Sir,

We thank Radke et al1 for their interest in our manuscript.2 Recent studies have shown a strong role for growth factors in the pathogenesis of proliferative vitreoretinopathy (PVR).3, 4 Vascular endothelial cell growth factor (VEGF) A has been reported to be able to activate the platelet-derived growth factor (PDGF) receptor α, a receptor tyrosine kinase that is key to pathogenesis of PVR.3 Interestingly, Pennock et al4 reported that ranibizumab protected the rabbits from developing PVR. In contrast to these findings, our results showed that intrasilicone injection of bevacizumab does not eliminate the risk of subsequent PVR and may be associated with subretinal proliferation.2

We generally close the eyes after silicone injection with an intraocular pressure (IOP) of around 20 mm Hg. To avoid an increase in IOP after bevacizumab injection, we injected bevacizumab before closure of inflow sclerotomy. Considering that the fluid is heavier than silicone oil and the injections were made in the mid-vitreous cavity, we did not expect to have drug regurgitation.

Several preclinical and clinical studies reported promising results of corticosteroid therapy via systemic, periocular and intraocular routes for prevention of PVR.5, 6, 7 Although the effect is still controversial, we consider corticosteroid therapy as an available and easy-to-use pharmacologic modality in high-risk patients to reduce the rate of subsequent PVR.

We agree with Radke et al about the reported detrimental effect from the injection of anti-VEGF agents on ‘fibrovascular’ membranes. However, such membranes are usually encountered in retinovascular diseases such as proliferative diabetic retinopathy (as depicted in their reference 3). In proliferative vitreoretinopathy the membranes are fibroglial and not fibrovascular.3 We did not find any previous study indicating detrimental effects from anti-VEGF agents on PVR. Actually this is the exact point that makes our study so unique. We look forward to future studies by other investigators to further elucidate the role of anti-VEGF agents in the management of proliferative vitreoretinopathy.