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Objective: To evaluate CD4+ Foxp3+ (forkhead box P3) T-regulatory cell populations in patients with uveitis and to determine if T-regulatory cell populations are associated with disease features. Methods: Patients with uveitis were evaluated for CD4+ Foxp3+ T-regulatory cells by flow cytometry. Systemic and ocular diagnoses, disease activity, and the presence of cystoid macular edema were reviewed. Percentages of CD4+ Foxp3+ lymphocytes were compared for patients with inactive vs active disease, systemic vs ocular diagnoses, and the presence or absence of cystoid macular edema. Real-time polymerase chain reaction testing was performed on 2 patients with extremely low CD4+ Foxp3+ cell populations to assess Foxp3 mRNA. Results: A total of 20 patients with intermediate uveitis, posterior uveitis, and panuveitis were evaluated. The mean age was 40.6 years and the mean visual acuity was 20/57. Percentages of CD4+ Foxp3+ cells were lower in patients with active compared with inactive uveitis (P.05). No differences in T-regulatory cells were observed between the other subgroups. Two patients with recalcitrant uveitis who demonstrated less than 1% CD4+ Foxp3+ lymphocytes showed extremely low or absent Foxp3 mRNA. Conclusion: T-regulatory cells are reduced in patients with active compared with inactive disease. Severe depletion of CD4+ Foxp3+ T cells and Foxp3 mRNA in 2 patients with severe uveitis suggests that loss of the T-regulatory cells of uveitis may be a salient feature in certain patients. [ABSTRACT FROM AUTHOR]

Objective: To characterize foveal atrophy in a heterogeneous group of patients with uveitis using clinical findings and high-definition (HD) optical coherence tomography (OCT). Design: Cross-sectional, retrospective case series. Results: The HD-OCT scans of 140 patients seen in a tertiary referral center were reviewed and 23 patients (33 eyes) with foveal atrophy were identified. All of the patients with foveal atrophy were diagnosed with intermediate uveitis, posterior uveitis, or panuveitis. The status of the photoreceptor layer as visualized with HD-OCT was associated with significant differences in mean visual acuity (P.001). Clinical findings associated with foveal atrophy included atrophy of the retinal pigment epithelium and choroid (30 eyes [91%]),macular ischemia (13 eyes [39%]), cystoid macular edema (5 eyes [15%]), choroidal neovascularization (4 eyes [12%]), retinal detachment involving themacula (2 eyes [6%]), and serum antiretinal antibodies (2 eyes [6%]). Conclusions: Foveal atrophy can be a complication of intraocular inflammation in a variety of uveitic syndromes. The cause of foveal atrophy is multifactorial and may include dysfunction and atrophy of the retinal pigment epithelium and choroid, cystoid macular edema, macular ischemia secondary to occlusive retinal vasculitis, choroidal neovascularization, retinal detachment, and possibly antibody-mediated damage directed against photoreceptors. Careful observation of the photoreceptor layer using HD-OCT may help to identify patients who are at risk for visual loss secondary to foveal atrophy. [ABSTRACT FROM AUTHOR]

Objectives: To describe the features, natural history, and management of an unusual manifestation of ocular von Hippel-Lindau disease in the form of fine vascular proliferation. Methods: Case series of 14 patients with definite or presumed von Hippel-Lindau disease. Results: Retinal vascular proliferation consisting of fine superficial vessels was found in 16 eyes of 14 patients with von Hippel-Lindau disease. The lesion was often found in a juxtapapillary location and associated with a fibrovascular component and/or a macular epiretinal membrane. In cases with follow-up (12 patients; mean [SD] follow-up, 10.9 [7.5] years), the lesion was stable in 7 of 13 eyes but showed growth and progression resulting in vision loss in the remainder. In 5 eyes, surgical intervention with pars plana vitrectomy, membrane peel, and excision of the fibrovascular lesion resulted in visual improvement in all of the cases. Conclusions: Ocular von Hippel-Lindau disease can uncommonly manifest as vascular proliferation that consists of fine, superficial, juxtapapillary vessels that are often associated with fibrovascular proliferation and epiretinal membrane formation. The natural history of this lesion is variable and can result in vision loss from tractional effects in progressive cases. Vision-threatening cases may be successfully managed by surgical excision. [ABSTRACT FROM AUTHOR]