Intravitreal bevacizumab treatment for neovascular glaucoma: histopathological analysis of trabeculectomy specimens

Background Neovascular glaucoma (NVG) is a serious complication for patients with proliferative diabetic retinopathy (PDR). Bevacizumab is a full-length humanized monoclonal antibody that binds all isoforms of vascular endothelial growth factor (VEGF). Recently, encouraging results regarding the off...

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Veröffentlicht in:Graefe's archive for clinical and experimental ophthalmology 2011-10, Vol.249 (10), p.1547
Hauptverfasser: Yoshida, Noriko, Hisatomi, Toshio, Ikeda, Yasuhiro, Kohno, Ri-ichiro, Murakami, Yusuke, Imaki, Hiroyuki, Ueno, Akifumi, Fujisawa, Kimihiko, Ishibashi, Tatsuro
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Sprache:eng
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Zusammenfassung:Background Neovascular glaucoma (NVG) is a serious complication for patients with proliferative diabetic retinopathy (PDR). Bevacizumab is a full-length humanized monoclonal antibody that binds all isoforms of vascular endothelial growth factor (VEGF). Recently, encouraging results regarding the off-label use of intravitreal bevacizumab (IVB) for the treatment of NVG have been reported. We evaluated the histology of bevacizumab-treated trabeculectomy specimens to clarify IVB’s biological effects on angle neovascularization. Methods We retrospectively reviewed the charts of a consecutive series of 15 eyes of 13 patients who underwent trabeculectomy to treat NVG caused by PDR. In ten eyes of eight patients, 1.25 mg bevacizumab was injected intravitreally via the pars plana. Using light or electron microscopy, the surgically excised trabecular tissue was compared to that without IVB. Results Light microscopy revealed decreased edema, fibrin deposition, inflammation and vascular congestion in the trabecular meshwork in specimens with IVB compared to those without IVB. Electron microscopy revealed endothelial cell degeneration in the bevacizumab-treated specimens. Conclusions The biological effects on angle neovascularization after IVB may involve reduced vascular permeability, decreased inflammatory reaction, loss of vascular function, and endothelial cell degeneration.
ISSN:0721-832X
1435-702X
DOI:10.1007/s00417-011-1761-2