Background Intravenous administration of the anti-TNF monoclonal antibody infliximab results in rapid and effective suppression of posterior eye segment inflammation, thus avoiding development of permanent lesions in the retina and optic disc, in many patients with Behcet’s disease (BD). Since infliximab may reactivate latent tuberculosis which is particularly prevalent in countries where BD is endemic, whereas history of cancer or congestive heart failure are contraindications for systemic anti-TNF treatment, an intravitreal injection with minimal systemic absorption could be preferable providing that therapeutic intraocular concentrations can be achieved. Along this line, recent experimental studies on intraocular administration of infliximab have been conducted.
Objectives To assess the efficacy and safety of a single intravitreal injection of the infliximab for sight–threatening uveitis attacks in BD.
Methods In this prospective, non-comparative, interventional study 15 patients with acute unilateral posterior uveitis were given intravitreal infliximab (1mg/0.05mL) at attack’s onset. Oral medications at the day of ocular attack included combinations of azathioprine/cyclosporine-A/corticosteroids (n=1), azathioprine/corticosteroids (n=2), cyclosporine-A/azathiorpine (n=3), or monotherapy with azathioprine (n=4), cyclosporine-A (n=1), or no treatment (n=4). Best corrected visual acuity (BCVA), anterior chamber cells, vitreous cells and posterior eye segment inflammation were assessed at baseline, 1, 7, 14, and 30 post-treatment days. Other medications remained unchanged.
Results Baseline BCVA (mean logarithm of the minimum angle of resolution of 0.74, range 0.15-1.7) improved significantly by day 7 and continued to improve through day 30 after infliximab (mean of 0.30, p<0.0001). Profound decreases in anterior chamber cells (p<0.0001), vitreous cells (p<0.0001), and beneficial effects in retinal vasculitis (p=0.0001) and retinitis (p=0.001) were evident through day 30. Although cystoid macular edema persisted at follow-up end in 9 of 11 eyes affected, central macular thickness decreased significantly by day 7 and continued to decrease through day 30 (p<0.0001). Total inflammation score decreased from 6.27 (baseline mean) to 4.13, 2.87 and 1.13 (days 7, 14 and 30, respectively), being 0 at follow-up end in 6/15 eyes. Background medications were not associated with response to infliximab. No ocular or extra-ocular side effects were noted.
Conclusions These findings confirm that intraocularly produced and/or acting TNF is crucial in BD-associated uveitis and suggest that intravitreal infliximab should be considered when systemic administration is not feasible or contraindicated. Further studies may identify patients for whom intravitreal delivery of infliximab could be preferable to systemic treatment.
Disclosure of Interest None Declared