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Search Results: 1 - 10 of 149867 matches for " Robyn H Guymer "
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Cost-effectiveness of smoking cessation to prevent age-related macular degeneration
Susan F Hurley, Jane P Matthews, Robyn H Guymer
Cost Effectiveness and Resource Allocation , 2008, DOI: 10.1186/1478-7547-6-18
Abstract: We fitted a function predicting the decline in risk of macular degeneration after quitting to data from 7 studies involving 1,488 patients. We assessed the cost-effectiveness of smoking cessation in terms of its impact on macular degeneration-related outcomes for 1,000 randomly selected U.S. smokers. We used a computer simulation model to predict the incidence of macular degeneration and blindness, the number of quality-adjusted life-years (QALYs), and direct costs (in 2004 U.S. dollars) until age 85 years. Cost-effectiveness ratios were based on the cost of the Massachusetts Tobacco Control Program. Costs and QALYs were discounted at 3% per year.If 1,000 smokers quit, our model predicted 48 fewer cases of macular degeneration, 12 fewer cases of blindness, and a gain of 1,600 QALYs. Macular degeneration-related costs would decrease by $2.5 million if the costs of caregivers for people with vision loss were included, or by $1.1 million if caregiver costs were excluded. At a cost of $1,400 per quitter, smoking cessation was cost-saving when caregiver costs were included, and cost about $200 per QALY gained when caregiver costs were excluded. Sensitivity analyses had a negligible impact. The cost per quitter would have to exceed $77,000 for the cost per QALY for smoking cessation to reach $50,000, a threshold above which interventions are sometimes viewed as not cost-effective.Smoking cessation is unequivocally cost-effective in terms of its impact on age-related macular degeneration outcomes alone.There is a strong association between tobacco smoking and age-related macular degeneration.[1] A pooled analysis of data from the 3 largest population-based prevalence surveys found risks for current smokers relative to never smokers were 4.55-fold higher for neovascular age-related macular degeneration and 2.54-fold higher for geographic atrophy.[2] These relative risks were approximately halved in ex-smokers, suggesting that the adverse effect of smoking is reversible.[1,2
Cost-effectiveness of ranibizumab for neovascular age-related macular degeneration
Susan F Hurley, Jane P Matthews, Robyn H Guymer
Cost Effectiveness and Resource Allocation , 2008, DOI: 10.1186/1478-7547-6-12
Abstract: We assessed the cost-effectiveness of ranibizumab compared with no ranibizumab over 10 years, using randomized trial efficacy data for the first 2 years, post-trial efficacy assumptions, and ranibizumab acquisition costs ranging from the wholesale price ($1,950 per dose) to the price of bevazicumab ($50), a similar molecule which may be equally efficacious. We used a computer simulation model to estimate the probability of blindness, the number of quality-adjusted life-years (QALYs), direct costs (in 2004 U.S. dollars), and cost-effectiveness ratios for a 67-year old woman. Costs and QALYs were discounted at 3% per year.The probability of blindness over 10 years was reduced from 56% to 34% if ranibizumab was efficacious for only 2 years, 27% if efficacy was maintained for a further 2 years only (base-case scenario), and 17% if visual acuity at 4 years was then sustained. It was cost-saving under all price assumptions, when caregiver costs were included. When caregiver costs were excluded, the cost per QALY for the base-case ranged from $5,600, assuming the bevazicumab price, to $91,900 assuming the wholesale ranibizumab price. The cost per QALY was < $50,000 when the cost of ranibizumab was less than $1000.From a societal perspective, ranibizumab was cost-saving. From a health care funder's perspective, ranibizumab was an efficient treatment when it cost less than $1000 per dose.Ranibizumab's efficacy has been described as miraculous [1]. This humanized, recombinant, monoclonal antibody fragment is the first treatment for neovascular age-related macular degeneration that improves visual acuity. In 2 recent randomized controlled trials, MARINA (the Minimally Classic/Occult Trial of the Anti-VEGF Antibody Ranibizumab in the Treatment of Neovascular Age-Related Macular Degeneration)[2] and the ANCHOR study (Anti-VEGF Antibody for the Treatment of Predominantly Classic Choroidal Neovascularization in Age-Related Macular Degeneration) [3], it prevented vision loss and im
Comprehensive Analysis of Copy Number Variation of Genes at Chromosome 1 and 10 Loci Associated with Late Age Related Macular Degeneration
Stuart Cantsilieris, Stefan J. White, Andrea J. Richardson, Robyn H. Guymer, Paul N. Baird
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035255
Abstract: Copy Number Variants (CNVs) are now recognized as playing a significant role in complex disease etiology. Age-related macular degeneration (AMD) is the most common cause of irreversible vision loss in the western world. While a number of genes and environmental factors have been associated with both risk and protection in AMD, the role of CNVs has remained largely unexplored. We analyzed the two major AMD risk-associated regions on chromosome 1q32 and 10q26 for CNVs using Multiplex Ligation-dependant Probe Amplification. The analysis targeted nine genes in these two key regions, including the Complement Factor H (CFH) gene, the 5 CFH-related (CFHR) genes representing a known copy number “hotspot”, the F13B gene as well as the ARMS2 and HTRA1 genes in 387 cases of late AMD and 327 controls. No copy number variation was detected at the ARMS2 and HTRA1 genes in the chromosome 10 region, nor for the CFH and F13B genes at the chromosome 1 region. However, significant association was identified for the CFHR3-1 deletion in AMD cases (p = 2.38×10?12) OR = 0.31, CI-0.95 (0.23–0.44), for both neovascular disease (nAMD) (p = 8.3×10?9) OR = 0.36 CI-0.95 (0.25–0.52) and geographic atrophy (GA) (p = 1.5×10?6) OR = 0.36 CI-0.95 (0.25–0.52) compared to controls. In addition, a significant association with deletion of CFHR1-4 was identified only in patients who presented with bilateral GA (p = 0.02) (OR = 7.6 CI-0.95 1.38–41.8). This is the first report of a phenotype specific association of a CNV for a major subtype of AMD and potentially allows for pre-diagnostic identification of individuals most likely to proceed to this end stage of disease.
Can HMG Co-A reductase inhibitors (“statins”) slow the progression of age-related macular degeneration? The Age-Related Maculopathy Statin Study (ARMSS)
Robyn H Guymer,Peter N Dimitrov,Mary Varsamidis,Lyndell L Lim
Clinical Interventions in Aging , 2008,
Abstract: Robyn H Guymer1,3, Peter N Dimitrov1, Mary Varsamidis1, Lyndell L Lim1,3, Paul N Baird1, Algis J Vingrys2, Luba Robman1,31Centre for Eye Research Australia, University of Melbourne, Melbourne, Victoria, Australia; 2Department of Optometry and Visual Sciences, University of Melbourne, Melbourne, Victoria, Australia; 3Royal Victorian Eye and EAR Hospital, Melbourne, AustraliaAbstract: Age-related macular degeneration (AMD) is responsible for the majority of visual impairment in the Western world. The role of cholesterol-lowering medications, HMG Co-A reductase inhibitors or statins, in reducing the risk of AMD or of delaying its progression has not been fully investigated. A 3-year prospective randomized controlled trial of 40 mg simvastatin per day compared to placebo in subjects at high risk of AMD progression is described. This paper outlines the primary aims of the Age-Related Maculopathy Statin Study (ARMSS), and the methodology involved. Standardized clinical grading of macular photographs and comparison of serial macular digital photographs, using the International grading scheme, form the basis for assessment of primary study outcomes. In addition, macular function is assessed at each visit with detailed psychophysical measurements of rod and cone function. Information collected in this study will assist in the assessment of the potential value of HMG Co-A reductase inhibitors (statins) in reducing the risk of AMD progression.Keywords: age-related macular degeneration, progression, randomized controlled trial, HMG Co-A reductase inhibitor, statin, visual function
Visual Impairment as a Function of Visual Acuity in Both Eyes and Its Impact on Patient Reported Preferences
Robert P. Finger, Eva Fenwick, Christoph W. Hirneiss, Arthur Hsueh, Robyn H. Guymer, Ecosse L. Lamoureux, Jill E. Keeffe
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0081042
Abstract: Purpose To assess the impact of VA loss on patient reported utilities taking both eyes into account compared to taking only the better or the worse eye into account. Methods In this cross-sectional study 1085 patients and 254 controls rated preferences with the generic health-related (EQ-5D; n = 868) and vision-specific (Vision and Quality of Life Index (VisQoL); n = 837) multi-attribute utility instruments (MAUIs). Utilities were calculated for three levels of VA in the better and worse eyes, as well as for 6 different vision states based on combinations of the better and worse eye VA. Results Using the VisQoL, utility scores decreased significantly with deteriorating vision in both the better and worse eyes when analysed separately. When stratified by the 6 vision states, VisQoL utilities decreased as VA declined in the worse eye despite stable VA in the better eye. Differences in VisQoL scores were statistically significant for cases where the better eye had no vision impairment and the worse seeing fellow eye had mild, moderate or severe vision impairment. In contrast, the EQ-5D failed to capture changes in better or worse eye VA, or any of the six vision states. Conclusions Calculating utilities based only on better eye VA or using a generic MAUI is likely to underestimate the impact of vision impairment, particularly when the better eye has no or little VA loss and the worse eye is moderately to severely visually impaired. These findings have considerable implications for the assessment of overall visual impairment as well as economic evaluations within eye health.
Clinical validation of a genetic model to estimate the risk of developing choroidal neovascular age-related macular degeneration
Gregory S Hageman, Karen Gehrs, Serguei Lejnine, Aruna T Bansal, Margaret M DeAngelis, Robyn H Guymer, Paul N Baird, Rando Allikmets, Cosmin Deciu, Paul Oeth, Lorah T Perlee
Human Genomics , 2011, DOI: 10.1186/1479-7364-5-5-420
Abstract: Many diseases of ageing characterised by complex inheritance patterns are progressive; the individual may be asymptomatic in the early stages. One of these diseases, age-related macular degeneration (AMD), is the most common cause of visual impairment and the leading cause of blindness in the elderly population in the developed world. The prevalence of AMD increases with advancing age in all populations studied. Thus, in developed nations such as the USA, UK, Canada and Australia, with increasingly aged populations, the condition affects a progressively larger segment of the population and has become a major public health issue. Early- or late-stage AMD is present in 15 per cent of individuals over the age of 60 years [1]. It is estimated that there are currently 9.1 million patients in the USA with AMD, of which 1.7 million suffer with the vision-threatening late-stage complications of choroidal neovascularisation (CNV) or geographic atrophy [1]. Moreover, it is predicted that the number of cases of early AMD will increase to 17.8 million by 2050 and, if untreated, cases of late-stage blinding AMD will increase to 3.8 million [1]. It has been determined that vision loss from AMD decreases quality of life by 60 per cent, similar to the experience of dealing with a stroke that requires intensive nursing care [2].The clinical presentation and natural course of AMD are highly variable. The disease may present as early as the fifth decade of life or as late as the ninth decade. The clinical symptoms of AMD range from no visual disturbances in early disease to profound loss of central vision in the advanced late stages of the disease. Some patients never progress beyond early AMD; however, in 10-15 per cent of Caucasian patients with early-stage disease, the condition progresses to an exudative neovascular (or 'wet' form) or geographic atrophic (or 'dry' form) AMD, which threatens vision. The phenotype is characterised by development of subretinal choroidal neovascular c
Proof of Concept, Randomized, Placebo-Controlled Study of the Effect of Simvastatin on the Course of Age-Related Macular Degeneration
Robyn H. Guymer, Paul N. Baird, Mary Varsamidis, Lucy Busija, Peter N. Dimitrov, Khin Zaw Aung, Galina A. Makeyeva, Andrea J. Richardson, Lyndell Lim, Liubov D. Robman
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0083759
Abstract: Background HMG Co-A reductase inhibitors are ubiquitous in our community yet their potential role in age-related macular degeneration (AMD) remains to be determined. Methodology/Principal Findings Objectives: To evaluate the effect of simvastatin on AMD progression and the effect modification by polymorphism in apolipoprotein E (ApoE) and complement factor H (CFH) genes. Design: A proof of concept double-masked randomized controlled study. Participants: 114 participants aged 53 to 91 years, with either bilateral intermediate AMD or unilateral non-advanced AMD (with advanced AMD in fellow eye), BCVA≥20/60 in at least one eye, and a normal lipid profile. Intervention: Simvastatin 40 mg/day or placebo, allocated 1:1. Main outcome measures: Progression of AMD either to advanced AMD or in severity of non-advanced AMD. Results. The cumulative AMD progression rates were 70% in the placebo and 54% in the simvastatin group. Intent to treat multivariable logistic regression analysis, adjusted for age, sex, smoking and baseline AMD severity, showed a significant 2-fold decrease in the risk of progression in the simvastatin group: OR 0.43 (0.18–0.99), p = 0.047. Post-hoc analysis stratified by baseline AMD severity showed no benefit from treatment in those who had advanced AMD in the fellow eye before enrolment: OR 0.97 (0.27–3.52), p = 0.96, after adjusting for age, sex and smoking. However, there was a significant reduction in the risk of progression in the bilateral intermediate AMD group compared to placebo [adjusted OR 0.23 (0.07–0.75), p = 0.015]. The most prominent effect was observed amongst those who had the CC (Y402H) at risk genotype of the CFH gene [OR 0.08 (0.02–0.45), p = 0.004]. No evidence of harm from simvastatin intervention was detected. Conclusion/Significance Simvastatin may slow progression of non-advanced AMD, especially for those with the at risk CFH genotype CC (Y402H). Further exploration of the potential use of statins for AMD, with emphasis on genetic subgroups, is warranted. Trial Registration Australian New Zealand Clinical Trial Registry (ANZCTR) ACTRN1260500032065
Novel measures of cardiovascular health and its association with prevalence and progression of age-related macular degeneration: the CHARM study
Catherine A McCarty, Adam Dowrick, James Cameron, Barry McGrath, Luba D Robman, Peter Dimitrov, Gabriella Tikellis, Caroline Nicolas, John McNeil, Robyn Guymer
BMC Ophthalmology , 2008, DOI: 10.1186/1471-2415-8-25
Abstract: Measures of the cardiovascular system: included intima media thickness (IMT), pulse wave velocity (PWV), systemic arterial compliance (SAC), carotid augmentation index (AI). For the prevalence study, hospital-based AMD cases and population-based age- and gender-matched controls with no signs of AMD in either eye were enrolled. For the progression component, participants with early AMD were recruited from two previous studies; cases were defined as progression in one or both eyes and controls were defined as no progression in either eye.160 cases and 160 controls were included in the prevalence component. The upper two quartiles of SAC, implying good cardiovascular health, were significantly associated with increased risk of AMD (OR = 2.54, 95% CL = 1.29, 4.99). High PWV was associated with increased prevalent AMD. Progression was observed in 82 (32.3%) of the 254 subjects recruited for the progression component. Higher AI (worse cardiovascular function) was protective for AMD progression (OR = 0.30, 95%CL = 0.13, 0.69). Higher aortic PWV was associated with increased risk of AMD progression; the highest risk was seen with the second lowest velocity (OR = 6.22, 95% CL = 2.35, 16.46).The results were unexpected in that better cardiovascular health was associated with increased risk of prevalent AMD and progression. Inconsistent findings between the prevalence and progression components could be due to truly different disease etiologies or to spurious findings, as can occur with inherent biases in case control studies of prevalence. Further investigation of these non-invasive methods of characterizing the cardiovascular system should be undertaken as they may help to further elucidate the role of the cardiovascular system in the etiology of prevalent AMD and progression.Age-related macular degeneration (AMD) is the leading cause of blindness in elderly Caucasians in the US [1], Australia [2] and other industrialized nations. The prevalence of AMD rises dramatically wit
Equidistribution of Horocyclic Flows on Complete Hyperbolic Surfaces of Finite Area
John H. Hubbard,Robyn L. Miller
Mathematics , 2007,
Abstract: We provide a self-contained, accessible introduction to Ratner's Equidistribution Theorem in the special case of horocyclic flow on a complete hyperbolic surface of finite area. This equidistribution result was first obtained in the early 1980s by Dani and Smillie and later reappeared as an illustrative special case of Ratner's work on the equidistribution of unipotent flows in homogeneous spaces. We also prove an interesting probabilistic result due to Breuillard: on the modular surface an arbitrary uncentered random walk on the horocycle through almost any point will fail to equidistribute, even though the horocycles are themselves equidistributed. In many aspects of this exposition we are indebted to Bekka and Mayer's more ambitious survey, "Ergodic Theory and Topological Dynamics for Group Actions on Homogeneous Spaces."
CuradermBEC5 for Skin Cancers, Is It? An Overview  [PDF]
Tania Robyn Chase
Journal of Cancer Therapy (JCT) , 2011, DOI: 10.4236/jct.2011.25099
Abstract: Skin cancer incidence is increasing at alarming rates and is considered by some as an epidemic. Its incidence is higher than all other cancers combined. The developments of new treatments have not parallelled the increased incidences of this disease. A variety of treatments are available with differing outcomes. More recently a novel topical treatment, consisting of the antineoplastic compounds solasodine rhamnosyl glycosides, solamargine and solasonine, which are derived from plant material, has been described that claims to have many advantages over the currently used skin cancer therapies. This review investigates such claims.
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