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Serum anti‐endothelial cell antibodies in patients with age‐related macular degeneration treated with intravitreal bevacizumab
Author(s) -
KubickaTrząska Agnieszka,
Wilańska Joanna,
RomanowskaDixon Bożena,
Sanak Marek
Publication year - 2016
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/aos.13033
Subject(s) - macular degeneration , medicine , pathogenesis , bevacizumab , antibody , endothelial stem cell , umbilical vein , eye disease , immune system , vascular disease , immunology , pathology , ophthalmology , chemotherapy , biology , in vitro , biochemistry
Abstract Purpose To analyse the prevalence and changes in circulating anti‐endothelial cell antibodies ( AECA ) during anti‐vascular endothelial growth factor (anti‐VEGF) therapy. Methods Ninety‐eight patients with exudative age‐related macular degeneration ( AMD ) were treated with intravitreal bevacizumab. Fifty sex‐ and age‐matched healthy subjects were used as controls. Serum AECA were detected using indirect immunofluorescence on primate skeletal muscle and cultivated human umbilical vein endothelial cells ( HUVEC ). These investigations were repeated at 4‐week intervals within 8 months of follow‐up. Results At baseline examination, 30 of the 98 patients (30.6%) were positive for AECA . The titres of AECA ranged from 1:10 to 1:320. In the control group, AECA were present in only nine sera (18%) with titres ranging between 1:20 and 1:80 (p = 0.0000). The greatest rates of reduction of AECA titres were observed during the ‘loading’ phase of therapy. During the ‘maintenance’ phase, the rates of changes in serum AECA levels were less significant and remained constant. In follow‐up period in 13 patients (13.3%), serum AECA were detected de novo in titres of 1:10 to 1:80. Statistical analysis did not show any significant correlation between the presence of AECA and activity of the disease. Conclusions There is growing evidence that AMD is an immune‐mediated disease, and thus it cannot be excluded that AECA may be involved in its pathogenesis and progression. We also speculate that AECA develop in response to retinal damage and anti‐ VEGF therapy.