Primary intravitreal bevacizumab for the management of pseudophakic cystoid macular edema

Arévalo, J. Fernando; Garcia-Amaris, Rafael A.; Roca, José A.; Sánchez, J. García; Wu, Lihteh; Berrocal, María H.; Maia, Maurício

doi:10.1016/j.jcrs.2007.07.046

Cited by 54 publications

(40 citation statements)

References 33 publications

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“…Tumor necrosis factor-a (TNF-a) plays a central role in the pathogenesis of ocular inflammation and the level of TNF-a is increased in ocular fluids of patients with uveitis [6,7]. Over the years, numerous treatment options have been used in an attempt to treat pseudophakic CME, including the use of systemic, periocular, intravitreal, and topical corticosteroids [1,8,9], oral and topical nonsteroidal anti-inflammatory drugs (NSAIDs) [1,10], oral and topical carbonic anhydrase inhibitors [1], laser surgery [11], pars plana vitrectomy [12], and intravitreal anti-vascular endothelial growth factor (VEGF) agents [13,14]. Despite these treatment options, a number of patients remain that do not respond to any of these treatment modalities.…”

Section: Introductionmentioning

confidence: 99%

Intravitreal infliximab for refractory pseudophakic cystoid macular edema: results of the Pan-American Collaborative Retina Study Group

Arévalo²,

Hernández-Bogantes

et al. 2012

Int Ophthalmol

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Inflammation is the major etiologic factor in the development of pseudophakic cystoid macular edema (CME). Several soluble mediators of inflammation such as tumor necrosis factor alpha (TNF-α) have been implicated in the pathogenesis of ocular inflammation. The purpose of this study is to report the short-term visual and anatomic outcomes following intravitreal injections of infliximab in eyes with refractory CME secondary to cataract surgery. An interventional, retrospective study of 7 eyes with refractory CME that were injected with 1 mg of infliximab. The main outcome measures were best-corrected visual acuity (BCVA) and central macular thickness (CMT) at 6-month follow-up. At the 6 month follow-up, BCVA improved from 1.14 ± 0.59 logMAR at baseline to 0.51 ± 0.35 logMAR (p = 0.0156). CMT also improved from 584 ± 159 μm at baseline to 327 ± 127 μm at 6 months (p = 0.0111). No systemic adverse events were reported in these patients. There was a single episode of uveitis that responded to topical steroids. Inhibition of TNF-α may be beneficial in the treatment of refractory pseudophakic CME.

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Section: Introductionmentioning

confidence: 99%

Intravitreal infliximab for refractory pseudophakic cystoid macular edema: results of the Pan-American Collaborative Retina Study Group

Arévalo²,

Hernández-Bogantes

et al. 2012

Int Ophthalmol

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“…Even if these cases represented postoperative pseudophakic CME, an inflammatory rather than a neovascular process, the edema should be responsive to anti-VEGF therapy, as is typical CME. 8 In this report, we present edema within thick ERMs that is responsive to anti-VEGF therapy. The membranes in our patients share many SD-OCT characteristics with vitreoretinal membranes that have been previously described but are distinguished by the presence of intramembranous fluid and by the ocular comorbidities in our patients, which may predispose to more complex ERM formation.…”

Section: Case Reportmentioning

confidence: 68%

Epiretinal Macular Edema Associated With Thick Epiretinal Membranes

Doshi¹,

Lowrance²,

Kim³

et al. 2013

Ophthalmic Surg Lasers Imaging Retina

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High-resolution imaging with spectraldomain optical coherence tomography has identified an unusual group of epiretinal membranes (ERMs) in the presence of lamellar macular holes. These ERMs are unusually thick. The authors present the case of a patient with age-related macular degeneration who developed edema within a thickened ERM in both eyes after cataract surgery. The edema resolved with anti-vascular endothelial growth factor (VEGF) therapy. The authors propose that the VEGF-responsive fluid within these thick ERMs arose from fibrovascular tissue derived from the retina. Further studies with histopathology will be required to determine whether neovascular tissue is present in all cases of thickened ERMs with epiretinal edema.

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“…The 2 critical COX isoforms are COX-1 and COX-2, and the later is the major isoform expressed in the retina [14]. The treatment option is topical corticosteroids, Periocular ocular corticosteroids, intraocular triamcinolone, avastin therapy and surgically pars plana vitrectomy [15,16].…”

Section: Pseudophakic Macular Edema (Irvine-gass Syndrome)mentioning

confidence: 99%

Advances in Management of Subretinal Choroidal Neovascularization Membrane Clinically

Shah¹

2017

AOVS

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Primary intravitreal bevacizumab for the management of pseudophakic cystoid macular edema

Abstract: Short-term results suggest that primary intravitreal Avastin is well tolerated in patients with pseudophakic CME. Treated eyes had a significant improvement in BCVA and decrease in macular thickness by OCT.

Cited by 54 publications

References 33 publications

Intravitreal infliximab for refractory pseudophakic cystoid macular edema: results of the Pan-American Collaborative Retina Study Group

Intravitreal infliximab for refractory pseudophakic cystoid macular edema: results of the Pan-American Collaborative Retina Study Group

Epiretinal Macular Edema Associated With Thick Epiretinal Membranes

Advances in Management of Subretinal Choroidal Neovascularization Membrane Clinically

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