Autoimmune retinopathy (AIR) is a rare and still poorly understood immune-mediated disease that may cause inflammation from circulating autoantibodies against the retina. It may be related to history of autoimmune disease in the patient or in a family member or the presence of neoplastic disease in the individual. The disease may be subdivided into paraneoplastic and non-paraneoplastic AIR. When related to melanoma, it is referred to as MAR, and when related to other cancers, it is called CAR. The exact prevalence of AIR is unknown. It mainly affects older adults. Patients present with bilateral and asymmetric scotomas, photopsias, visual field defects, with rapidly progressive visual loss in late onset. In the initial stage, fundus examination is unremarkable, and in late stages, there is limited retinal epitheliopathy and vascular attenuation, with or without optic disc pallor, associated or not with intraocular inflammation and with no evidence of degenerative retinal disease. A clinical investigation with detailed anamnesis and laboratory tests should be performed to search for an associated neoplasm. Ophthalmologic and complementary examinations such as full-field electroretinogram, optical coherence tomography, visual field and fundus autofluorescence, help the diagnosis. Blood tests to search for autoantibodies should be requested. Management consists of prolonged immunosuppression, which may be combined with antioxidant vitamins. In general, the prognosis is uncertain, so the disease still needs to be better understood. More studies should be performed to improve diagnostic measures and define specific management that could preserve or even restore vision.

Patients with VKH and long-standing disease had thinner choroids when compared to controls. Progressive choroidal thinning related to disease duration was observed at the macula of these patients. Whether this finding is part of the natural history of the disease or the result of a clinically undetected choroidal inflammation remains to be determined.

Objective: To evaluate a technique of autologous internal limiting membrane (ILM) fragment transplantation for the treatment of large, chronic, and/or refractory macular holes (MH). Design: This was a 6-month prospective interventional case series. Method: Ten eyes of 10 patients with MH underwent pars plana vitretomy (PPV) and ILM peeling followed by transplantation of an autologous ILM fragment to the MH. Six patients had primary MH with an internal diameter greater than 500 µm and a duration of more than 18 months, including 1 patient with nonproliferative diabetic retinopathy previously treated with panretinal photocoagulation. Four eyes with MH had previously been submitted to PPV (i.e. 1 for retinal detachment and 3 to attempt to close large MH). One of the latter also displayed juxtapapillary choroidal neovascularization due to age-related macular degeneration. The primary and secondary outcomes were MH closure and improvement of the best corrected visual acuity (BCVA), respectively. Results: Complete MH closure was achieved in all cases. A statistically significant improvement in the average BCVA was observed after 6 months of follow-up (p = 0.018; paired t test). The BCVA improved in 8 eyes (80%), and in 6 of those eyes it improved by ≥15 letters. In 1 patient, the BCVA remained unchanged after the surgery, but the visual field reportedly improved. One patient experienced a slight worsening (0.16 logMAR). Two cases developed atrophy of the retinal pigment epithelium despite MH closure and BCVA improvement. Conclusion: Treatment with autologous ILM fragment transplantation seems to be an efficient alternative for large, chronic, and refractory MH.

Diabetes mellitus (DM) is a highly prevalent complex genetic disorder. There has been a worldwide effort in the identification of susceptibility genes for DM and its complications, and the 5-10-methylenetetrahydrofolate reductase (MTHFR) and apolipoprotein-E (APOE) genes have been considered good candidate susceptibility genes to this condition. The objectives of the present study were to determine if the 677T MTHFR and ε2/ε3/ε4 APOE alleles are risk factors for DM and for severity of diabetic retinopathy (DR). A total of 248 individuals were studied: 107 healthy individuals and 141 diabetic patients (46 with type 1 diabetes and 95 with type 2 diabetes), who also had DR (81 with non-proliferative DR and 60 with proliferative DR). The polymorphisms were analyzed by PCR followed by digestion with restriction enzyme or the single-nucleotide primer extension method. No evidence of association between the 677TT genotype of MTHFR gene and DM [cases: TT = 10/95 (10.6%); controls: TT = 14/107 (13%)] or with severity of DR was observed [cases: TT = 5/60 (8.5%); controls: TT = 9/81 (11.1%); P > 0.05]. We also did not find evidence of an association between APOE alleles and proliferative DR (ε2, ε3 and ε4 in cases: 9, 76, and 15%, and in controls: 5, 88, and 12%, respectively) but the carriers of ε2 allele were more frequent among patients with type 2 DM and DR than in controls [cases: 15/95 (15.8%); controls: 7/ 107 (6.5%); P < 0.05]. Therefore, our results suggest that the ε2 allele/ APOE might be a risk factor for diabetes in the Brazilian population.

Escalating doses of intravitreous adalimumab in rabbit eyes caused no detectable functional or structural ocular toxicity up to a dose of 0.50 mg. Administration of 1.0 mg in 0.1 ml was associated with an inflammatory reaction and retinal necrosis.