Chronic Vascular Arrest as a Predictor of Bevacizumab Treatment Failure in Retinopathy of Prematurity

Toy, Brian C.; Schachar, Ira H.; Tan, Gavin Siew Wei; Moshfeghi, Darius M.

doi:10.1016/j.ophtha.2016.06.055

Cited by 78 publications

(54 citation statements)

References 40 publications

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“…However, one study recently found that fluorescein angiography revealed a scalloped regression pattern in eyes treated with an anti-VEGF drug. The presence of that pattern in conjunction with chronic vascular arrest and peripheral retinal ischemia (in nearly 90% of eyes) that persisted beyond standard screening timelines has significant implications for the management of ROP [19]. This is a new finding worthy of further study.…”

Section: Discussionmentioning

confidence: 99%

Recurrence of Retinopathy of Prematurity in Zone II Stage 3+ after Ranibizumab Treatment: A Retrospective Study

Bai

Chen

et al. 2017

Journal of Ophthalmology

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Objective. To determine the prevalence and risk factors for the recurrence of retinopathy of prematurity (ROP) in Zone II Stage 3+ after ranibizumab treatment. Methods. This was a retrospective, nonrandomized, noncontrolled study that excluded Zone I and aggressive posterior ROP (APROP) cases. Infants who developed Zone II Stage 3 ROP with plus disease and underwent initial intravitreal injection of ranibizumab (IVR) were recruited. Patients were divided into 2 groups based on the outcome after initial ranibizumab treatment: recurrence of ROP or favorable outcome. Data was collected and analyzed by SPSS 16.0. Results. Forty-two patients were included, and 80 eyes with Zone II Stage 3+ were subjected to IVR treatment. Eleven of 42 patients (26.2%, 18 eyes) had a recurrence of ROP after the initial treatment. On univariate analysis, preretinal hemorrhage before treatment was significantly different between the two groups (P = 0.000). Multivariate analysis found that preretinal hemorrhage before treatment was the only factor associated with the recurrence of ROP in our study (P = 0.004). Conclusions. The recurrence rate of ROP in Zone II Stage 3+ after initial ranibizumab treatment was notable and preretinal hemorrhage before treatment was associated with the recurrence of ROP in our study.

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Section: Discussionmentioning

confidence: 99%

Recurrence of Retinopathy of Prematurity in Zone II Stage 3+ after Ranibizumab Treatment: A Retrospective Study

Bai

Chen

et al. 2017

Journal of Ophthalmology

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“…95,96,99 Another small retrospective study that included 58 eyes noted that those infants requiring earlier bevacizumab treatment or had lower initial birth weights required significantly higher The Role of Anti-vascular Endothelial Growth Factor Agents in the Management of Retinopathy of Prematurity rates of rescue treatment. 100 In the rat 50/10 OIR model, it was shown that inhibition of VEGF bioactivity using a neutralizing antibody led to later intravitreal neovascularization in part associated with activation of other angiogenic pathways. 101 The late reactivation in infants also makes extended follow up a necessity compared to laser therapy in a world where providers are already difficult to find.…”

Section: Anti-vascular Endothelial Growth Factormentioning

confidence: 99%

The Role of Anti-vascular Endothelial Growth Factor Agents in the Management of Retinopathy of Prematurity

Conrady¹,

Hartnett²

2017

US Ophthalmic Review

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“…While anti‐VEGF agents represent a major breakthrough in the treatment of retinal diseases with an angiogenic component, they have been used with limited success (Usui et al, ). Not all patients respond to anti‐VEGF treatment (Ashraf, Souka, Adelman, & Forster, ; Chin‐Yee, Eck, Fowler, Hardi, & Apte, ) and increasing evidence suggests that, in some cases, prolonged treatment with anti‐VEGF may lead to hypoxia, exacerbate retinal ischemia (Lee, Kang, & Koh, ; Toy, Schachar, Tan, & Moshfeghi, ) and lead to degeneration of retinal neurons and retinal pigment epithelium (RPE) (Ashraf et al, ; Gemenetzi et al, ; Keir et al, ). Thus, there is a large unmet medical need to develop new, targeted therapies that will either improve efficacy or reduce off‐target effects when used in combination with anti‐VEGF drugs.…”

Section: Introductionmentioning

confidence: 99%

“…VEGF may lead to hypoxia, exacerbate retinal ischemia (Lee, Kang, & Koh, 2017;Toy, Schachar, Tan, & Moshfeghi, 2016) and lead to degeneration of retinal neurons and retinal pigment epithelium (RPE) (Ashraf et al, 2016;Gemenetzi et al, 2017;Keir et al, 2017). Thus, there is a large unmet medical need to develop new, targeted therapies that will either improve efficacy or reduce off-target effects when used in combination with anti-VEGF drugs.…”

mentioning

confidence: 99%

miR‐30a‐5p inhibition promotes interaction of Fas⁺endothelial cells and FasL⁺microglia to decrease pathological neovascularization and promote physiological angiogenesis

Murinello

Usui

Sakimoto

et al. 2018

Glia

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Ischemia‐induced angiogenesis contributes to various neuronal and retinal diseases, and often results in neurodegeneration and visual impairment. Current treatments involve the use of anti‐VEGF agents but are not successful in all cases. In this study we determined that miR‐30a‐5p is another important mediator of retinal angiogenesis. Using a rodent model of ischemic retinopathy, we show that inhibiting miR‐30a‐5p reduces neovascularization and promotes tissue repair, through modulation of microglial and endothelial cell cross‐talk. miR‐30a‐5p inhibition results in increased expression of the death receptor Fas and CCL2, to decrease endothelial cell survival and promote microglial migration and phagocytic function in focal regions of ischemic injury. Our data suggest that miR‐30a‐5p inhibition accelerates tissue repair by enhancing FasL–Fas crosstalk between microglia and endothelial cells, to promote endothelial cell apoptosis and removal of dead endothelial cells. Finally, we found that miR‐30a levels were increased in the vitreous of patients with proliferative diabetic retinopathy. Our study identifies a role for miR‐30a in the pathogenesis of neovascular retinal disease by modulating microglial and endothelial cell function, and suggests it may be a therapeutic target to treat ischemia‐mediated conditions.

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Chronic Vascular Arrest as a Predictor of Bevacizumab Treatment Failure in Retinopathy of Prematurity

Cited by 78 publications

References 40 publications

Recurrence of Retinopathy of Prematurity in Zone II Stage 3+ after Ranibizumab Treatment: A Retrospective Study

Recurrence of Retinopathy of Prematurity in Zone II Stage 3+ after Ranibizumab Treatment: A Retrospective Study

The Role of Anti-vascular Endothelial Growth Factor Agents in the Management of Retinopathy of Prematurity

miR‐30a‐5p inhibition promotes interaction of Fas⁺endothelial cells and FasL⁺microglia to decrease pathological neovascularization and promote physiological angiogenesis

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Chronic Vascular Arrest as a Predictor of Bevacizumab Treatment Failure in Retinopathy of Prematurity

Cited by 78 publications

References 40 publications

Recurrence of Retinopathy of Prematurity in Zone II Stage 3+ after Ranibizumab Treatment: A Retrospective Study

Recurrence of Retinopathy of Prematurity in Zone II Stage 3+ after Ranibizumab Treatment: A Retrospective Study

The Role of Anti-vascular Endothelial Growth Factor Agents in the Management of Retinopathy of Prematurity

miR‐30a‐5p inhibition promotes interaction of Fas+endothelial cells and FasL+microglia to decrease pathological neovascularization and promote physiological angiogenesis

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Product

Resources

About

miR‐30a‐5p inhibition promotes interaction of Fas⁺endothelial cells and FasL⁺microglia to decrease pathological neovascularization and promote physiological angiogenesis