Beta blocker use and age‐related macular degeneration

in reducing prednisolone to 5 mg (original maintenance dosage) without any recurrences (Fig. 1). To date, there has been no flare-up of scleritis for 12 months. According to previous reports, TNFa may play a role in uveitis and scleritis in patients with RA (Di Girolamo et al. 1997; Braun et al. 2005; Smith et al. 2005), but anecdotal reports paradoxically implicated etanercept as a cause of uveitis and scleritis (Lim et al. 2007; Le Garrec et al. 2009). On the other hand, another anti-TNF medication, infliximab, is effective in controlling eye involvements (Braun, et al. 2005). Our case suggests that etanercept may induce intractable scleritis or is ineffective in treating scleritis. Switching antiTNF treatment from etanercept to infliximab was effective in controlling both RA and scleritis. The discrepancy of efficacy in the treatment of eye involvements might come from the mechanisms of these anti-TNF medications. Infliximab can bind to transmembrane forms of TNF-a, resulting in a breaking down of TNF-a-producing cells, while etanercept cannot affect TNF-a-producing cells because of its lack of binding to transmembrane forms of TNF. Our report does not suggest that infliximab should be preferred over etanercept in treatment of patients with inflammatory disease that may or may not be associated with eye involvements. However, if a patient has scleritis during etanercept therapy, then a change to infliximab therapy may be valuable.