Long-term real-world outcomes in retinal vein occlusions: How close are we to the trials?

Purpose:To assess and analyze the visual outcomes of patients with retinal vein occlusions in a real-world setting with a long-term follow-up of more than 5 years.Methods:Retrospective analysis of 56 patients having retinal vein occlusions from a tertiary eye center, with a mean follow-up of 7 years was performed. Primary outcome measures were mean change in best-corrected visual acuity (BCVA) from baseline at 6 months, 1 year, 2 years, 3 years, and final visit (≥5 years), proportion of patients having BCVA better than 20/40 and worse than 20/200, and mean number of injections. Secondary outcome measures were change in central macular thickness (CMT), development of subsequent retinal vein occlusion (RVO) in same eye or the other eye, and development of neovascular complications.Results:The mean change in letter score was + 11.84 in branch RVO (BRVO), +7.14 in non-ischemic central RVO (CRVO), and −9.5 in ischemic CRVO at 1 year, which changed to + 8.57, −5 and − 24, respectively, at the end of follow-up. CMT had improved from 506 ± 98.8 µm, 576.44 ± 149 µm, and 618 ± 178.27 µm, respectively, at baseline to 267 ± 94 µm, 345.20 ± 122.61 µm, and 265.50 ± 107.75 µm, respectively, in BRVO, non-ischemic, and ischemic hemi RVO (HRVO)/CRVO groups. The total mean number of injections given in BRVO, non-ischemic CRVO, and ischemic CRVO groups were 4.6, 6.6, and 4.1, respectively. None of the patients with BRVO developed neovascular glaucoma (NVG). Non-ischemic to ischemic HRVO/CRVO conversion was noted in 4/11 eyes at a mean duration of 12.6 months. NVG was noted in 7/9 eyes (77.8%) in initial ischemic CRVO/HRVO group and 3/4 (75%) converted eyes.Conclusion:Patients with BRVO have good visual outcomes with anti-VEGF, while in CRVO results may vary considerably owing to patient compliance and treatment burden on long-term follow-up in a real-world setting.     

How strong is the relationship between glaucoma,the retinal nerve fibre layer,and neurodegenerative diseases such as Alzheimer's disease and multiple sclerosis?

Glaucoma is a neurodegenerative disorder with established relationships with ocular structures such as the retinal nerve fibre layer (RNFL) and the ganglion cell layer (GCL). Ocular imaging techniques such as optical coherence tomography (OCT) allow for quantitative measurement of these structures. OCT has been used in the monitoring of glaucoma, as well as investigating other neurodegenerative conditions such as Alzheimer''s disease (AD) and multiple sclerosis (MS). In this review, we highlight the association between these disorders and ocular structures (RNFL and GCL), examining their usefulness as biomarkers of neurodegeneration. The average RNFL thickness loss in patients with AD is 11 μm, and 7 μm in MS patients. Most of the studies investigating these changes are cross-sectional. Further longitudinal studies are required to assess sensitivity and specificity of these potential ocular biomarkers to neurodegenerative disease progression.     

Screening and treating amblyopia: are we making a difference?

PURPOSE: To determine the rate of amblyopia in native Jewish Israelis compared with those who immigrated from the former Soviet Union (U.S.S.R.) after they were 10 years of age. METHODS: Health records of all 16-year-old subjects examined in the Israel Defense Forces Recruitment Center between 1998 and 2003 were analyzed. The number of subjects with best corrected visual acuity (BCVA) of 6/12 or less in at least one eye among native Israelis and among those who immigrated to Israel from the U.S.S.R. after they were 10 years of age was determined. Subjects who had any ocular disease except cataract, corneal opacity, strabismus, or ptosis were excluded. RESULTS: Of 305,712 subjects examined between 1998 and 2003, 292,255 were enrolled in the study. Of those, 260,186 (89%) were born in Israel and 32,069 (11%) were born in the U.S.S.R. and immigrated to Israel after they were 10 years of age. There were 2565 (0.98%) native Israelis and 483 (1.5%) immigrants who had BCVA of 6/12 or less in at least one eye (chi(2) test, P < 0.00001). The rate of amblyopia among subjects who had refractive errors was 14.6% among immigrants, as opposed to 8.0% among native Israelis (P < 0.0001), whereas amblyopia rates among those with strabismus, cataract, or ptosis were similar in native Israelis and immigrants (34.4%, 38.6%, 12.8% as opposed to 34%, 37.5%, 15.4%, respectively, P = 0.5-0.61). CONCLUSIONS: The difference in the rate of refractive amblyopia as opposed to strabismic and deprivation amblyopia may be due to the difference in vision screening methods between both countries.     

Glaucoma genetics: where are we? Where will we go?

The understanding of the genetic basis of the glaucomas has advanced rapidly. Mutations in the myocilin gene (previously known as TIGR) at the GLC1A locus on chromosome 1q21-q31 occur in a subset of patients with juvenile- and adult-onset primary open-angle glaucoma. Five other genetic localizations for primary open-angle glaucoma have now been reported. In patients with primary congenital glaucoma, mutations have been found in the CYP1B1 gene on chromosome 2p21. At least one other locus for primary congenital glaucoma is mapped. In the developmental glaucomas, mutations in the PITX2 gene on chromosome 4q25 have been associated with Rieger syndrome, iris hypoplasia, and iridogoniodysgenesis. A second locus for Rieger syndrome resides on chromosome 13q14. Mutations in the FKHL7 gene on chromosome 6p25 have been described in patients with Axenfeld-Rieger anomaly. A new ocular finding of glaucoma in pedigrees with the nailpatella syndrome has been described, and mutations in the LMX1B gene on chromosome 9q34 are now known to underlie nail-patella syndrome. Two loci for the pigment dispersion syndrome have been mapped. This paper provides an overview of recent literature, summarizes developments in glaucoma genetics, and addresses their potential relevance to the clinical management of glaucoma.     

A decade of age-related macular degeneration risk models: What have we learned from them and where are we going?

The genomic revolution has revealed the complexity of multifactorial diseases, making the development of effective diagnostics extremely challenging. In turn, the prospect of precision medicine as applied through targeted therapeutic treatments continues to remain largely elusive. Age-related macular degeneration (AMD) as a complex disease falls under this category, despite it being one of the most well characterized multifactorial diseases. This reflects both the extent of identified genetic components and known environmental risk factors. Additional considerations in dissecting out the roles played by genetic and non-genetic risk factors arise through the rapid increase in prevalence of AMD with age and the varying time periods over which disease progression can occur, complicating efforts to discriminate between “progressors” and non-“progressors.” As a consequence, extensive research into the aetiology of AMD is yet to realize a clinically acceptable predictive test. This review covers the current climate of risk models in late AMD but will focus mainly on genetic risk factors as well as the types of models that have currently been employed in the AMD modelling literature.     

Pathologic myopia: where are we now?

PURPOSE: To describe current concepts and available treatments for pathologic myopia. DESIGN: Review of experimental and clinical studies. METHODS: The demography, natural history, medical and surgical treatments for choroidal neovascular membrane, vitreoretinal interface disorders and future strategies for pathologic myopia are reviewed. RESULTS: Several medical and surgical modalities are currently available to treat various complications of pathologic myopia. Macular translocation appears to stabilize or improve visual function in many eyes with choroidal neovascularization. CONCLUSION: Newer strategies are emerging to better ameliorate or prevent the complications of pathologic myopia.