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Intravitreal ranibizumab (Lucentis) for choroidal neovascularization associated with vitelliform macular dystrophy

Editor, C horoidal neovascularization (CNV) is a rare complication of Best’s disease (Miller et al. 1976; Noble et al. 1978). Ranibizumab (Lucentis , Genentech, Inc., San Francisco, CA, USA) is a recombinant, humanized, monoclonal antibody antigen-binding fragment (Fab) that neutralizes all biologically active forms of vascular endothelial growth factor (VEGF) and is effectively used in the treatment of neovascular agerelated macular degeneration (AMD) (Brown et al. 2006; Rosenfeld et al. 2006). We present an interventional case report describing a young patient affected with retrofoveolar CNV associated with Best’s vitelliform macular dystrophy, who underwent treatment with intravitreal ranibizumab. A 13-year-old boy was referred to our department for a sudden decrease in vision in his left eye (LE). Three years before, the patient had been diagnosed with extrafoveal CNV in the right eye (RE) occurring as a complication of bilateral vitelliform macular dystrophy, which had been treated by argon laser photocoagulation. The parents of the young patient signed a comprehensive consent form before proceeding with any examinations or treatments. The subject’s best corrected visual acuity (BCVA) was 20 ⁄32 RE and 20 ⁄ 126 LE. On fundus biomicroscopy, the macula of the LE showed a subfoveal greenish-grey lesion, and a subretinal haemorrhage inferonasal to the fovea associated with a serous detachment, within the egg-yolk lesion area. Fluorescein angiography (FA) in the LE showed blocking hypofluorescence caused by subretinal haemorrhage, and hyperfluorescence resulting from CNV leakage into the subretinal space at the superior border of the fovea (Fig. 1A). Indocyanine green angiography (ICGA) late frames showed focal hyperfluorescence in the area corresponding with the CNV (Fig. 1B). Optical coherence tomography (OCT3; Humphrey-Zeiss, San Leandro, CA, USA) confirmed the presence of a subfoveal CNV, characterized by a moderately reflective mass protruding from the retinal pigment epithelium, associated with neurosensory retina elevation in the macular area (Fig. 1C). After discussing treatment options, including that of intravitreal ranibizumab, the parents of the young patient requested that intravitreal ranibizumab be given. Intravitreal ranibizumab 0.05 ml ⁄ 0.5 mg was administered with no complications. At the 1-month follow-up, BCVA in the LE had improved to 20 ⁄ 40, fundus biomicroscopy revealed resolution of the subretinal haemorrhage, FA and ICGA revealed the CNV closure, and OCT revealed total resolution of the associated serous retinal detachment as a result of the CNV closure. Three months after the injection, BCVA remained at 20 ⁄ 40, with no recurrence as evaluated by fundus biomicroscopy, FA (Fig. 2A), ICGA (Fig. 2B) and OCT (Fig. 2C). Moreover, at the time of writing, 6 months after the injection, we documented the absence of recurrence by high-definition spectral domain OCT (HD-OCT) (OCT 4000 Cirrus; Humphrey-Zeiss) (Fig. 2D–G). In this patient we performed intravitreal ranibizumab because of the subfoveal localization of the CNV. One month after the injection, BCVA had improved to 20 ⁄ 40, and fundus biomicroscopy, FA, ICGA and OCT revealed total regression of the CNV. No subsequent recurrence and no complications from the intravitreal injection of ranibizumab have arisen during follow-up (6 months). A B