Korean J Ophthalmol Vol.23, No.1, 2009 A B Fig. 3. Development of central retinal thickness measured by optical coherence tomography after 1 month (A) and 3 months (B) of follow-up. respectively) (Fig. 1). However, at 3-month follow-up, mean central retinal thickness significantly increased to 421.40± 192.76 µm, compared with 1-month follow-up (334.40± 121.76 µm, p=0.044). Figure 3 summarizes OCT-measured retinal thickness results. Changes in visual acuity and changes in central retinal thickness did not vary substantially according to subject age (p=0.54 and p=0.95, respectively), diabetic retinopathy severity (p=0.88 and p=0.14), previous focal laser treatment (p=0.09 and p=0.76), previous panretinal photocoagulation (p=0.31 and p=0.93), or previous IVTA injection (p=0.79 and p=0.83). There was a suggestion of greater effect on visual acuity in eyes that had not undergone pars plana vitrectomy compared with previously vitrectomized eyes (p=0.025). The same effect was not observed concerning central retinal thickness (p=0.98). Eyes with thicker retinas at baseline experienced a greater absolute and relative reduction in central retinal thickness at 1 month (p=0.001 and p=0.031, respectively), but changes in visual acuity did not differ according to baseline visual acuity or baseline central retinal thickness (p=0.06 and p=0.63, respectively). There were no cases of endophthalmitis, uveitis, IOP increase, or severe decrease in vision immediately after injection. At 3 months, no ocular or systemic adverse events were reported, including thromboembolic events (cerebro- vascular accidents, transient ischemic attacks, myocardial infarctions, or peripheral vascular disease). D iscussion DME is a manifestation of diabetic retinopathy that produces severe visual impairment. Although several treatment mo- dalities are under investigation, the only demonstrated means to reduce the risk of vision loss from DME are laser photo- coagulation, as demonstrated by the ETDRS2; intensive 20 glycemic control, as demonstrated by the Diabetes Control and Complications Trial and the United Kingdom Pro- spective Diabetes Study; and blood pressure control, as demonstrated by the United Kingdom Prospective Diabetes Study.18,19 However, there has been interest in other treatment modalities, such as pharmacologic therapy with oral protein kinase C inhibitors and the use of intravitreal corticosteroids, because most laser-treated DME eyes do not exhibit satis- factory improvements in VA.20,21 Antibodies targeted to VEGF have also generated considerable interest and are being investigated. VEGF is an endothelial cell-specific mitogen and angio- genic inducer in a variety of in vitro and in vivo models.22 It is upregulated by hypoxia, and it plays a role in DME and contributes to the excessive vascular permeability that leads to macular edema in diabetic patients. Bevacizumab is a full-length humanized monoclonal antibody that binds and inhibits all biologically active isoforms of VEGF. Although preclinical experimental data from primates suggested that the full-length antibody might not penetrate the internal limiting membrane of the retina, recent studies have shown full-thickness penetration of the retina within 24 hours.23,24 To our knowledge, all clinical and experimental studies presented thus far have not noted drug-related toxic effects in any retinal structure.14-17,25-30 Intravitreal injection of bevacizumab appears to have good efficacy in the treatment of wet AMD as a new treatment option. Injection of bevaci- zumab into the vitreous cavity, as is presently done mostly for patients with AMD, is based on the results of clinical reports clearly indicating an increase in visual acuity and a decrease in retinal thickness.15,16,27 In addition, other VEGF inhibitors, such as pegaptanib sodium (Macugen)－which binds to one VEGF isoform－have also been successfully used to treat DME in a published randomized, controlled, double-masked phase II multicenter trial. Subjects treated