Purpose To evaluate 6-and 9-month follow-up data including the effect on vision and anatomic outcome in patients treated with intravitreal bevacizumab for neovascular age-related macular degeneration (AMD). Study design Interventional consecutive retrospective case series. Patients received intravitreal bevacizumab for the treatment of neovascular AMD including choroidal neovascular membranes, pigment epithelial detachment, and macular haemorrhage. Ophthalmic evaluation included log MAR or Snellen acuity, ophthalmic examination, optical coherence tomography, and fluorescein angiography. Repeat injections were given in the presence of persistent leakage or retinal oedema. Change in vision and foveal thickness from baseline was evaluated using the paired Student's t-test.

Ophthalmic assessments of 120 patients with homozygous sickle cell (SS) disease and of 222 with sickle cell haemoglobin-C (SC) disease were conducted over a period of ten years. Visual acuity loss (V.A. less than or equal to 6/18) attributable to sickle cell retinopathy occurred in 10% of untreated eyes during a mean observation period of 6.9 years. Visual loss was strongly associated with proliferative sickle retinopathy (p less than 0.001) and most commonly resulted from vitreous haemorrhage, tractional retinal detachment and epiretinal membranes. The incidence of visual loss was 31 per 1000 eye-years observation among eyes with proliferative disease compared to 1.4 per 1000 eye-years observation among eyes with non-proliferative disease.

Background/aims-Sympathetic ophthalmia (SO) is a classic example of autoimmune disease where human leucocyte antigen (HLA) genomic associations could provide further understanding of mechanisms of disease. This study sought to assess HLA genetic polymorphism in British and Irish patients with SO, and to assess whether HLA gene variants are associated with clinical phenotype or disease severity. Methods-High resolution DNA based HLA typing using polymerase chain reaction sequence specific primers was performed in 27 patients with SO and 51 matched healthy controls. Clinical phenotype and markers of disease severity were determined prospectively in 17 newly diagnosed patients and from medical record review and repeat clinical examination in 10 previously diagnosed patients. Results-HLA-Cw*03 (p=0.008), DRB1*04 (p=0.017), and DQA1*03 (p=0.014) were significantly associated with SO. For class II alleles at higher resolution, only HLA-DRB1*0404 (relative risk (RR) = 5.6, p = 0.045) was significantly associated with SO. The highest relative risk for any of the associated haplotypes was with HLA-DRB1*0404-DQA1*0301 (RR=10.9, p=0.019). Patients with the DRB1*04-DQA1*03 associated haplotype were significantly more likely to develop SO earlier, with fewer inciting ocular trauma events, and to require more systemic steroid therapy to control inflammatory activity. Conclusions-Sympathetic ophthalmia is associated with HLA-DRB1*04 and DQA1*03 genotypes in white patients, similar to Japanese patients. DiVerences in DRB1*04 gene variant associations (−0404 in Britain and Ireland and −0405 in Japan) may have implications for HLA peptide binding in disease initiation. The DRB1*04-DQA1*03 haplotype is a marker of increased SO susceptibility and severity, as in Vogt-Koyanagi-Harada disease, which also has similar clinicopathological and HLA associations. (Br J Ophthalmol 2001;85:281-286)

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