That, in part, prompted researchers to develop uveitis applications for targeted biological-response modifiers such as TNF-α inhibitors like infliximab and adalimumab (Humira, AbbVie).2,8 Adalimumab was approved in June 2016 by the US Food and Drug Administration (FDA) for the treatment of noninfectious intermediate, posterior and panuveitis—the first FDA-approved non-corticosteroid treatment for noninfectious uveitis. The FDA’s approval was based on submitted findings from the Phase 3 VISUAL-I (ClinicalTrials.gov Identifier NCT01138657) and VISUAL-II (ClinicalTrials.gov Identifier NCT01124838) clinical studies, which reportedly included a halving of the risk of uveitis flare and worsened visual acuity.

A multicenter study of 160 patients published in the June 2016 issue of the journal Arthritis & Rheumatology found that among patients with noninfectious uveitis (associated in most cases with systemic autoimmune diseases like Behçet’s disease, juvenile idiopathic arthritis, spondyloarthropathy, and sarcoidosis) refractory to previous treatments, infliximab and adalimumab were both effective, and that Behçet’s disease and occurrence of more than 5 uveitic flares before initiating anti-TNF-α therapy were associated with improved likelihood of anti-TNF-α treatment response.2 Overall response rate and complete-response rate at 12 months were 93% and 28%, respectively.2


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In addition to other TNF-α blocking agents like certolizumab and etanercept, investigational targeted therapies under development as potential treatments for noninfectious uveitis include tocilizumab (which inhibits cytokine signaling of innate immune inflammation response), natalizumab, secukinumab, ustekinumab, and antivascular endothelial growth factor agents like bevacizumab and ranizumab.5

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References:

1. De Smet MD, Taylor SRJ, Bodaghi B, et al. Understanding uveitis: the impact of research on visual outcomes. Progress in Retinal and Eye Research. 2011;30:452-470.

2. Vallet H, Seve P, Biard L, et al. Infliximab versus adalimumab in the treatment of refractory inflammatory uveitis. Arthritis & Rheumatology. 2016;68(6):1522-1530.

3. Prete M, Guerriero S, Dammacco R, et al. Autoimmune uveitis: a retrospective analysis of 104 patients from a tertiary reference center. Journal of Ophthalmic Inflammation and Infection. 2014;4:17. doi: 10.1186/s12348-014-0017-9.

4. Barisani-Asenbauer T, Maca SM, Mejdoubi L, et al. Uveitis—a rare disease often associated with systemic diseases and infections—a systematic review of 2619 patients. Orphanet J Rare Diseases. 2012;7:57. doi: 10.1186/1750-1172-7-57.

5. Prete M, Dammacco R, Fatone MC, Racanelli V. Autoimmune uveitis: clinical, pathogenetic, and therapeutic features. Clinical and Experimental Medicine. 2016;16(2):125-136.

6. Deschenes J, Murray PI, Rao NA, Nussenblatt RB. International Uvenitis Study Group (IUSG): clinical classification of uveitis. Ocular Immunology and Inflammation. 2008;16(1):1-2. doi: 10.1080/09273940801899822.

7. Renfro L, Snow JS. Ocular effects of topical and systemic steroids. Dermatology Clinics. 1992;10(3):505-512.

8. Maleki A, Meese H, Sahawneh H, Foster CS. Progress in the understanding and utilization of biologic response modifiers in the treatment of uveitis. Expert Review of Clinical Immunology. 2016;12(7):775-786.

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This article originally appeared on MPR