Findings From the 15-Year Follow-up of an Australian Cohort
Early age-related macular degeneration (AMD) is characterized by the presence of drusen and retinal pigmentary abnormalities.1,2 Drusen vary in size (diameter range, ≤63 to ≥250 μm) and type (hard, soft, distinct, and indistinct). Pigmentary abnormalities include clusters of pigment granules within the sensory retina (increased pigmentation) and sharply demarcated areas of retinal pigment epithelium (RPE) depigmentation.
The international classification and grading system for AMD categorizes medium drusen as intermediate soft drusen, defined as drusen with a maximum diameter of 63 to less than 125 μm, larger than the maximum diameter of hard drusen (‹63 μm) but smaller than the minimum diameter of large soft drusen (≥ 125 μm).1 A similar definition of this drusen type was used by the Age-Related Eye Disease Study2 and clinical classification system,3 categorized as medium drusen. urthermore, the Wisconsin Age-Related Maculopathy Grading System4 defines medium drusen by the maximum diameter, although the categorization of medium drusen is not used. In this study, we describe this type of drusen as medium drusen.
Despite recent interest in medium drusen and their inclusion in AMD incidence studies,5,6 knowledge of the associated risk factors and the progression of medium drusen is limited. Medium drusen have been underrepresented in studies3,7-9 compared with large drusen, soft drusen, and pigmentary lesions. In this study, we aimed to assess the 15-year incidence and progression of medium drusen in an older Australian cohort, as well as associations between common AMD risk factors and the development and progression of medium drusen.
Full Paper: Incidence, Progression, and Associated Risk Factors of Medium Drusen in Age-Related Macular Degeneration
The role of the vitreomacular interface (VMI) in the pathophysiologic features and treatment of neovascular age-related macular degeneration (AMD) has generated much recent interest. In retrospective and prospective observational case series, a higher prevalence of vitreomacular adhesion (VMA) has been reported in eyes with neovascular AMD compared with eyes with nonneovascular AMD.1-3 In a paired eye study, VMA was observed more frequently in eyes with neovascular AMD compared with the fellow nonneovascular AMD eye that served as a control.4 Some investigators also have observed that VMA occurs at the vitreoretinal interface overlying the choroidal neovascularization (CNV).1,2,4 Vitreomacular adhesion also influences treatment and outcomes in neovascular AMD; the absence of VMA has been associated with slightly better visual acuity (VA),5,6 and eyes with VMA may require more frequent dosing compared with neovascular AMD eyes without VMA.5,6 This combined body of evidence suggests thatVMA may have a role in the pathogenesis and management of CNV.
The purpose of our study was to assess the relationship of the VMI to treatment frequency in neovascular AMD, as well as to VA and anatomic outcomes in the Comparison of AMD Treatments Trials (CATT),7 one of the largest prospective treatment trials for neovascular AMD conducted to date.
Full Paper: Influence of the Vitreomacular Interface on Treatment Outcomes in the Comparison of Age-Related Macular Degeneration Treatments Trials
AGE-RELATED MACULAR DEGENERATION (AMD) IS the leading cause of late-onset visual impairment and blindness in persons over 65 years of age.1,2 Age-related macular degeneration is staged as early, intermediate, or late. Small drusen are the hallmark of earlystage AMD; intermediate-stage AMD consists of extensive medium-size drusen or any large drusen, with or without pigment changes. Late-stage AMD is defined by either choroidal neovascularization or geographic atrophy.3–6 In the United States, it is estimated that ~1.2 million persons have neovascular AMD; 970,000 have geographic atrophy; and 8 million have intermediate-stage AMD.1
Antiretroviral-treated, immune-restored, human immunodeficiency virus (HIV)-infected persons have a marked reduction in opportunistic infections and a substantially increased lifespan compared to those from the era before modern combination antiretroviral therapy.7–10 However, despite the improved immune function and increased lifespan, antiretroviral therapy does not fully restore health. Compared to similarly-aged, non-HIV-infected peers, antiretroviral-treated, immune-restored, HIV-infected persons have a substantially shortened lifespan, largely owing to an increased risk of non–acquired immunodeficiency syndrome (AIDS) diseases associated with aging.11–14 These diseases include cardiovascular disease, non-AIDS cancers, metabolic diseases, and neurocognitive decline, and collectively suggest that antiretroviral-treated, immune-restored HIV infection is associated with an “accelerated/accentuated aging” phenotype.11 Therefore, we undertook to evaluate whether persons with AIDS had an increased prevalence of AMD, using retinal photographs taken at enrollment in the Longitudinal Study of the Ocular Complications of AIDS (LSOCA) cohort.
Full Paper: Prevalence of Intermediate-Stage Age-Related Macular Degeneration in Patients With Acquired Immunodeficiency Syndrome