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Reactivation of retinopathy of prematurity after ranibizumab treatment
Ryan K Wong1, Sasha Hubschman, Irena Tsui
1Retina Division, Department of Ophthalmology, Jules Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, California.
Insights
Bevacizumab showed no ROP reactivation, unlike ranibizumab which reactivated in 83% of eyes. Close infant monitoring is crucial after anti-VEGF treatment for retinopathy of prematurity.
Area of Science:
- Ophthalmology
- Neonatology
- Pharmacology
Background:
- Retinopathy of prematurity (ROP) is a leading cause of childhood blindness.
- Vascular endothelial growth factor (VEGF) drives ROP neovascularization.
- Anti-VEGF agents are used for ROP, with bevacizumab and ranibizumab being common choices.
Purpose of the Study:
- To compare the clinical outcomes of bevacizumab and ranibizumab in treating retinopathy of prematurity.
- To evaluate the efficacy and safety of anti-VEGF agents in ROP management.
Main Methods:
- Retrospective chart review of infants screened for ROP.
- Analysis of infants treated with bevacizumab (0.625 mg) or ranibizumab (0.25 mg).
- Minimum 6-month follow-up to assess ROP regression and reactivation.
Main Results:
- Six infants received anti-VEGF treatment for ROP.
- All treated eyes showed initial regression.
- ROP reactivation occurred in 83% of eyes treated with ranibizumab, but none treated with bevacizumab (P < 0.05).
Conclusions:
- Bevacizumab demonstrated superior efficacy in preventing ROP reactivation compared to ranibizumab.
- Ranibizumab's shorter half-life may contribute to ROP recurrence.
- Extended infant monitoring is essential following anti-VEGF therapy for ROP.
Introduction:
Retinopathy of prematurity (ROP) is a vasoproliferative disorder of the developing retina and a significant cause of childhood blindness around the world. Vascular endothelial growth factor (VEGF) plays an important role in the neovascular phase of ROP, and treatment with an anti-VEGF agent is justified in select cases. Bevacizumab is the most commonly used anti-VEGF agent in ROP, but ranibizumab has a shorter half-life with the potential for decreased systemic toxicity. The purpose of this study is to report our experience with anti-VEGF agents for the treatment of ROP.
Methods:
A retrospective chart review was performed on consecutive infants screened for ROP. Infants treated with peripheral retinal ablation, bevacizumab 0.625 mg/0.025 mL, or ranibizumab 0.25 mg/0.025 mL were specifically identified for review of their clinical outcomes. All treated infants had at least 6 months of follow-up with the treating team and were examined until total regression of ROP.
Results:
One hundred and forty-two infants were screened over a two-year period. Six infants received anti-VEGF agents, with a mean gestational age of 23.48 weeks and mean birth weight of 620 g. Ten eyes from the six infants received anti-VEGF treatment. All ten eyes demonstrated initial regression of ROP. However, ROP reactivation occurred in 5/6 (83%) eyes treated with ranibizumab, on average 5.9 weeks after treatment; whereas none of the 4 eyes treated with bevacizumab experienced reactivation (P < 0.05). One infant who received a unilateral injection of ranibizumab demonstrated bilateral regression of ROP.
Conclusion:
The role of anti-VEGF treatment for ROP is still being evaluated. Although the shorter half-life of ranibizumab makes it an attractive option, reactivation of ROP is possible. Physicians and families should be aware of this to follow infants closely for an extended period of time.
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