Uveitis, the Comparison of Age-Related Macular Degeneration Treatments Trials (CATT), and intravitreal biologics for ocular inflammation.
OBJECTIVE
To provide perspective on the implications of the Comparison of Age-Related Macular Degeneration Treatments Trials (CATT) on intravitreal biologic agents in uveitis and retinal diseases in which ocular inflammatory pathways are central to their pathogenesis.


METHODS
Interpretative essay.


METHODS
Literature review and interpretation.


RESULTS
Besides the clear importance of CATT from a patient treatment perspective in age-related macular degeneration (AMD), these data highlight the critical relevance of highly specific protein immunotherapies offered with biologic agents. The CATT trial also provides a reminder regarding the importance of rigorous efficacy and safety monitoring required when administering intravitreal biologic therapy. Within the field of uveitis, systemic and local biologics have been used to effectively treat uveitis, targeting pathways implicated in both angiogenesis and inflammation (eg, tumor necrosis factor-α [TNF-α] and interleukin-2 pathways), and research on intravitreal biologic therapy for uveitis and AMD will continue to expand. With over 25 ongoing clinical trials on intravitreal biologic therapy for AMD, enthusiasm for vanguard biologic therapies should be tempered by judicious monitoring for adverse events.


CONCLUSIONS
The importance of the CATT trial encompasses day-to-day treatment decisions for AMD, as well as lessons on how biologics for ocular disease should be implemented into clinical practice. Specifically, the introduction of intravitreal biologic therapies into clinical practice for uveitis, AMD, and other ocular diseases in which inflammation is involved should be guided by a clear understanding of the immunotherapeutic agent and its molecular target and with rigorous monitoring for both patient benefit and patient safety.
Emory Eye Center, Emory University School of Medicine, Atlanta, Georgia, USA.
Steven
S
Yeh
Thomas A
TA
Albini
Andrew A
AA
Moshfeghi
Robert B
RB
Nussenblatt
D020533:Angiogenesis Inhibitors / Q000009:adverse effects / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects / Q000627:therapeutic use*; D058846:Antibodies, Monoclonal, Murine-Derived / Q000009:adverse effects / Q000627:therapeutic use*; D000068258:Bevacizumab; D002986:Clinical Trials as Topic; D006801:Humans; D007155:Immunologic Factors / Q000009:adverse effects / Q000627:therapeutic use; D000069285:Infliximab; D058449:Intravitreal Injections; D008268:Macular Degeneration / Q000188:drug therapy*; D016032:Randomized Controlled Trials as Topic; D000069579:Ranibizumab; D000069283:Rituximab; D014605:Uveitis / Q000188:drug therapy*; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors
D020533:Angiogenesis Inhibitors; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D007155:Immunologic Factors; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab; D000069283:Rituximab; D000069285:Infliximab; D000069579:Ranibizumab