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Infliximab for chronic cystoid macular edema associated with uveitis.
American Journal of Ophthalmology 2004 October
PURPOSE: To assess the efficacy of the anti-TNF monoclonal antibody infliximab in uveitis patients without clinically evident ocular inflammation and impaired visual acuity because of chronic cystoid macular edema (CME).
DESIGN: Prospective, noncomparative, interventional case series.
METHODS: Patients with refractory CME (14 eyes, mean duration of 14 months), associated with intermediate uveitis (n = 6), Adamantiades-Behcet disease (n = 2), adult-type vascular pseudotumor (n = 1), and HLAB27+-related uveitis (n = 1) received an intravenous infliximab infusion (5 mg/kg); five patients were retreated after 1 month.
RESULTS: Macular thickness, measured by ocular coherence tomography, was reduced from 428 +/- 138 microm to 219 +/- 51 microm at 2 months postbaseline (P = .0001), while visual acuity increased from 0.41 +/- 0.18 to 0.83 +/- 0.17 (P < .00001). Anatomic and functional improvement was sustained at 6 months in all. No ocular or extra-ocular side effects were noted.
CONCLUSION: These promising results suggest that TNF may play an important pathogenetic role in chronic CME, thus, a controlled trial is warranted.
DESIGN: Prospective, noncomparative, interventional case series.
METHODS: Patients with refractory CME (14 eyes, mean duration of 14 months), associated with intermediate uveitis (n = 6), Adamantiades-Behcet disease (n = 2), adult-type vascular pseudotumor (n = 1), and HLAB27+-related uveitis (n = 1) received an intravenous infliximab infusion (5 mg/kg); five patients were retreated after 1 month.
RESULTS: Macular thickness, measured by ocular coherence tomography, was reduced from 428 +/- 138 microm to 219 +/- 51 microm at 2 months postbaseline (P = .0001), while visual acuity increased from 0.41 +/- 0.18 to 0.83 +/- 0.17 (P < .00001). Anatomic and functional improvement was sustained at 6 months in all. No ocular or extra-ocular side effects were noted.
CONCLUSION: These promising results suggest that TNF may play an important pathogenetic role in chronic CME, thus, a controlled trial is warranted.
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