The authors undertook a study based on their own patient records to elucidate whether Avastin does have a viable role to play in the treatment of neovascular glaucoma associated with retinal ischaemic disease.
Bevacizumab (Avastin) was the first commercially available angiogenesis inhibitor targeted against the natural protein vascular endothelial growth factor (VEGF), and approved for the treatment of various types of cancer. It is a full-length monoclonal antibody that is usually administered intravenously, and stops tumour growth by preventing angiogenesis.
Ophthalmologists have recently expanded its uses to include the treatment of neovascular retinopathy from wet age-related macular degeneration (AMD), neovascularization from retinal ischaemia, as well as neovascular glaucoma (NVG). The literature contains many reports of impressive clinical results when Avastin, injected intravitreally, is used to treat NVG; however, the number of patients and length of follow-up presented by these studies have prevented the drawing of any meaningful conclusion. We therefore undertook a study based on our own patient records to elucidate whether Avastin does indeed have a viable role to play in the treatment of NVG associated with retinal ischaemic disease.
What's the problem with current treatment options?
Intravitreal Avastin provides a novel adjunctive treatment modality that works quickly and is less invasive than surgery. The literature on NVG and Avastin is limited, however, with the largest case series published involving only six patients.1 Most of these studies also have a short follow-up, the longest being 16 weeks,2 with the average of around eight weeks.3,4,5 Consequently, many questions remain regarding the use of Avastin in NVG treatment including safety and toxicity profile (systemic and ocular side effects), and ocular pharmacokinetics (duration and persistence of effect, for example). Moreover, ophthalmologists are unsure whether Avastin can be used as a first-line treatment, whether patients will need adjunctive treatments, whether the effect of Avastin is long-term, and what the therapeutic regimen with this agent actually is.
To better answer these questions, we studied the medical records of all our patients who had NVG from ischaemia-related conditions (e.g. proliferative diabetic retinopathy, central retinal vein occlusion, branch retinal vein occlusion) and who were treated with intravitreal Avastin for a six-month period, from March to October 2006. Demographic data, primary eye diagnosis, baseline visual acuity, gonioscopy, intraocular pressure (IOP) at baseline prior to injection, IOP immediately after injection, and IOP at one week, one month, three months, six months, nine months, and 12 months, and final outcome was recorded.
Dramatic regression of disease