Clinical Classification of Age-related Macular Degeneration

Ferris, Frederick L.; Wilkinson, Charles P.; Bird, Alan C.; Chakravarthy, Usha; Chew, Emily Y.; Csaky, Karl G.; Sadda, Srinivas R

doi:10.1016/j.ophtha.2012.10.036

Cited by 1,338 publications

(1,198 citation statements)

References 19 publications

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“…17 AMD is the leading cause of irreversible severe visual loss in high-income countries in individuals aged > 60 years. 18 It is the most common cause of adult blind registration in many high-income countries, including the UK.…”

Section: Age-related Macular Degenerationmentioning

confidence: 99%

“…There was no evidence for independent age or sex effects, with the estimated differences (95% CI) per year of 0.03 (-0.05 to 0.11; p = 0.49) and between males and females of 1.09 (-0.05 to 2.24; p = 0.06). For the analysis of the range of sMMSE scores in our sample (Tables 5 and 6), each participant was allocated to one of five levels of cognitive impairment based on their total sMMSE score: severe cognitive impairment (sMMSE score of 0-9), moderate cognitive impairment (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20), mild cognitive impairment (21)(22)(23)(24), very mild cognitive impairment (25)(26)(27) and no cognitive impairment (28)(29)(30). In the context of the PrOVIDe study, the term mild cognitive impairment is being taken to include people in the sMMSE range of 21-24, although mild cognitive impairment has a different meaning in the general literature, where it often refers to people without dementia but who have a performance of 1.5-2 SDs lower on cognitive (usually memory) testing than age-matched norms.…”

Section: Levels Of Cognitive Impairment In the Samplementioning

confidence: 99%

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The Prevalence of Visual Impairment in People with Dementia (the PrOVIDe study): a cross-sectional study of people aged 60–89 years with dementia and qualitative exploration of individual, carer and professional perspectives

Bowen

Edgar

Hancock

et al. 2016

Health Serv Deliv Res

121

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BackgroundThe prevalence of visual impairment (VI) and dementia increases with age and these conditions may coexist, but few UK data exist on VI among people with dementia.ObjectivesTo measure the prevalence of eye conditions causing VI in people with dementia and to identify/describe reasons for underdetection or inappropriate management.DesignStage 1 – cross-sectional prevalence study. Stage 2 – qualitative research exploring participant, carer and professional perspectives of eye care.SettingStage 1 – 20 NHS sites in six English regions. Stage 2 – six English regions.ParticipantsStage 1 – 708 participants with dementia (aged 60–89 years): 389 lived in the community (group 1) and 319 lived in care homes (group 2). Stage 2 – 119 participants.InterventionsStage 1 gathered eye examination data following domiciliary sight tests complying with General Ophthalmic Services requirements and professional guidelines. Cognitive impairment was assessed using the Standardised Mini-Mental State Examination (sMMSE) test, and functional ability and behaviour were assessed using the Bristol Activities of Daily Living Scale and Cambridge Behavioural Inventory – Revised. Stage 2 involved individual interviews (36 people with dementia and 11 care workers); and separate focus groups (34 optometrists; 38 family and professional carers).Main outcome measures.VI defined by visual acuity (VA) worse than 6/12 or worse than 6/18 measured before and after refraction.ResultsStage 1 – when participants wore their current spectacles, VI prevalence was 32.5% [95% confidence interval (CI) 28.7% to 36.5%] and 16.3% (95% CI 13.5% to 19.6%) for commonly used criteria for VI of VA worse than 6/12 and 6/18, respectively. Of those with VI, 44% (VA < 6/12) and 47% (VA < 6/18) were correctable with new spectacles. Almost 50% of remaining uncorrectable VI (VA < 6/12) was associated with cataract, and was, therefore, potentially remediable, and one-third was associated with macular degeneration. Uncorrected/undercorrected VI prevalence (VA < 6/12) was significantly higher in participants in care homes (odds ratio 2.19, 95% CI 1.30 to 3.73;p < 0.01) when adjusted for age, sex and sMMSE score. VA could not be measured in 2.6% of group 1 and 34.2% of group 2 participants (p < 0.01). The main eye examination elements (excluding visual fields) could be performed in > 80% of participants. There was no evidence that the management of VI in people with dementia differed from that in older people in general. Exploratory analysis suggested significant deficits in some vision-related aspects of function and behaviour in participants with VI. Stage 2 key messages – carers and care workers underestimated how much can be achieved in an eye examination. People with dementia and carers were unaware of domiciliary sight test availability. Improved communication is needed between optometrists and carers; optometrists should be informed of the person’s dementia. Tailoring eye examinations to individual needs includes allowing extra time. Optometrists wanted training and guidance about dementia. Correcting VI may improve the quality of life of people with dementia but should be weighed against the risks and burdens of undergoing examinations and cataract surgery on an individual basis.LimitationsSampling bias is possible owing to quota-sampling and response bias.ConclusionsThe prevalence of VI is disproportionately higher in people with dementia living in care homes. Almost 50% of presenting VI is correctable with spectacles, and more with cataract surgery. Areas for future research are the development of an eye-care pathway for people with dementia; assessment of the benefits of early cataract surgery; and research into the feasibility of specialist optometrists for older people.FundingThe National Institute for Health Research Health Services and Delivery Research programme.

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Section: Age-related Macular Degenerationmentioning

confidence: 99%

Section: Levels Of Cognitive Impairment In the Samplementioning

confidence: 99%

The Prevalence of Visual Impairment in People with Dementia (the PrOVIDe study): a cross-sectional study of people aged 60–89 years with dementia and qualitative exploration of individual, carer and professional perspectives

Bowen

Edgar

Hancock

et al. 2016

Health Serv Deliv Res

121

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“…Retinal angiomatous proliferation is also a discrete neovascular AMD subtype; in this condition, intraretinal neovascular lesions connect with vessels from the choroidal circulations. The Beckman Initiative for Macular Research has published a phenotypic classification of AMD based on consensus of 30 opinion leaders in the field (Ferris et al 2013). A current goal of AMD genetics is to identify biomarkers that can be used to distinguish these heterogeneous clinical subtypes (Gorin 2012).…”

Section: Amd Phenotypesmentioning

confidence: 99%

“…Gorin also stresses the point that accurate quantitation of AMD phenotype is paramount in classifying disease progression for drug response studies. A recently published position statement is expected to offer guidance on this matter (Ferris et al 2013). Finally, regarding constraints to progress in AMD pharmacogenomics, there currently are no established biomarkers with which to monitor response to preventive interventions in AMD-free people at moderate risk for developing the disease.…”

Section: Genetic Basis Of Drug Activity and Toxicitymentioning

confidence: 99%

Clinical Applications of Age-Related Macular Degeneration Genetics

SanGiovanni

Chew

2014

Cold Spring Harbor Perspectives in Medicine

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Understanding genetic causes of age-related macular degeneration (AMD) will eventually yield effective discoveries and improvements in predictive/prognostic methods. These include, but are not limited to, reliable disease prediction (screening for increased discrimination of clinical risk), differential classification of AMD subtypes with biomarkers (development of risk-linked molecular taxonomies), selection of optimal preventive and therapeutic interventions (guided by a biologically meaningful understanding of treatment response), and drug dosing. In this review, we discuss clinical applications informed by key findings in AMD genetics, and provide commentary on leveraging extant and forthcoming evidence to improve AMD risk prediction, AMD classification, and knowledge on the genetic basis of drug activity and toxicity. Advances in translating AMD genetics findings for AMD risk prediction require development of a genetics-based causality for AMD incidence and progression. Molecular subtyping of AMD phenotypes requires a set of dynamic biomarkers presenting prognostic value; although these have yet to be identified, the formation of multidisciplinary teams and their participation in large-scale consortia may yield promising results. Drugs targeting complement and vascular endothelial growth factor (VEGF) systems are under evaluation, and forthcoming work on rare variants and noncoding DNA in AMD pathogenesis will likely reveal biochemical pathways enriched with AMD-associated genetic variants. Pharmacologic targets in these pathways may inform a rational and effective therapeutic approach to preventing and treating this sight-threatening disease.A ge-related macular degeneration (AMD) is a complex sight-threatening disease of public health significance . Knowledge on the nature of AMD phenotypes and related pathogenic processes (as well as on constraints in approaches to investigation) has influenced our ability to make inferences on a geneticsbased causality of this disease. Such inferences are necessary in the development of feasible clinic-based approaches for effective AMD prevention, prognosis, and treatment (Gorin 2012). In this review we discuss clinical applications informed by key findings in AMD genetics, and provide commentary on leveraging extant and forthcoming evidence to improve AMD risk prediction, classification, and knowledge on the genetic basis of drug activity and toxicity. We start with a definition of AMD phenotypes and follow with an overview of what research in AMD genetics has told us about the nature and

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“…1 The increase in the size of drusen is considered a risk factor for the progression to late AMD, which includes geographic atrophy (GA) and macular neovascularization. [1][2][3] Historically, drusen were imaged and quantified using color fundus imaging, but drusen morphology can now be reproducibly measured and their natural history followed using spectral-domain optical coherence tomography (SD-OCT) imaging. [4][5][6][7] The natural history of drusen morphology was followed for 2 years, and three different growth patterns were identified.…”

Section: Introductionmentioning

confidence: 99%

Change in Drusen Volume as a Novel Clinical Trial Endpoint for the Study of Complement Inhibition in Age-related Macular Degeneration

Filho¹,

Yehoshua²,

Gregori³

et al. 2014

Ophthalmic Surg Lasers Imaging Retina

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BACKGROUND AND OBJECTIVE:To evaluate the change in drusen volume following treatment with eculizumab, a systemic inhibitor of complement component 5. PATIENTS AND METHODS:Single-center, prospective, randomized, double-masked clinical trial. Patients were randomized 2:1 to receive intravenous eculizumab or placebo over 26 weeks. Main outcome measure: decrease in drusen volume of at least 50% at 26-week follow-up. RESULTS:Mean drusen cube root volumes were 0.49 mm and 0.47 mm (P = .64) at baseline and 0.51 mm and 0.42 mm (P = .17) at 26 weeks in the eculizumab and placebo groups, respectively. In the placebo group, one eye had a decrease in drusen volume of at least 50% and two eyes developed neovascularization through 26 weeks. CONCLUSION:Systemic complement inhibition with eculizumab did not significantly reduce drusen volume. Drusen growth was dependent on the number of complement at-risk alleles. Future trials should consider the use of a composite clinical trial endpoint in which efficacy is defined by the treatment's ability to prevent drusen growth, neovascularization, and the formation of geographic atrophy over 1 year.

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Clinical Classification of Age-related Macular Degeneration

Cited by 1,338 publications

References 19 publications

The Prevalence of Visual Impairment in People with Dementia (the PrOVIDe study): a cross-sectional study of people aged 60–89 years with dementia and qualitative exploration of individual, carer and professional perspectives

The Prevalence of Visual Impairment in People with Dementia (the PrOVIDe study): a cross-sectional study of people aged 60–89 years with dementia and qualitative exploration of individual, carer and professional perspectives

Clinical Applications of Age-Related Macular Degeneration Genetics

Change in Drusen Volume as a Novel Clinical Trial Endpoint for the Study of Complement Inhibition in Age-related Macular Degeneration

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