PURPOSE: To describe the effects of the antitumor necrosis factor (TNF) monoclonal antibody Infliximab systemic therapy on choroidal neovacularisation (CNV) secondary to age-related macular degeneration (AMD). DESIGN: Prospective, noncomparative series of three patients. METHODS: A subretinal membrane secondary to AMD was documented by fluoroangiography at baseline in three elderly patients scheduled to receive Infliximab therapy for inflammatory arthritis (infusions of 5 mg/kg at weeks 0, 2, 6, and every 8 weeks thereafter). Follow-up was performed at three months post-baseline, as well as during 18 months of continuing treatment in the first patient. RESULTS: CNV regressed partially at three months and resolved at six months in the first patient. Best-corrected visual acuity (BCVA) increased from 0.05 to 0.2; this effect was sustained at 18 months. Regression of subretinal membrane and increase of BCVA was also documented in the other patients. No ocular or extra-ocular side effects were noted. CONCLUSIONS: These findings suggest a plausible pathogenetic role of TNF in CNV secondary to AMD. Additional patients should be studied to confirm the promising clinical results.
PURPOSE: To describe the effects of the antitumor necrosis factor (TNF) monoclonal antibody Infliximab systemic therapy on choroidal neovacularisation (CNV) secondary to age-related macular degeneration (AMD). DESIGN: Prospective, noncomparative series of three patients. METHODS: A subretinal membrane secondary to AMD was documented by fluoroangiography at baseline in three elderly patients scheduled to receive Infliximab therapy for inflammatory arthritis (infusions of 5 mg/kg at weeks 0, 2, 6, and every 8 weeks thereafter). Follow-up was performed at three months post-baseline, as well as during 18 months of continuing treatment in the first patient. RESULTS: CNV regressed partially at three months and resolved at six months in the first patient. Best-corrected visual acuity (BCVA) increased from 0.05 to 0.2; this effect was sustained at 18 months. Regression of subretinal membrane and increase of BCVA was also documented in the other patients. No ocular or extra-ocular side effects were noted. CONCLUSIONS: These findings suggest a plausible pathogenetic role of TNF in CNV secondary to AMD. Additional patients should be studied to confirm the promising clinical results.
Authors: Panagiotis G Theodossiadis; Vasilios S Liarakos; Petros P Sfikakis; Alexander Charonis; Georgios Agrogiannis; Nikolaos Kavantzas; Ioannis A Vergados Journal: Graefes Arch Clin Exp Ophthalmol Date: 2008-11-04 Impact factor: 3.117
Authors: Roberta P A Manzano; Gholam A Peyman; Petros E Carvounis; Muhamet Kivilcim; Palwasha Khan; Patricia Chevez-Barrios; Walter Takahashi Journal: Graefes Arch Clin Exp Ophthalmol Date: 2008-04-15 Impact factor: 3.117