Intravitreal Ranibizumab (Lucentis) for Branch Retinal Vein Occlusion-Induced Macular Edema

Rouvas, Alexandros; Petrou, Petros; Ntouraki, Amalia; Douvali, Maria; Ladas, Ioannis; Vergados, Ioannis

doi:10.1097/iae.0b013e3181cd4894

Cited by 25 publications

(18 citation statements)

References 28 publications

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“…Changes in thickness and shape of the central segment of the retina in occlusive processes in the central retinal vein and its tributaries are described in other studies that address this issue. (9)(10)(11)(12) This paper describes a 30% increase in average thickness of the macular area of the retina to 386.97 ± 16.26 microns with the highest index in the center corresponding approximately to the results presented by other authors with a similar index of 416 microns at average indices of the central part, and a thickness from 552 microns to 150 ± 668.18 ± 245.58 microns. (9) According to the authors of the paper, the changes in the macula in the retina vein thrombosis affect the outer plexiform layer, the inner nuclear layer and the retinal nerve fiber layer with the internal limiting membrane.…”

Section: Discussionsupporting

confidence: 59%

Morphometric of the interface of the central retina in patients with retinal vein occlusion

Бикбов¹,

Fayzrakhmanov²,

Gilmanshin³

et al. 2016

Revista Brasileira De Oftalmologia

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Section: Discussionsupporting

confidence: 59%

Morphometric of the interface of the central retina in patients with retinal vein occlusion

Бикбов¹,

Fayzrakhmanov²,

Gilmanshin³

et al. 2016

Revista Brasileira De Oftalmologia

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“…2 ) disturbs the retinal osmohomeostasis and hinders edema resolution. Intravitreally applied anti-VEGF agents are used clinically for treating macular edema secondary to CRVO [14,15] . Bevacizu mab prevents the receptor binding of VEGF, resulting in decreased vascular permeability as a major cause of edema.…”

Section: Discussionmentioning

confidence: 99%

“…The downregulation of Kir4.1 and aquaporins might result in a disruption of the regular potassium and water transport through glial cells, which may hinder the clearance of edema [1] . In addition to intravitreal steroids, an intravitreal injection of anti-VEGF agents such as bevacizumab (Avastin) and ranibizumab (Lucentis) was shown to be efficient in reducing retinal edema due to CRVO [13][14][15] . Because bevacizumab is a full-length humanized monoclonal IgG antibody that binds to the moiety of VEGF responsible for receptor binding, it is assumed that it preferentially inhibits the action of VEGF at the level of target cells.…”

Section: Effect Of Intravitreal Anti-vascular Endothelialmentioning

confidence: 99%

Effect of Intravitreal Anti-Vascular Endothelial Growth Factor Treatment on the Retinal Gene Expression in Acute Experimental Central Retinal Vein Occlusion

et al. 2011

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Purpose: To determine the effect of intravitreal bevacizumab and anti-vascular endothelial growth factor (VEGF) antibodies on the gene expression in the neural retina in a rat model of central retinal vein occlusion (CRVO). Methods: The CRVO was induced by laser photocoagulation of all retinal veins. The animals were divided into 3 groups (in each, n = 16): group CRVO only without any further treatment, group CRVO with bevacizumab, and group CRVO with anti-VEGF antibodies. The intravitreal injection of bevacizumab or anti-VEGF antibodies was performed 15 min after CRVO induction. The left eyes in all animals served as untreated controls. The expression of factors which influence the development of vascular edema (VEGF-A, pigment epithelium-derived factor, PEDF), of channels implicated in retinal osmohomeostasis (Kir4.1, AQP4, AQP1) and of the proinflammatory cytokines interleukin (IL)-1β and IL-6 was determined by using real-time RT-PCR after 1 and 3 days of CRVO. Results: CRVO induced a rapid transient upregulation of Vegfa after 1 day, and a delayed upregulation of Pedf after 3 days of CRVO. The expression levels of Kir4.1, Aqp4 and Aqp1 were strongly decreased, and the levels of Il1β and Il6 were strikingly increased after CRVO. Intravitreal bevacizumab and anti-VEGF antibodies fully prevented the upregulation of Vegfa after 1 day, and the upregulation of Pedf after 3 days of CRVO, and decreased the upregulation of Il1β after 1 day of CRVO. Anti-VEGF treatment had no effect on the expression levels of Kir4.1, Aqp4, Aqp1, and Il6. Conclusions: It is suggested that the inhibitory effect on the upregulation of Vegfa and Il1β contributes to the edema-resolving effect of anti-VEGF treatment.

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“…At the 6th month of follow-up, mean logMAR visual acuity reached 0.41 ± 0.06. In a previous study, Rouvas et al (20) reported that baseline logMAR visual acuity improved from 0.74 ± 0.28 to 0.48 ± 0.3. Similarly, Ahn et al (31) reported an improvement from 0.61 ± 0.35 logMAR to 0.35 ± 0.30 logMAR.…”

Section: Discussionmentioning

confidence: 92%

“…In addition, these studies did not address the issue of the ischemic or nonischemic nature of the retinal perfusion. Moreover, despite promising results with different dose regimens for bevacizumab injections, clinical trials for intravitreal ranibizumab injections in BRVO are very limited (15)(16)(17)(18)(19)(20)(21). We aimed to assess the efficacy of pro re nata (PRN) intravitreal ranibizumab injection from the start in the treatment of ME in patients with ischemic or nonischemic BRVO.…”

Section: Introductionmentioning

confidence: 99%

Intravitreal PRN ranibizumab treatment for macular edemadue to branch retinal vein occlusion

et al. 2017

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Background/aim: To evaluate the effect of intravitreal pro re nata (PRN) ranibizumab treatment from the start on the best-corrected visual acuity (BCVA) and the central retinal thickness (CRT) in macular edema (ME) due to branch retinal vein occlusion (BRVO). Materials and methods:Patients with ME secondary to BRVO, who were treated on a PRN basis after a single intravitreal ranibizumab injection, were retrospectively evaluated. The main outcome measures were changes in BCVA and CRT as measured by optical coherence tomography. Results:The number of injections over 6 months was 2.43 ± 1.16. The mean BCVA of the patients was 0.84 ± 0.10 logMAR at baseline and 0.41 ± 0.06 at the 6th month (P < 0.001). Mean BCVA of the ischemic BRVO group was 1.06 ± 0.68 logMAR at baseline and 0.44 ± 0.30 logMAR at the 6th month (P < 0.05). Similarly, the mean BCVA of the nonischemic BRVO group was 0.77 ± 0.53 logMAR at baseline and 0.41 ± 0.36 logMAR at the 6th month (P < 0.05). Between groups, there was no significant difference in mean BCVA at any examination. Conclusion:Intravitreal ranibizumab is a safe and effective treatment option for ME due to ischemic and nonischemic BRVO using PRN from the start.

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Intravitreal Ranibizumab (Lucentis) for Branch Retinal Vein Occlusion-Induced Macular Edema

Cited by 25 publications

References 28 publications

Morphometric of the interface of the central retina in patients with retinal vein occlusion

Morphometric of the interface of the central retina in patients with retinal vein occlusion

Effect of Intravitreal Anti-Vascular Endothelial Growth Factor Treatment on the Retinal Gene Expression in Acute Experimental Central Retinal Vein Occlusion

Intravitreal PRN ranibizumab treatment for macular edemadue to branch retinal vein occlusion

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