Pneumatic vitreolysis with C3F8 gas is effective in releasing focal vitreomacular traction in a high percentage of eyes with few adverse events, especially with limited vitreomacular traction (within 1 disk area), lack of thick cellophane membranes, no diabetes mellitus, younger age (mean age of 69.1 years vs. 78.1 years), better baseline best spectacle–corrected visual acuity (mean of 20/50 vs. 20/66), small Stage 2 macular hole, and female gender.

Cytotoxic T-lymphocyte-associated antigen (CTLA-4) is a naturally occurring inhibitor of T-cell costimulation. Monoclonal antibody inhibition of CTLA-4 with ipilimumab blocks this negative regulator of costimulation, promoting T-cell activation and survival, and leads to melanoma regression. Findings of the Vogt-Koyanagi-Harada syndrome, an uveomeningitic syndrome that features neurologic, auditory, ophthalmologic, and cutaneous involvement due to autoimmune targeting of melanocytic antigen, have rarely been described in association with melanoma immunotherapy. We describe a case of Vogt-Koyanagi-Harada (VKH)-like syndrome in a 45-year-old HLA-A02-positive patient with metastatic melanoma treated with ipilimumab. Disruption of immune tolerance by ipilimumab led to melanoma remission while also inciting systemic and ophthalmic autoimmunity towards melanocytic antigen. These observations provide insight into the pathophysiology of the VKH syndrome, as well as the balance between tumor-associated tolerance and autoimmunity.

Background: Age-related macular degeneration (AMD), a leading cause of irreversible vision impairment in the United States and globally, is a disease of the photoreceptor support system involving the retinal pigment epithelium (RPE), Bruch's membrane, and the choriocapillaris in the setting of characteristic extracellular deposits between outer retinal cells and their blood supply. Research has clearly documented the selective vulnerability of rod photoreceptors and rod-mediated (scotopic) vision in early AMD, including delayed rod-mediated dark adaptation (RMDA) and impaired rod-mediated light and pattern sensitivity. The unifying hypothesis of the Alabama Study on Early Macular Degeneration (ALSTAR2) is that early AMD is a disease of micronutrient deficiency and vascular insufficiency, due to detectable structural changes in the retinoid re-supply route from the choriocapillaris to the photoreceptors. Functionally this is manifest as delayed rod-mediated dark adaptation and eventually as rod-mediated visual dysfunction in general. Methods: A cohort of 480 older adults either in normal macular health or with early AMD will be enrolled and followed for 3 years to examine cross-sectional and longitudinal associations between structural and functional characteristics of AMD. Using spectral domain optical coherence tomography, the association between (1) subretinal drusenoid deposits and drusen, (2) RPE cell bodies, and (3) the choriocapillaris' vascular density and rodand cone-mediated vision will be examined. An accurate map and timeline of structure-function relationships in aging and early AMD gained from ALSTAR2, especially the critical transition from aging to disease, will identify major characteristics relevant to future treatments and preventative measures.