In response to the correspondence of Gonzales and associates, we thank the authors for contributing their experience with 2 patients treated by intravitreal bevacizumab injections for vision-threatening subretinal bleeding in peripheral exudative hemorrhagic chorioretinopathy (PEHCR).
Although PEHCR usually shows a benign outcome with spontaneous stabilization and regression of the peripheral lesions, we fully agree with Gonzales and associates that cases with vision-threatening exudation into the macula may benefit from treatment, ideally before the fovea is affected. Our recent description of 56 eyes in 45 patients with PEHCR focused on the clinical characteristics of the entity without discussing possible therapeutic measures. We described in up to 55% of patients visual acuity reduction attributable to PEHCR, in most cases attributable to serous and/or lipid exudation extending into the macula. Anti–vascular endothelial growth factor (VEGF) therapy was not yet available for these patients. A variety of different treatment approaches had been applied for selected cases (laser photocoagulation, photodynamic therapy with Visudyne [Novartis Pharma, Basel, Switzerland], transpupillary thermotherapy). Treated patients showed no further progression but mostly regression of lesion and exudation. However, in the absence of any systematic therapeutic approach, we do not consider it justified to speculate about the treatment benefit in our cases, even more so as untreated patients often showed similar outcome. Having said so, we nevertheless consider anti-VEGF treatment an interesting treatment modality in present times. Particularly in cases of highly active PEHCR with spreading hemorrhage or exudation threatening the foveal function, a potent therapeutic intervention may be vision-saving. If anti-VEGF injections prove effective, as suggested by the preliminary experience of Gonzales and associates, the mere fact of VEGF apparently being implicated in the pathology may add to the indirect evidence of peripheral neovascularization being responsible for the pathology, despite the absence of direct histologic proof. Obviously, further studies about the role of VEGF and anti-VEGF treatment in PEHCR are needed.