Clinical and electrophysiologic outcome in patients with neovascular glaucoma treated with and without bevacizumab.
ABSTRACT To investigate the clinical and electrophysiologic effect of a single intravitreal injection of bevacizumab for neovascular glaucoma (NVG) after ischemic central retinal vein occlusion (iCRVO).
Nineteen eyes from 19 patients with NVG secondary to iCRVO were randomly allocated to either an intravitreal bevacizumab injection and panretinal photocoagulation (PRP) (10 eyes) or PRP alone (9 eyes). The primary outcome measure was the change in the total retinal function 6 months after treatment, demonstrated by full-field electroretinography (ERG). Secondary outcomes included visual acuity, intraocular pressure (IOP), glaucoma medication, additional IOP-lowering treatment, and the presence of ocular neovascularization before treatment, and 1 week, 2 months, and 6 months after treatment.
The regression of ocular neovascularization in the bevacizumab/PRP group was confirmed 1 week after injection. Patients in both study groups had very poor visual acuity at baseline. This remained unchanged. There was no significant difference in the mean IOP between the groups at any point in time. The a-wave amplitudes of combined rod-cone response were significantly decreased after 6 months in the bevacizumab/PRP group (p=0.028), compared with the baseline values. The a- and b-wave amplitudes of combined rod-cone response and the b-wave amplitudes of the 30-Hz flicker response were also markedly reduced compared with the PRP group (-60%, -43%, -47% vs +23%, -36%, -16%, respectively).
This study suggests that intravitreal injection of bevacizumab is valuable in the treatment of NVG by hastening the resolution of neovascularization, while the full-field ERG results indicate that bevacizumab may reduce the photoreceptor function in NVG patients.
- SourceAvailable from: Yin-Shan Ng[show abstract] [hide abstract]
ABSTRACT: Vascular endothelial growth factor A (VEGF-A) is a validated therapeutic target in several angiogenic- and vascular permeability-related pathological conditions, including certain cancers and potentially blinding diseases, such as age-related macular degeneration and diabetic retinopathy. We and others have shown that VEGF-A also plays an important role in neuronal development and neuroprotection, including in the neural retina. Antagonism of VEGF-A function might, therefore, present a risk to neuronal survival as a significant adverse effect. Herein, we demonstrate that VEGF-A acts directly on retinal ganglion cells (RGCs) to promote survival. VEGF receptor-2 signaling via the phosphoinositide-3-kinase/Akt pathway was required for the survival response in isolated RGCs. These results were confirmed in animal models of staurosporine-induced RGC death and experimental hypertensive glaucoma. More important, we observed that VEGF-A blockade significantly exacerbated neuronal cell death in the hypertensive glaucoma model. Our findings highlight the need to better define the risks associated with use of VEGF-A antagonists in the ocular setting.American Journal Of Pathology 02/2013; · 4.52 Impact Factor