and 10 months after the first injection, her foveal thickness was decreased to 293 μm and the visual acuity improved to 20/20. There was no recurrence of macular edema during the infliximab injections. However, the infliximab injection was stopped because the patient developed pneumonia. Eight months after stopping the infliximab injection, her foveal thickness increased to 494 μm. To treat the RA, her orthopedists began weekly subcutaneous injections of etanercept, a fusion protein of a section of the TNF receptor and immunoglobulin. Five months later, the foveal thickness had decreased to 260 μm, and the visual acuity remained at 20/25+. Because TNF-α is known to break down the blood–retinal barrier, the improvements in our case suggest that TNF-α plays a role in the pathogenesis of macular edema in some patients with BRVO.