Intravitreal Bevacizumab for Macular Oedema Secondary to BRVO or CRVO
Intravitreal Bevacizumab for Macular Oedema Secondary to BRVO or CRVO
Aims: The aim of the study was to evaluate functional and anatomical changes after intravitreal bevacizumab (Avastin®) in eyes with persistent macular oedema secondary to branch retinal vein occlusion (BRVO) or central retinal vein occlusion (CRVO).
Methods: Twenty-nine consecutive eyes with macular oedema secondary to BRVO (21 eyes) or CRVO (eight eyes) were included in a prospective clinical trial. Eyes were treated with three initial intravitreal bevacizumab injections of 1 mg at a monthly interval. Retreatment was based on central retinal thickness (CRT) based on optical coherence tomography. If continuous injections were indicated up to month 6, the dose was increased to 2.5 mg.
Results: After 12 months of follow-up, mean visual acuity increased from 50 letters (20/100) at baseline to 66 letters (20/50; +16 letters; p < 0.001) at month 12 and CRT decreased from 558 µm at baseline to 309 µm at month 12 (-249 µm; p < 0.001). Patients received a mean of eight out of 13 possible injections. No drug-related systemic or ocular side effects following intravitreal bevacizumab treatment were observed. Fluorescein angiography revealed no progression of avascular areas.
Conclusions: Intravitreal therapy using bevacizumab appears to be a safe and effective treatment in patients with macular oedema secondary to retinal vein occlusion. However, the main limitations of this treatment modality are its short-term effectiveness and high recurrence rate.
With a cumulative 10-year incidence of 1.6%, retinal vein occlusion (RVO) is the most common retinal vascular disease after diabetic retinopathy. Although the pathogenesis is still not fully understood, several risk factors have been associated with central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO), including age, hypertension, atherosclerotic retinal vessel changes, diabetes, hyperhomocysteinaemia and open-angle glaucoma. Both CRVO and BRVO seem to have a comparable risk profile, although recent publications hypothesise that the development of CRVO may be multifactorial and not be explicable by a simple thrombus formation alone.
The most common sequela of RVO is the development of cystoid macular oedema (CMO) with a consecutive deterioration in vision. The major stimulus for the formation of macular oedema and neovascularisation in patients with RVO seems to be hypoxia-induced production of vascular endothelial growth factor (VEGF), an angiogenic factor that promotes angiogenesis and increases permeability.
The only proven treatment method for eyes with CMO secondary to BRVO is macular grid laser photocoagulation. However, according to the Branch Vein Occlusion Study, only patients with macular oedema associated with BRVO and a visual acuity of 20/40 or less showed a significant visual benefit compared with the untreated control group. In patients with macular oedema secondary to CRVO, there was no difference between eyes treated with macular grid laser photocoagulation and observation only.
Several studies have evaluated the efficacy of intravitreal triamcinolone in the treatment of macular oedema secondary to both BRVO and CRVO, but were only able to show stabilisation or a moderate improvement in visual acuity. However, the main limitation of intravitreal triamcinolone therapy is the high rate of side effects, such as cataract formation or increased intraocular pressure.
An alternative for patients with macular oedema secondary to RVO is anti-VEGF therapy. Since the first report of the efficacy of intravitreal bevacizumab (a recombinant monoclonal antibody binding to all isoforms of VEGF) in a patient with macular oedema secondary to CRVO in 2005, several retrospective case series have shown the benefit of this treatment, with an improvement in visual acuity and a decrease of central retinal thickness (CRT) in patients with macular oedema associated with both BRVO and CRVO. We have designed a prospective clinical trial to evaluate the effect of intravitreal bevacizumab therapy in patients with macular oedema in retinal vein occlusion (BRVO and CRVO). Consecutive patients with BRVO or CRVO were included and treated based on a standardised protocol over a period of 12 months with monthly follow-up visits. A previous report describes the 6-month results of this trial.
Abstract and Introduction
Abstract
Aims: The aim of the study was to evaluate functional and anatomical changes after intravitreal bevacizumab (Avastin®) in eyes with persistent macular oedema secondary to branch retinal vein occlusion (BRVO) or central retinal vein occlusion (CRVO).
Methods: Twenty-nine consecutive eyes with macular oedema secondary to BRVO (21 eyes) or CRVO (eight eyes) were included in a prospective clinical trial. Eyes were treated with three initial intravitreal bevacizumab injections of 1 mg at a monthly interval. Retreatment was based on central retinal thickness (CRT) based on optical coherence tomography. If continuous injections were indicated up to month 6, the dose was increased to 2.5 mg.
Results: After 12 months of follow-up, mean visual acuity increased from 50 letters (20/100) at baseline to 66 letters (20/50; +16 letters; p < 0.001) at month 12 and CRT decreased from 558 µm at baseline to 309 µm at month 12 (-249 µm; p < 0.001). Patients received a mean of eight out of 13 possible injections. No drug-related systemic or ocular side effects following intravitreal bevacizumab treatment were observed. Fluorescein angiography revealed no progression of avascular areas.
Conclusions: Intravitreal therapy using bevacizumab appears to be a safe and effective treatment in patients with macular oedema secondary to retinal vein occlusion. However, the main limitations of this treatment modality are its short-term effectiveness and high recurrence rate.
Introduction
With a cumulative 10-year incidence of 1.6%, retinal vein occlusion (RVO) is the most common retinal vascular disease after diabetic retinopathy. Although the pathogenesis is still not fully understood, several risk factors have been associated with central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO), including age, hypertension, atherosclerotic retinal vessel changes, diabetes, hyperhomocysteinaemia and open-angle glaucoma. Both CRVO and BRVO seem to have a comparable risk profile, although recent publications hypothesise that the development of CRVO may be multifactorial and not be explicable by a simple thrombus formation alone.
The most common sequela of RVO is the development of cystoid macular oedema (CMO) with a consecutive deterioration in vision. The major stimulus for the formation of macular oedema and neovascularisation in patients with RVO seems to be hypoxia-induced production of vascular endothelial growth factor (VEGF), an angiogenic factor that promotes angiogenesis and increases permeability.
The only proven treatment method for eyes with CMO secondary to BRVO is macular grid laser photocoagulation. However, according to the Branch Vein Occlusion Study, only patients with macular oedema associated with BRVO and a visual acuity of 20/40 or less showed a significant visual benefit compared with the untreated control group. In patients with macular oedema secondary to CRVO, there was no difference between eyes treated with macular grid laser photocoagulation and observation only.
Several studies have evaluated the efficacy of intravitreal triamcinolone in the treatment of macular oedema secondary to both BRVO and CRVO, but were only able to show stabilisation or a moderate improvement in visual acuity. However, the main limitation of intravitreal triamcinolone therapy is the high rate of side effects, such as cataract formation or increased intraocular pressure.
An alternative for patients with macular oedema secondary to RVO is anti-VEGF therapy. Since the first report of the efficacy of intravitreal bevacizumab (a recombinant monoclonal antibody binding to all isoforms of VEGF) in a patient with macular oedema secondary to CRVO in 2005, several retrospective case series have shown the benefit of this treatment, with an improvement in visual acuity and a decrease of central retinal thickness (CRT) in patients with macular oedema associated with both BRVO and CRVO. We have designed a prospective clinical trial to evaluate the effect of intravitreal bevacizumab therapy in patients with macular oedema in retinal vein occlusion (BRVO and CRVO). Consecutive patients with BRVO or CRVO were included and treated based on a standardised protocol over a period of 12 months with monthly follow-up visits. A previous report describes the 6-month results of this trial.
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