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anti-VEGF Therapy (anti-vegf + therapy)

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Medical Sciences	100%

Selected Abstracts

3412: Anti-VEGF and corticosteroids therapy in macular edema secondary to venous occlusions

ACTA OPHTHALMOLOGICA, Issue 2010
JAC POURNARAS
Purpose To assess the evidence on interventions to improve visual acuity (VA) and to treat macular edema (ME) secondary to central (CRVO) and branch retinal vein occlusion (BRVO) Methods Recent randomized studies have evaluated the safety and efficacy of corticosteroids (triamcinolone, dexamethasone) and anti-VEGF therapies (ranibizumab). Score study evaluates preservative-free intravitreal triamcinolone with standard care in BRVO and CRVO. In Geneva study, dexamethasone (DEX) intravitreal implant is compared with sham in BRVO and CRVO. BRAVO and Cruise studies evaluate intraocular injections of ranibizumab in patients with ME following BRVO and CRVO, respectively. Results In SCORE study, there was no difference identified in visual acuity at 12 months for the standard care group compared with the triamcinolone groups in BRVO patients. Intravitreal triamcinolone is superior to observation for treating vision loss associated with ME secondary to CRVO. Improvements in BCVA with DEX implant were seen in patients with BRVO and CRVO, although the patterns of response differed. Intraocular injections of 0.3 mg or 0.5 mg ranibizumab provided rapid, effective treatment for ME following BRVO and CRVO Conclusion Grid photocoagulation remains the standard care for patients with vision loss associated with ME secondary to BRVO. Intravitreal triamcinolone is superior to observation for treating vision loss associated with ME secondary to CRVO. Dexamethasone intravitreal implant can both reduce the risk of vision loss and improve the speed and incidence of visual improvement in eyes with ME secondary to BRVO or CRVO. Anti-VEGF therapies represent new therapeutical option in the treatment of ME secondary to BRVO and CRVO. Further randomized studies are needed [source]

Toxicity testing of the VEGF inhibitors bevacizumab, ranibizumab and pegaptanib in rats both with and without prior retinal ganglion cell damage

ACTA OPHTHALMOLOGICA, Issue 5 2010
Sebastian Thaler
Abstract. Purpose:, To evaluate the effects of intravitreally introduced vascular endothelial growth factor (VEGF) inhibitors in rat eyes with healthy retinal ganglion cells (RGC) and into others with N-methyl-D-aspartate (NMDA)-induced RGC damage. Methods:, Bevacizumab, ranibizumab and pegaptanib were intravitreally injected each at two different concentrations. Respective vehicles of the three substances served as controls. In a different group, additionally a rat anti-VEGF antibody was injected after NMDA treatment. Retrogradely labelled RGC were counted on retinal wholemounts 1 week or 2 months after intravitreal introduction of the VEGF inhibitors. Electron microscopy (EM) was performed on normal rat eyes 2 months after introduction of the VEGF inhibitors. Results:, RGC counts in healthy rat eyes were essentially unchanged from those of the control animals after the administration of both low and high concentrations of bevacizumab, ranibizumab or pegaptanib. Compared to the other two substances, however, high doses of pegaptanib and its respective vehicle significantly decreased RGC after 1 week and led to a marked increase of mitochondrial swelling in EM. In eyes with NMDA-induced RGC damage, no changes of RGC numbers were detected after rat anti-VEGF antibody or bevacizumab, ranibizumab and pegaptanib at both tested concentrations. Conclusions:, Even at higher doses, bevacizumab and ranibizumab showed no toxic effects on RGC in vivo in either untreated rats or in the NMDA-induced RGC damage model. Also a rat anti-VEGF antibody showed no adverse effects after NMDA. Anti-VEGF therapy therefore appears safe even for eyes with additional excitotoxic RGC damage. Potential harm from the pegaptanib carrier solution at very high local concentrations cannot be excluded. [source]

Retinal artery occlusion following intravitreal anti-VEGF therapy

ACTA OPHTHALMOLOGICA, Issue 2 2010
Therese Von Hanno
Abstract. Purpose:, Anti-vascular endothelial growth factor (anti-VEGF) therapy effectively inhibits angiogenesis and is now enjoying widespread use in the treatment of age-related macular degeneration (AMD). It may also have a role in the treatment of macular oedema secondary to other conditions. VEGF is a signalling molecule that has a variety of roles, including vasoregulation and effects on the coagulation homeostasis. Anti-VEGF therapy may therefore have adverse effects on ocular blood flow. Methods:, Two cases of retinal artery occlusion after intravitreal injection of anti-VEGF are presented. Both patients were given the treatment to reduce macular oedema secondary to central retinal vein occlusion. Possible mechanisms are discussed. Results:, Patient 1 developed a central retinal artery occlusion within 1 month of an intravitreal injection of ranibizumab (Lucentis®). The macular oedema was totally resolved at 1 month; final visual acuity (VA) was light perception. Patient 2 developed a branch retinal artery occlusion in the macula 2 days after an intravitreal injection of bevacizumab (Avastin®). The macular oedema was almost resolved within 1 week and did not recur; final VA was 0.6. Conclusions:, Anti-VEGF therapy may have a role in the treatment of macular oedema caused by central retinal vein occlusions. However, our report indicates that the therapeutic principle may be associated with an increased risk of retinal arterial occlusions. [source]

Anti-VEGF therapy: riding the wave of change

CLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 5 2008
Alex P Hunyor FRANZCO
No abstract is available for this article. [source]

3412: Anti-VEGF and corticosteroids therapy in macular edema secondary to venous occlusions

3363: VEGF in aqueous humor of eyes with uveal melanoma

ACTA OPHTHALMOLOGICA, Issue 2010
JP CAUJOLLE
Purpose To analyze in uveal melanomas (UM) the expression of angiogenic factors in pre- and post-treatment neovascular glaucomas (NVG). To study Vascular Endothelial Growth Factor (VEGF-A; VEGFxxxb) and interleukin 8 (IL-8) levels in the aqueous humor of eyes with UM prior to treatment. Methods The cytokines rates in UM have been studied by performing anterior chamber tap. In a few cases, we also analyzed these rates both in vitreous (V) and aqueous (A) humors to compare their concentrations. In addition, some control measurements were made. The concentrations were determined using dedicated enzyme-linked immunosorbent assay kits (ELISA) with a threshold of 5pg/ml. Results We have found no VEGF-A in A humor of control patients. Regarding our samples, virtually no VEGFxxxb isoforms were detected in V and A humors. Moreover, production of cytokine IL-8 was found in a few tumors producing or not VEGF. In the first series on patients with NVG, we have collected 11 samples of A humor and 5 of V humor. The VEGF-A concentrations between A and V humor were nearly equivalent. Concerning A humor samples, VEGF-A levels were ranged from 70.1 to 5680 pg/ml. The second series was obtained with A humor samples from 31 UM eyes prior to treatment. VEGF-A levels were ranged from undetectable to 1532 pg/ml. The correlation between VEGF-A levels and the different tumor features was studied. In both series, the highest rates of VEGF-A were found in A humor of NVG UM eyes. Conclusion VEGF-A and IL-8 can be produced in the context of UM. However, their expression is not systematic. Our results suggest that VEGF determination should be determined prior to anti-VEGF therapy in order to prevent post-protontherapy complications or to improve protontherapy efficiency. [source]

4265: Inhibitory isoforms of VEGF in uveal melanoma

ACTA OPHTHALMOLOGICA, Issue 2010
SE COUPLAND
Purpose Uveal melanoma (UM) affects around 600 new patients in the UK each year with half of these being treated at the Liverpool Ocular Oncology Centre. UM is an unusual tumour in that gross chromosomal abnormalities are strongly associated with metastatic spread, especially monosomy 3 & chromosome 8q gain. Mechanisms that underlie this remain unclear. Methods Angiogenesis is a requirement for tumour survival & metastasis. Vascular Endothelial Growth Factor (VEGF) is known to be the most potent stimulator of angiogenesis and increased expression of VEGF-A is linked to enhanced metastatic potential in UM. Treatment with bevacizumab (anti-VEGF therapy) suppresses hepatic micrometastasis of ocular melanoma cells in animal models. However, VEGF-A data in UM are variable, with some studies demonstrating no correlation between VEGF-A expression and metastasis or survival. Results VEGF-A was accepted as a single pro-angiogenic family of protein isoforms generated from alternatively spliced mRNA (VEGF189, VEGF165 etc). However, recently a family of sister isoforms named VEGFxxxb, where xxx is the amino acid number and b a different six C-terminus amino acids (VEGF189b, VEGF165b) has been discovered. The VEGFxxxb variants are exactly the same size as pro-angiogenic VEGFxxx, yet are antiangiogenic. VEGF165b is down-regulated in primary cutaneous melanoma that later metastasises, and over-expression of VEGFxxxb isoforms confers a protective anti-tumour effect. Conclusion Immunohistochemical expression of pro- and anti-angiogenic VEGF-A in 19 UM was assessed using pan-VEGF-A and VEGF165b specific antibodies. A statistically significant reduction in expression of VEGF165b was observed in monosomy 3 UM (non-parametric ANOVA; p<0.05). This suggests that VEGF165b expression may be a useful predictor of UM metastasis. [source]

4366: Treatment of choroidal neovascularization associated with choroidal nevus

ACTA OPHTHALMOLOGICA, Issue 2010
E PILOTTO
Purpose Purpose:To evaluate safety and efficacy of different treatments of choroidal neovascularization (CNV) associated with choroidal nevus at the posterior pole. Methods Methods: Six patients affected by choriodal nevus complicated by CNV were treated with photodynamic therapy with verteporfin (PDT; 50 J/cm2, 83 seconds) (five cases), or intravitreal anti-VEGF (bevacizumab, 1.25 mg) (one case). All patients underwent an ophthalmologic evaluation, including fluorescein and indocyanine green angiography, A-and B scan ultrasonography and OCT at presentation and at each follow-up examination. CNV was extrafoveal in all PDT treated cases, and a foveal serous detachment was detectable. CNV was subfoveal in the eye treated with anti-VEGF. Results Results: Mean follow-up was 15.5 months (range: 6 , 24). Visual acuity improved in four of the PDT treated cases and in the anti-VEGF treated eye, while it remained unchanged in the remaining PDT treated lesion. In all eyes resolution of the foveal serous detachment was detectable. In all PDT treated eyes a single treatment was performed with no recurrence during follow-up. Meanwhile anti-VEGF was repeated after three months for CNV recurrence. Conclusion Conclusions: PDT and anti-VEGF seem both effective in the treatment of CNV secondary to choroidal nevus but a larger study is required to evaluate long-term efficacy and safety expecially of anti-VEGF therapy. [source]

4367: Intravitreal injection of anti-VEGF and diagnosis of primary intraocular-central nervous system lymphoma

ACTA OPHTHALMOLOGICA, Issue 2010
J GAMBRELLE
Purpose We report the case of the diagnosis of primary intraocular- central nervous system (CNS) lymphoma in a patient treated by anti-VEGF. Methods An 88-year old female, with a medical history of bilateral ARMD treated by intravitreal injections of ranibizumab for 1 year, was referred to our department for bilateral vitritis diagnosed 10 days after the last anti-VEGF injection. A complete vitritis work-up including aqueous humour analysis, magnetic resonance imaging of the brain and vitreous biopsy enabled us to confirm the diagnosis of primary intraocular-CNS lymphoma. Results To the best of our knowledge, this is the first report of the diagnosis of primary intraocular-CNS lymphoma in a patient treated by anti-VEGF for ARMD. In our opinion, the occurrence of lymphoma in this case was coincidental and not due to the anti-VEGF injections. The differential diagnosis of vitritis in elderly patients is relatively large. Endophthalmitis or uveitis has been described after anti-VEGF injections. In such a situation, there is actually a risk of overlooking a diagnosis of intraocular lymphoma in the mistaken belief that the observed vitritis may be a reaction to administred anti-VEGFs. If no direct time-relationship with the anti-VEGF injections can be found, a classic vitritis work-up should be performed. Anti-VEGF treatment did not impede cytological diagnosis in our patient. Conclusion Although in some none-CNS non-Hodgkin lymphomas (NHL) systemic anti-VEGF therapy is added to chemotherapy schedules, the use of anti-VEGF did not halt the spread of the lesion within the eye in this case. It can, therefore, be presumed that local anti-VEGF therapy has no adjuvant effect in primary intraocular lymphoma. [source]