Intravitreal bevacizumab for choroidal neovascularization secondary to inflammation

Wolf, Armin; Thurau, Stephan; Kook, Daniel; Hoeing, Anna; Priglinger, Siegfried; Haritoglou, Christos

doi:10.1111/j.1755-3768.2009.01681.x

Cited by 3 publications

(3 citation statements)

References 6 publications

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“…Most CNV occurs in macular lesions at the center of the retina and directly causes a severe loss of visual acuity [1,2,3,4]. Inflammation-induced VEGF-A production is essential for development of CNV [5,6,7,8,9,10,11,12]. However, although anti-VEGF-A treatments have proven therapeutic effects, the outcome remains unsatisfactory.…”

Section: Discussionmentioning

confidence: 99%

“…Inflammatory processes are thought to be critical in generating CNV [5,6,7]. Many experimental and clinical studies have indicated that the vascular endothelial growth factor A (VEGF-A) family, especially VEGF-A, is essential for promoting CNV [8,9,10,11,12].…”

Section: Introductionmentioning

confidence: 99%

“…This growth factor also influences the production of various pro-inflammatory cytokines. However, although anti-angiogenic treatments have proven therapeutic effects with antagonist against VEGF-A, the therapeutic outcome in patients is not always satisfactory [1,2,3,4,5,6,7,8,9,10,11,12]. …”

Section: Introductionmentioning

confidence: 99%

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Inhibition of Ocular Neovascularization by Co-Inhibition of VEGF-A and PLGF

Huo

Li²,

Jiang³

et al. 2015

Cell Physiol Biochem

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Background/Aims: Age-related macular degeneration (AMD) appears to be a disease with increasing incidence in Western countries and may develop into acquired blindness. Choroidal neovascularization (CNV) is the most frequent cause for AMD, and is commonly induced by regional inflammation. Past studies have highlighted vascular endothelial growth factor A (VEGF-A) as a major trigger for CNV. However, studies on the associated angiogenic factors other than VEGF-A are lacking. Methods: Here, we used a well-established laser burn (LB)-induced experimental CNV mouse model to study the molecular mechanisms underlying the development of CNV after ocular injury. We analyzed vessel density by lectin labeling. We isolated macrophages, endothelial cells and other cell types by flow cytometry, and analyzed levels of different angiogenic factors in these populations. We used antisera against VEGF-A (aVEGF) and/or antisera against placental growth factor (PLGF; aPLGF) to antagonize CNV. We used an antibody-driven toxin to selectively eliminate macrophages to evaluate the role of macrophages in CNV. We also examined expression of PLGF in macrophage subtypes. Results: The choroidal vessel density increased significantly 7 days after LB. LB increased significantly the levels of VEGF-A and PLGF in mouse eyes. Treatment with aVEGF significantly blunted increases in vessel density by LB. Treatment with aPLGF alone did not significantly reduce increases in vessel density. However, aPLGF significantly increased the inhibitory effects of aVEGF on vessel density increases. While VEGF-A was produced by endothelial cells, macrophages and other types at similar levels, PLGF seemed to be predominantly produced by macrophages. Selective macrophage depletion significantly reduced CNV. M2, but M1 macrophages produced high levels of PLGF. Conclusions: Together, our data suggest a previously unappreciated role of PLGF in coordination with VEGF-A to regulate CNV during ocular injury. Our study highlights macrophages and their production of PLGF as novel targets for CNV therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Inhibition of Ocular Neovascularization by Co-Inhibition of VEGF-A and PLGF

Huo

Li²,

Jiang³

et al. 2015

Cell Physiol Biochem

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Intravitreal Antivascular Endothelial Growth Factor Treatment for Inflammatory Choroidal Neovascularization in Noninfectious Uveitis

Woronkowicz

Niederer

Lightman

et al. 2022

American Journal of Ophthalmology

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Intravitreal aflibercept for choroidal neovascularization associated with chorioretinitis: a pilot study

Korol¹,

Zborovska²,

Kustryn³

et al. 2017

OPTH

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PurposeThe purpose of this study was to evaluate the potential benefits of intravitreal aflibercept injections for the treatment of choroidal neovascularization (CNV) secondary to chorioretinitis.MethodsIn this uncontrolled, prospective cohort study, 15 eyes of 14 consecutive patients affected by CNV associated with ocular toxoplasmosis were treated with intravitreal aflibercept (2 mg) pro re nata and observed over a 12-month follow-up period. The primary outcome was the change in best-corrected visual acuity (BCVA) from baseline to month 12. Secondary outcomes included change in central retinal thickness (CRT) in the foveal area on optical coherence tomography (OCT) from baseline to month 12, the number of intravitreal aflibercept injections administered, and safety.ResultsMean (standard deviation [SD]) BCVA improved significantly from 0.36 (0.23) at baseline to 0.64 (0.3) at month 12 (P=0.0002). Mean (SD) CRT on OCT showed a reduction from 317 (74) µm at baseline to 254 (43) µm (P=0.0002) at month 12. A mean (SD) of 1.7 (0.5) injections (range, 1–2 injections) were performed during the study period. No cases of endophthalmitis, uveitis, stroke, or retinal detachment were noted. No patient demonstrated an intraocular pressure >20 mmHg at any study visit.ConclusionIntravitreal aflibercept showed a positive clinical effect and was well tolerated for the treatment of CNV associated with chorioretinitis. The results could be helpful for selecting a treatment for CNV secondary to chorioretinitis.

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Intravitreal bevacizumab for choroidal neovascularization secondary to inflammation

Cited by 3 publications

References 6 publications

Inhibition of Ocular Neovascularization by Co-Inhibition of VEGF-A and PLGF

Inhibition of Ocular Neovascularization by Co-Inhibition of VEGF-A and PLGF

Intravitreal Antivascular Endothelial Growth Factor Treatment for Inflammatory Choroidal Neovascularization in Noninfectious Uveitis

Intravitreal aflibercept for choroidal neovascularization associated with chorioretinitis: a pilot study

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