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• W2044283334 abstract "Editor, The possible effects of intraocular injection of bevacizumab on the contralateral non-injected eye have been reported in the literature. Bevacizumab was detected in the untreated fellow eye as well as in the systemic circulation in animal models (Bakri et al. 2007; Heiduschka et al. 2008) and an acute retinal pigment epithelial (RPE) tear was reported in the fellow eye of a patient with age-related macular degeneration (AMD) (Mennel et al. 2007). The present report describes the rapid development of a subclinical choroidal neovascular membrane (choroidal neovascularization [CNV]) in the untreated fellow eyes of two AMD patients treated with intravitreal bevacizumab. A 78-year-old woman presented with a 1-month history of decreased visual acuity (VA) in the right eye (OD). Visual acuity was 20/80 OD and 20/25 in the asymptomatic left eye (OS). Fundoscopic examination, fluorescein angiography (FA) and optical coherence tomography (OCT) indicated a subfoveal CNV and pigment epithelial detachment (PED) OD, and some drusens and exudates without active CNV OS (Fig. 1A–F). After the first bevacizumab injection, the subject’s VA OD improved. However, 1 week after the second injection, metamorphopsia and decreased vision developed in the untreated eye. Repeated FA and OCT demonstrated activation of a subclinical CNV OS (Fig. 1G–I). Case 1. Fundus photographs, optical coherence tomography (OCT) and fluorescein angiography (FA) taken (A–C) prior to bevacizumab injection in the right eye (OD). (D–F) Note the drusens and some exudates in the untreated left eye, in which OCT reveals a small extrafoveal pigment epithelial detachment, and late phase FA shows mild hyperfluorescence. (G–I) One week after the second bevacizumab injection OD, visual acuity had decreased to 20/100 in the untreated eye, and OCT and FA of the untreated eye show an increase in and activation of an occult choroidal neovascular membrane. A 91-year-old man presented with a 5-month history of visual decrease OD (20/300 OD, 20/40 OS). Funduscopy revealed exudative maculopathy and PED OD, and multiple drusens OS. Fluorescein angiography and OCT showed a CNV at the edge of the PED OD, but no sign of a CNV OS (Fig. 2A–F). One week after the second bevacizumab injection, VA in the untreated eye had decreased to 20/400. Retinal haemorrhage and thickening of the macula suggested rapid progression of a preclinical lesion, which was confirmed by OCT and FA (Fig. 2G–I). Case 2. Fundus photographs, optical coherence tomography (OCT) and fluorescein angiography (FA) taken (A–C) prior to bevacizumab injection in the right eye (OD). (D–F) In the untreated left eye, note the multiple drusens that correspond to retinal pigment epithelial irregularities revealed by OCT, and minimal hyperfluorescence revealed by late phase FA at 8′35″. (G–I) One week after the second bevacizumab injection OD, visual acuity in the untreated eye had decreased to 20/400; OCT shows a serous detachment and pigment epithelial detachment and FA reveals dye leakage. In both patients, the unexpected worsening of early AMD was noted 1 week after the second bevacizumab injection. Although baseline examinations indicated early AMD in both patients, both denied any prior episodes of symptomatic maculopathy in the untreated eye. Previous authors have reported that intravitreal bevacizumab injection may cause systemic complications associated with anti-vascular endothelial growth factor (anti-VEGF) activity (Avery et al. 2006; Shima et al. 2008), and result in similar effects in untreated eyes as in treated eyes, which may be either therapeutic (Avery et al. 2006) or of adverse impact (Mennel et al. 2007). Interestingly, the present cases showed a paradoxical effect of bevacizumab, whereby improvement occurred in the treated eye and pre-/subclinical lesions worsened in the untreated eye. The mechanism underlying rapid worsening of early AMD in the untreated fellow eye is unknown. In the CNV of AMD patients, levels of angiogenesis-stimulating VEGF and angiogenesis-inhibiting pigment epithelial-derived factor (PEDF) increase with an unfavourable equilibrium shift (Tong & Yao 2006). Intravitreal bevacizumab may reach the fellow eye via the systemic circulation within 1 week (Heiduschka et al. 2008). If the fellow eye also has a compromised blood–retinal barrier caused by early AMD lesions, anti-VEGF activity can disturb the equilibrium between VEGF and PEDF, resulting in the growth and activation of subclinical lesions. As there is an inherent risk of developing fellow eye lesions (Brantley et al. 2007), it is unclear whether the acute worsening of early AMD observed in the present patients resulted from bevacizumab treatment or was a characteristic of the natural course of the disease. Given the increasing use of intravitreal bevacizumab, further studies of its effects on fellow eyes, especially those with pre-/subclinical lesions, are warranted." @default.
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• W2044283334 date "2009-09-01" @default.
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• W2044283334 title "Rapid progression of subclinical age-related macular degeneration in the untreated fellow eye after intravitreal bevacizumab" @default.
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• W2044283334 doi "https://doi.org/10.1111/j.1755-3768.2008.01281.x" @default.
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