Comparison of the Effect of Unilateral Intravitreal Bevacizumab and Ranibizumab Injection on Diabetic Macular Edema of the Fellow Eye

Bakbak, Berker; Öztürk, Bayram; Gonul, Saban; Yılmaz, Mevlüt; Gedik, Şansal

doi:10.1089/jop.2013.0049

Cited by 43 publications

(30 citation statements)

References 23 publications

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“…A fellow-eye effect has been demonstrated in multiple clinical studies involving anti-VEGF treatment of Diabetic Macular Edema (DME) (Avery et al, 2006; Bakbak et al, 2013; Hanhart et al, 2014). A possible fellow-eye therapeutic effect was also reported in diabetics, after bevacizumab injection (Avery et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Norrin treatment improves ganglion cell survival in an oxygen-induced retinopathy model of retinal ischemia

Dailey

Drenser

Wong

et al. 2017

Experimental Eye Research

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Treatment of a mouse model of oxygen-induced retinopathy (OIR) with recombinant human Norrin (Norrie Disease Protein, gene: NDP) accelerates regrowth of the microvasculature into central ischemic regions of the neural retina, which are generated after treatment with 75% oxygen. While this reduces the average duration and severity of ischemia overall, we do not know if this accelerated recovery of the microvasculature results in any significant survival of retinal ganglion cells (RGCs). The purpose of this study was to investigate ganglion cell survival with and without the intravitreal injection of Norrin in the murine model of oxygen induced retinopathy (OIR), using two strains of mice: C57BL/6J and Thy1-YFP mice. Intravitreal injections of Norrin or vehicle were done after five days of exposure to 75% oxygen from ages P7 to P12. The C57BL/J mice were followed by Spectral-Domain Optical Coherence Tomography (SD-OCT), and the average nerve fiber layer (NFL) and inner-plexiform layer (IPL) thicknesses were measured at twenty-four locations per retina at P42. Additionally, some C57BL/J retinas were flat mounted and immunostained for the RGC marker, Brn3a, to compare the population density of surviving retinal ganglion cells. Using homozygous Thy1-YFP mice, single intrinsically fluorescent RGCs were imaged in live animals with a Micron-III imaging system at ages P21, 28 and P42. The relative percentage of YFP-fluorescent RGCs with dendritic arbors were compared. At age P42, the NFL was thicker in Norrin-injected OIR eyes, 14.4 μm, compared to Vehicle-injected OIR eyes, 13.3 μm (p=0.01). In the superior retina, the average thickness of the IPL was greater in Norrin-injected OIR eyes, 37.7 μm, compared to Vehicle-injected OIR eyes, 34.6 μm (p = 0.04). Retinas from Norrin injected OIR mice had significantly more surviving RGCs (p = 0.03) than vehicle-injected mice. Based upon NFL thickness and counts of RGCs, we conclude that Norrin treatment, early in the ischemic phase, increased the relative population density of surviving RGCs in the central retinas of OIR mice.

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Section: Discussionmentioning

confidence: 99%

Norrin treatment improves ganglion cell survival in an oxygen-induced retinopathy model of retinal ischemia

Dailey

Drenser

Wong

et al. 2017

Experimental Eye Research

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“…Intravitreal RAN and BEV are known to enter systemic circulation [29,30] . There are even some reports on a fellow-eye treatment effect for intravitreal RAN and BEV [31,32] . None of the prior vessel diameter studies [19][20][21]23] , except 1 [22] , presented any results pertaining to noninjected fellow eyes following anti-VEGF delivery.…”

Section: Discussionmentioning

confidence: 99%

Comparative Retinal Vessel Size Study of Intravitreal Ranibizumab and Bevacizumab in Eyes with Neovascular Age-Related Macular Degeneration

et al. 2017

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Purpose: The aim of this paper was to assess and compare the effects of intravitreal ranibizumab and bevacizumab on retinal vessel diameter in eyes with neovascular age-related macular degeneration (AMD). Methods: Patients with neovascular AMD who underwent intravitreal injection of either ranibizumab or bevacizumab were included. Noninjected fellow eyes served as a control. The main outcome measures were central retinal artery equivalent (CRAE), central retinal vein equivalent (CRVE), and the artery-vein ratio (AVR). Results: In the ranibizumab group, the mean CRAE value decreased significantly at 1 week and 1 month (p = 0.002). The AVR value decreased significantly at 1 month (p = 0.028). CRVE values did not change at 1 week and 1 month (p = 0.083). In the bevacizumab group, the preinjection CRAE, CRVE, and AVR values did not change through the study period (p = 0.128, p = 0.600, and p = 0.734, respectively). Conclusion: These results suggest that intravitreal ranibizumab led to significant retinal arteriolar vasoconstriction in eyes with neovascular AMD.

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“…Hence, I reduced the injected dose of bevacizumab down by 200-fold to 6.25 µg and was still able to see an effect on leakage of neovascularisation in the injected eye 1. Although many fellow eye cases have now been reported, and I have observed it with ranibizumab, aflibercept and bevacizumab, most clinicians have not seen fellow eye effects and discount the plausibility that they occur 2 3…”

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confidence: 99%

What is the evidence for systemic effects of intravitreal anti-VEGF agents, and should we be concerned?

Avery

2013

Br J Ophthalmol

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Comparison of the Effect of Unilateral Intravitreal Bevacizumab and Ranibizumab Injection on Diabetic Macular Edema of the Fellow Eye

Abstract: Compared with ranibizumab, intravitreal administration of bevacizumab resulted in a greater decrease in macular thickness in the untreated eye, in patients with bilateral DME.

Cited by 43 publications

References 23 publications

Norrin treatment improves ganglion cell survival in an oxygen-induced retinopathy model of retinal ischemia

Norrin treatment improves ganglion cell survival in an oxygen-induced retinopathy model of retinal ischemia

Comparative Retinal Vessel Size Study of Intravitreal Ranibizumab and Bevacizumab in Eyes with Neovascular Age-Related Macular Degeneration

What is the evidence for systemic effects of intravitreal anti-VEGF agents, and should we be concerned?

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