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Posters

Serum anti-enothelial cell antibodies (AECA) in patients with exudative age-related macular degeneration treated with intravitreal injections of bevacizumab

Poster Details

First Author: A.Kubicka-Trz─ůska POLAND

Co Author(s):    I. Karska-Basta   B. Romanowska-Dixon               0   0 0   0 0   0 0   0 0

Abstract Details



Purpose:

To analyze the prevalence and changes in circulating anti-endothelial cell antibodies (AECA) during anti-VEGF therapy in patients with exudative age-related macular degeneration (AMD) and to assess the correlation between AECA and disease activity.

Setting:

There is growing evidence of a chronic inflammation and autoimmunity against retinal antigens that might be involved in AMD pathogenesis and progression. Ocular diseases in which inflammatory and autoimmune components play an important role, may be associated with the presence of circulating autoantibodies.

Methods:

The study comprised ninety eight patients (108 eyes) treated with intravitreal bevacizumab. The ophthalmic examination included best corrected visual acuity (BCVA), slit lamp biomicroscopy, fundoscopy, fluorescein angiography (FA), and optical coherence tomography (OCT). In all cases serum anti-retinal antibodies (ARAs) levels were assessed by indirect immunofluorescence (IIF) on normal monkey retina substrate. In cases with positive reaction within retinal vessels, AECA were detected using IIF on primate skeletal muscle and cultivated human umbilical vein endothelial cells (HUVEC). These studies were repeated at 4 week intervals within 8 months of a follow-up. The sera of 50 sex- and age-matched healthy subjects were used as controls.

Results:

At baseline examination, 94 (95.5%) of the 98 patients were positive for ARAs. In 30 patients (30.6%) ARAs showed positive reaction within retinal vessels. IIF testing performed on monkey iliopsoas muscle and HUVEC cells confirmed the presence of AECA in these patients at titres ranging from 1:10 to 1:320. In the control group AECA were present in only 9 sera (18%) with titres ranging between 1:20 and 1:80. During a follow-up period AECA occurred de novo in in sera of 13 patients (13.3%) in titres ranging from 1:10 to 1:80. Statistical analysis did not show any significant correlation between the presence of AECA and activity of the disease.

Conclusions:

To our knowledge the presence of AECA in sera of AMD patients has not been reported previously. There is growing evidence that AMD is an immune-mediated disease, and thus it could not be excluded that AECA may be involved in its pathogenesis and progression. There are also suggestions that AECA may develop in response to retinal damage and anti-VEGF therapy. The precise determination of a role of circulating AECA in AMD patients requires further investigations.

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