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1/5. Subretinal fibrosis and choroidal neovascularization in Vogt-Koyanagi-Harada syndrome.

    BACKGROUND: To describe clinical findings of subretinal fibrosis and choroidal neovascularization in patients with Vogt-Koyanagi-Harada (VKH) syndrome. methods: We retrospectively reviewed 75 medical records of patients with VKH seen at the National eye Institute, Bethesda, maryland between 1978 and 1996. Recorded data included age, gender, race, duration of disease, extraocular manifestations, best-corrected visual acuity, slit-lamp biomicroscopy, retinal examination, retinal photographs and fluorescein angiograms. We sought features that correlated with the visual outcome. RESULTS: Thirty of 75 (40%) patients developed subretinal fibrosis. Eleven patients (14.7%) had choroidal neovascularization. Presence of subretinal fibrosis was associated with a longer duration of the disease (42.6 vs 19.1 months, P = 0.07). patients with subretinal fibrosis had worse visual acuity than those without subretinal fibrosis (26.2 vs 57.3 ETDRS letters read, P < 0.001) after adjusting for duration of disease (P = 0.021), degree of vitreous haze (P = 0.074), and use of immunosuppressive therapy (P = 0.008). CONCLUSIONS: Presence of subretinal fibrosis in patients with VKH is associated with a poor visual prognosis. The diagnosis of choroidal neovascularization and subretinal fibrosis presents a challenge in the management of this disease.
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ranking = 1
keywords = neovascularization
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2/5. Photodynamic therapy with verteporfin for subfoveal choroidal neovascularization in Vogt-Koyanagi-Harada syndrome.

    PURPOSE: To assess the role of photodynamic therapy using verteporfin in the treatment of subfoveal choroidal neovascularization in Vogt-Koyanagi-Harada syndrome. DESIGN: Interventional case report. methods: A 9-year-old patient with subfoveal choroidal neovascularization received a single photodynamic therapy with verteporfin session (one eye) and was prospectively followed with fluorescein angiography. RESULTS: A complete regression of the lesion was achieved within 1 week after treatment. visual acuity improved from 20/800 to 20/320 by 6 months of follow-up. fluorescein angiography disclosed unexpected retinal pigment epithelium alteration within the treatment area. CONCLUSION: Although regression of the choroidal neovascularization occurred, unpredicted findings involving normal retina in the vicinity of the lesion suggest that further studies are required to assess the clinical value of this treatment for subfoveal choroidal neovascularization in Vogt-Koyanagi-Harada syndrome.
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ranking = 1.1428571428571
keywords = neovascularization
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3/5. Formation of pseudodiscs in chronic recurrent Vogt-Koyanagi-Harada syndrome.

    We report an unusual form of chorioretinal anastomosis in a 20-year-old man with chronic recurrent Vogt-Koyanagi-Harada syndrome. Several subretinal optic disc-like lesions of subretinal fibrosis were found in the vicinity of the equator. No evidence of neovascularization or arteriovenous shunt was noted.
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ranking = 0.14285714285714
keywords = neovascularization
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4/5. choroidal neovascularization in long-standing case of Vogt-Koyanagi-Harada disease.

    The eyes in a case of Vogt-Koyanagi-Harada disease (VKH) with long-standing uveitis for 26 years after the onset were studied histopathologically. It was found that typical granulomatous inflammation was persistent in the uveal tract and the choroidal neovascularization occurred in the peripheral fundus accompanied by proliferation of the retinal pigment epithelial cells (RPE). Some of the new vessels under the pigment epithelium extended into the vitreous. It was concluded that the ocular inflammation of VKH was essentially granulomatous even in this long-standing case. Disappearance of choroidal melanocytes, existence of epithelioid cells containing pigment granules, and accumulation of lymphocytes and plasma cells in the lesion indicated that the inflammation was an autoimmune reaction against uveal melanocytes, although the trigger initiating the disease remains unknown. It was further concluded that the peripheral fundus as well as the peripapillary and macular areas was a predilected site for choroidal neovascularization in chronic uveitis. The choroidal neovascularization may develop in such a way that the uveal inflammation damages the Bruch's membrane and choriocapillaris and consequently causes retinal ischemia, thus stimulating the endothelium of the choriocapillaris and the overlying RPE to proliferate. There is a close relation between choroidal neovascularization and proliferation of RPE. choroidal neovascularization may cause reactive proliferation of the RPE and vice versa.
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ranking = 1.2857142857143
keywords = neovascularization
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5/5. Subretinal neovascularization in the Vogt-Koyanagi-Harada syndrome.

    Two Hispanic patients with Vogt-Koyanagi-Harada (VKH) syndrome each developed a disciform lesion involving the macula of one eye several months after the onset of symptoms. Each had extraocular manifestations which included pleocytosis of the cerebrospinal fluid. The disciform lesions were associated with retinochoroidal anastomoses, a finding not previously reported in VKH syndrome. Each patient had a separate extramacular disciform lesion in the same eye. Two other Hispanic patients with diffuse bilateral intraocular inflammation had ocular findings consistent with VKH syndrome. One of these patients developed bilateral peripapillary disciform lesions and the other developed a disciform macular scar in one eye. fluorescein angiography in each patient showed early irregular hyperfluorescence with late intense staining. The disciform detachments occurred in areas of reactive proliferation of the retinal pigment epithelium, and we postulate that growth of subretinal new vessels occurred through areas of Bruch's membrane that were damaged by the inflammation.
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ranking = 0.57142857142857
keywords = neovascularization
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