A 70-year-old man presented with progressive decrease of vision in right eye (OD) and relative central scotoma of 6 months duration.
No known personal or family history.
Diabetes mellitus type 2, three years of evolution, with good metabolic control, and hypertension in treatment.
The best visual acuity with correction in the initial examination was 4/10 in OD (+; -1.00×95o) and 8/10 in left eye (LE) (+D), -1.50×85o).
Biomicroscopy of the anterior pole was normal.
At the bottom of the eye, there was the presence of a vesicular lesion, elevated in the macular area of the right eye and macular pigmentary alteration in the left eye.
No signs of diabetic retinopathy were found in any of the eyes.
Optical coherence tomography (OCT) showed, in the macular area of the right eye, the presence of a mass of medium reflectivity, above the band of the retinal epithelium, with no evidence of intraretinal fluid.
Fluorescein angiography (FFA) showed the presence of a hyperfluorescent lesion with a center of hypofluorescence, which increased in intensity in late phases but without diffusion of contrast, which would confirm the diagnosis.
Electrophysiological tests, both electroretinogram and electrooculography were normal.
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From that moment on, periodic controls were established, which evidenced the progressive regression of the vitelliform lesion and the evolution towards the macular pigment epithelium in the RE.
Vision in the left eye remained stable (7/10), although macular pigmentary changes were increasingly evident.
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Two and a half years after the first visit, the patient complains of decreased vision in the left eye (2/10), indicating the appearance of a macular detachment in the right eye.
OCT showed an important macular detachment with detachment of the pigment epithelium, intraretinal cysts and presence of subretinal fluid (LSR) at the edges of the lesion.
Median AGF was found to be occult neovascular membrane with delayed dye diffusion.
At this time, it was decided to treat OI with intravitreal ranibizumab at the dose usually used for the treatment of exudative macular degeneration (0.5mg/0.05ml).
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Four weeks after the injection, visual acuity had improved to 3/10 in the left eye, with virtually complete resorption of the macular hemorrhage, and a minimal amount of LSR was observed on tomography.
After 8 weeks, VA was 4/10, and OCT showed a significant decrease in central macular thickness with minimal subretinal fibrosis.
At the 3-month follow-up visit, vision in the left eye had decreased (2/10), and an injection of ranitidine led to an increase in macular thickness greater than 100 micra, with the presence of subretinal fluid.
The response to this second injection was favorable, and at 12 weeks it was possible to verify the complete reabsorption of the subretinal fluid, leaving a minimal subretinal fibrosis as a result of the closure of the neovascular membrane.
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Twelve months after the last injection, visual acuity remained stable in the left eye (6/10), with no signs of membrane reactivation and no complications resulting from intravitreal treatment.
