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PURPOSE: To describe the effects of the antitumor necrosis factor (TNF) monocl onal antibody Infliximab systemic therapy on choroidal neovacularisation (CNV) secondary to age-related macular degeneration (AMD). DESIGN: Prospective, noncom parative series of three patients. METHODS: A subretinal membrane secondary to A MD was documented by fluoroangiography at baseline in three elderly patients sch eduled to receive Infliximab therapy for inflammatory arthritis (infusions of 5 mg/kg at weeks 0, 2, 6, and every 8 weeks thereafter). Followup was performed at three months post-baseline, as well as during 18 months of continuing treatmen t in the first patient. RESULTS: CNV regressed partially at three months and res olved at six months in the first patient. Best-corrected visual acuity (BCVA) i ncreased 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 patie nts. No ocular or extra-ocular side effects were noted. CONCLUSIONS: These find ings suggest a plausible pathogenetic role of TNF in CNV secondary to AMD. Addit ional patients should be studied to confirm the promising clinical results.
PURPOSE: To describe the effects of the antitumor necrosis factor (TNF) monocl onal 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 A MD was documented by fluoroangiography at baseline in three elderly patients sch eduled to receive Infliximab therapy for inflammatory arthritis (infusions of 5 mg / kg at weeks 0, 2, 6, and every 8 weeks thereafter). Followup was was RESULTS: CNV regressed partially at three months and res olved at six months in the first patient. Best-corrected visual acuity (BCVA) i ncreased 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 e CONCLUSIONS: These find ings suggest a plausible pathogenetic role of TNF in CNV secondary to AMD. Additional patients should be studied to confirm the promising clinical results.