Subretinal neovascular membranes complicating uveitis: frequency, treatments, and visual outcome.

PURPOSE: Retrospective evaluation in a uveitic population of subretinal neovascular membranes (SRNMs), their occurrence, visual impact, and outcome in differently treated subgroups of patients. METHODS: Medical records of patients were reviewed and cases with SRNM (n = 12) identified. Intraocular inflammation was classified according to vitreous examination records as high (2+ cells), low (1/2+ to 1+ cells), or inactive (0 cells). Visual outcome was considered to be +VA (same or gain of one or more Snellen lines) or -VA (loss of Snellen lines). In nine cases, treatment consisted of the oral administration of high doses of corticosteroids (CST) for one month, tapered down in favorable situations (+VA or SRNM angiographic regression) or maintained at half the dose in unfavorable situations (-VA or SRNM angiographic progression) while additional laser therapies, including photodynamic therapy (PDT), transpupillary thermotherapy (TTT), or argon laser therapy (CLT)), were performed in some of the cases. The above treatment scheme was not applied in three cases (pre-PDT period; undiagnosed underlying uveitis treated without CST). RESULTS: Twelve out of 648 patients (1.9%) with uveitis developed SRNM. The mean visual impact was 4.5 Snellen lines and mean follow-up time was 19.5 months. Two patients with high intraocular inflammation had a favorable visual outcome with CST alone. Eight patients with low intraocular inflammation had a favorable visual outcome with CST alone in three cases, with additional laser therapy in four cases (PDT in 3 cases and TTT in 1 case), and exclusively with PDT in one case (undiagnosed uveitis). Two patients with no intraocular inflammation had unfavorable visual outcome with CST alone (no PDT/TTT available). CONCLUSION: SRNMs occurred as a rare complication of uveitis. Their visual outcome was relatively favorable. Although high doses of CST seem to be the first step in the management of SRNMs, alternative laser treatments should be considered early, especially in cases of absence or low intraocular inflammation.

Massive vascular endothelium growth factor (VEGF) expression in Eales' disease.

BACKGROUND: Eales' disease is an idiopathic retinal vasculitic and vaso-occlusive process complicated by extensive retinal neovascularisation and vitreous hemorrhages. The great propensity to produce retinal neovessels is one of the particular aspects of the disease that deserves to be further investigated. We report a case of Eales' disease having evolved over more than three decades, with a typical clinical presentation in one eye, while the other eye had to be enucleated because of a terminal neovascular glaucoma, thus allowing pathological examination. METHODS: The functional right eye was treated by vitrectomy, cerclage, cryocoagulation and endolaser. The non-functional phthitic left eye was enucleated and submitted for histopathological and immunohistochemical examination using antibodies against vascular endothelial growth factor, T-cells, B-cells and Müller cells. RESULTS: Evolution was favourable in the operated right eye, following management of the inflammatory reaction. The histopathological examination of the left eye revealed an occlusion of the anterior chamber angle by rubeosis iridis, tractional retinal detachments, pre-, intra- and sub-retinal neovascular membranes, and vitrous hemorrhages. Diffuse positive anti-VEGF immunostaining was found at the level of the retinal neovascular membranes. The retina exhibited prominent Müller cell immunostaining, indicating extensive gliosis, and predominantly B cell infiltrates were found in the eye. CONCLUSION: The present study indicates a close relationship between the prominent neovascular proliferation in Eales' disease and the intense expression of VEGF. The increased expression of VEGF, when compared to other conditions inducing neovascularisation, might explain the severity of neovascular growth and the propensity of repeated vitrous hemorrhages in Eales' disease.