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HF Fine, ME Wright, KG Csaky, H Masur, MA Polis, MR Robinson; Peripheral Choroidal Neovascularization as a Late Finding in HIV-infected Patients with Inactive Cytomegalovirus Retinitis and Ocular Inflammation from Immune Recovery Uveitis . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2208.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: The natural history of cytomegalovirus (CMV) retinitis is marked by retinal necrosis and the formation of atrophic scar tissue. Highly active anti-retroviral therapy in HIV-infected patients with CMV retinitis may obviate the need for lifelong anti-CMV therapy, but may also be associated with vision-threatening immune recovery uveitis (IRU). IRU is characterized by cataract, vitritis, optic disc and macular edema, and epiretinal membrane formation. We report an observation not previously described in patients with IRU: the development of choroidal neovascularization (CNV) in areas of atrophic retina. Methods: We followed 16 HIV-infected patients who discontinued specific anti-CMV therapy in a 4.5-year prospective observational study. Patients received frequent complete eye examinations with fluorescein angiography (FA). Those with evidence of CNV underwent high-speed indocyanine green angiography (ICG) and optical coherence tomography (OCT) when possible. Results: Three of 16 patients with bilateral inactive CMV retinitis developed CNV: 2 patients had CNV in 1 eye, 1 patient in both eyes. The mean times to development of CNV from CMV diagnosis and from study enrollment were 73 months and 46 months, respectively. All 3 patients had IRU with a low-grade vitritis and diffuse macular edema in both eyes. The CNV was characterized by a fibrovascular proliferation which overlaid atrophic retina in all 3 cases, was hyperfluorescent by FA, and ranged in size from 3-10 disc areas. OCT performed in 2 eyes of 2 patients showed the fibrovascular membranes to be firmly attached to the underlying choroid. ICG performed in 2 eyes of 2 patients demonstrated an afferent feeder vessel emanating from the choroid into the lesion. One patient (1 eye) had vitreous traction to the fibrovascular lesion and experienced repeated vitreous hemorrhages with vision loss over a 2-year period. A pars plana vitrectomy with direct endophotocoagulation to the lesion was successful in eliminating the vitreous hemorrhages. Slow growth of the membranes in the other 2 patients (3 eyes with CNV) was apparent, but no hemorrhage occurred. Conclusion: Peripheral CNV is a late finding in patients with IRU. Recognition of CNV associated with atrophic CMV scars in persons with IRU is important because of the potential for vitreous hemorrhage and vision loss.
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