Intravitreal triamcinolone acetonide and bevacizumab injection as prevention of proliferative vitreoretinopathy in open globe injury

Author:

Kautsar Abiyoga ,Yulia Primitasari ,Delfitri Lutfi

Abstract

Link of Video Abstract: https://youtu.be/VVibnyUdBx4 Background: Proliferative vitreoretinopathy (PVR) is common following an open globe injury (OGI) due to aberrant wound healing that can result in retinal detachment or vitreous hemorrhage. Despite the anatomical success, visual acuity improvement remains unsatisfactory. Triamcinolone acetonide (TCA) and Bevacizumab are among these therapies. This study aims to explore the effect of TCA and Bevacizumab intravitreal injection as potential preventive therapies for PVR in OGI. Methods: This literature review compiles and elaborates on previous studies from many authors to support future experimental studies, which will be conducted to evaluate the intravitreal triamcinolone acetonide and bevacizumab injection as prevention of proliferative vitreoretinopathy in open globe injury through several relevant articles. Results: The healing process requires inflammation that stimulates inflammatory cells and mediators, such as transforming growth factor-β (TGF-β), tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), interleukin-1 (IL-1), IL-2, IL-3, IL-6, IL-8, and IL-10. Plasminogen activator inhibitor-1 (PAI) is upregulated during inflammation, resulting in continued collagen deposition due to fibrosis. The injection of corticosteroids as immunosuppressants and anti-VEGFs as antiangiogenesis is thought to have a positive impact by reducing inflammation and the development of new blood vessels, thus suppressing fibrosis. Conclusion: TCA injection was associated with improved anatomical and visual acuity in humans, pre-operatively or during pars plana vitrectomy. Anti-VEGFs, such as Bevacizumab, ranibizumab, conbercept, and aflibercept, demonstrated protective effects on the eyes of animal models and showed their ability to reduce VEGF, TGF-β, and PAI-1, thereby inhibiting wound fibrosis.

Publisher

DiscoverSys, Inc.

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