Cataract development in Norwegian patients with congenital aniridia

roidal neovascularization with similar efficacy as anti-VEGF antibodies (Rennel et al. 2011). Several studies have shown that the simultaneous blockade of Ang-2/Tie2 and VEGF pathways reduces vascular leakage and tumour sprouting angiogenesis and has an additive effect to single-agent treatment without apparent increased systemic toxicity (Koh et al. 2010). Combined inhibition of Tie-2 and VEGF signalling was also more effective in terminating pathological retinal neovascularization than anti-VEGF therapy alone (Takagi et al. 2003). In this study, we performed vitrectomy for the management of sightthreatening complications of ischaemic RVO in four patients (Table 1). Vitreous haemorrhage, neovascularization and some fibrosis formation were observed in all RVO eyes. None of the patients had previous ophthalmologic history or diabetes prior to RVO. Intravitreal injections of anti-VEGF blockade, such as with bevacizumab or ranibizumab, were not used in any of the study eyes preoperatively. The intravitreal concentrations of both Ang-2 and VEGF were significantly higher in eyes undergoing primary vitrectomy due to complicated RVO compared with eyes with a quiescent idiopathic macular hole or pucker (p 0.001; Table 1). This observation, together with the finding of normal intravitreal total protein and plasma Ang-2 levels among the patients with RVO, suggests that ischaemic retinal ECs secrete more Ang2 than arises due to leakage from blood as a result of blood–retinal barrier breakdown. Interestingly, Ang-1, a factor with known vasculoprotective properties, was induced in RVO eyes. Based on these findings, we suggest that the combination of Ang-2 inhibitors with anti-VEGF therapy may be a more potent treatment for RVO than anti-VEGF therapy alone. However, clinical trials are needed to confirm our hypothesis.