Format

Send to

Choose Destination
Curr Opin Ophthalmol. 2009 May;20(3):166-74. doi: 10.1097/ICU.0b013e328329d173.

Anti-vascular endothelial growth factor therapy for neovascular ocular diseases other than age-related macular degeneration.

Author information

1
Vitreoretinal Service, Midwest Eye Institute, Indianapolis, Indiana 46280, USA. thomasciulla@yahoo.com

Abstract

PURPOSE OF REVIEW:

Anti-vascular endothelial growth factor (anti-VEGF) therapies that arrest choroidal angiogenesis and reduce vascular permeability have revolutionized clinical practices for neovascular eye diseases. This review describes anti-VEGF strategies that are being evaluated in ocular diseases, other than neovascular age-related macular degeneration, in which neovascularization plays a critical role in pathogenesis.

RECENT FINDINGS:

Early studies of the anti-VEGF agents, pegaptanib sodium, ranibizumab, bevacizumab, VEGF trap, and bevasiranib in the treatment of various neovascular diseases (e.g., diabetic macular edema, retinal vein occlusion, choroidal neovascularization) have shown promising results. The efficacy and safety of these agents, either alone or combined with standard treatments (e.g., laser photocoagulation), anti-inflammatory agents, or other non-VEGF-based antiangiogenic therapies, is actively investigated. Non-VEGF-driven pathways and growth factors other than VEGF may play important roles in pathogenesis and are included in certain combination therapies with VEGF inhibitors.

SUMMARY:

The discovery of VEGF-A's role in the pathogenesis of neovascular ocular disease provided a strong rationale for the development of anti-VEGF-based therapies. There is now ample evidence that anti-VEGF therapies are viable treatment options for these diseases. Nevertheless, large, randomized controlled trials are still awaited to confirm early safety and efficacy findings from small, open-label prospective studies.

PMID:
19381089
DOI:
10.1097/ICU.0b013e328329d173
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center