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Background:The aim of our study was to evaluate the functional and anatomic outcomes of intravitreal ranibizumab for the treatment of symptomatic drusenoid pigment epithelial detachment without choroidal neovascularization in age-related macular degeneration.Methods:This was a prospective, single-center, uncontrolled, interventional pilot study. Six consecutive eyes (six patients) with drusenoid pigment epithelial detachment with a visual acuity of 20/63 to 20/100 and no evidence of choroidal neovascularization in age-related macular degeneration participated. Patients were given at least one intravitreal ranibizumab injection and were followed for a mean of 66.67 ± 10.3 weeks. Main outcome measures included best-corrected visual acuity (BCVA) measured by Early Treatment Diabetic Retinopathy Study charts and optical coherence tomography, and central macular thickness measured by optical coherence tomography.Results:The mean number of intravitreal ranibizumab injections was 3.0 at the end of follow-up. Regarding BCVA and optical coherence tomography, 33.3% of eyes gained between 19 and 21 letters of BCVA, with a median decrease in central macular thickness of 21 μm. There was a statistically significant difference between baseline and final BCVA (P = 0.046). There was a positive correlation between intraretinal fluid by optical coherence tomography and improved BCVA after intravitreal ranibizumab. Metamorphopsia disappeared completely after the first injection in all subjects, with no further recurrences. No patient developed choroidal neovascularization or atrophic changes.Conclusion:Intravitreal ranibizumab demonstrated anatomic and functional benefit in patients with symptomatic drusenoid pigment epithelial detachment without choroidal neovascularization in age-related macular degeneration. Further long-term, randomized, controlled trials should be performed to confirm our preliminary results.

Health Organization (WHO) grades I to III according to the histological appearance. Distant metastasis are exceptional in grade I but account for 10% of grade II and for 71% of grade III chondrosarcoma; these occurs in the lung, femur, sternum, liver, pleura and ureter. The presence of metastasis is associated with a 5-year survival rate of 18%. Heart and brain metastasis are exceptionally rare and scarcely documented [1]. Herein we report a case of chest-wall chondrosarcoma with metastasis to the lung, brain, and choroid.A 53-year-old female was referred to the department of ophthalmology because of progressive visual loss in her right eye (OD) for the 2 previous months. Her past medical history was significant for a rib chondrosarcoma grade II treated with excisional surgery 10 years before, and a recent mestastasic lesion in the right lung tissue which was being treated with chemotherapy using adriamycin.Her best-corrected visual acuity was 20/60 in the OD and 20/25 in the left eye. Fundus examination revealed an elevated yellowish choroidal lesion within the macular area in her OD (Fig. 1a). The left eye was unremarkable. In the OCT we observed a serous detachment with a swelling of macula (Fig. 1b). Fluorescence angiography was performed, revealing early hypofluorescence with late pinpoint hyperfluorescence (Fig. 1c 1-3 ).Standardized B-scan ultrasonography of the OD demonstrated a plateau-shaped choroidal mass of 8 ×3 mm (Fig. 2a). Cerebral magnetic resonance imaging showed metastatic lesions in the right cerebellum hemisphere and the OD choroid (Fig. 2b). Fine needle aspiration biopsy and photodynamic therapy was refused by the patient, who was lost to follow-up.Metastasic cells reach the eye exclusively by the hematogenous route, since there are no intraocular lymphatic channels. The most frequently affected ocular tissue is the choroid, which has the highest metastatic efficiency index of any tissue [2], because of its marked vascularization and its high blood flow. We are unaware of previously reported cases of chondrosarcoma metastatic to the choroid in the indexed literature [3]. This case report has not been presented at any conference.

These results suggest that ApoE knockout mice have changes in ON morphology and myelination.

The morphologic and morphometric results suggest that homozygous P27(Kip1) knock-out mice had hypertrophic, hyperplastic, and dystrophic ON.