Database : MEDLINE
Search on : Geographic and Atrophy [Words]
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[PMID]: 29224928
[Au] Autor:Pietraszkiewicz A; van Asten F; Kwong A; Ratnapriya R; Abecasis G; Swaroop A; Chew EY
[Ad] Address:Neurobiology, Neurodegeneration and Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland.
[Ti] Title:Association of Rare Predicted Loss-of-Function Variants in Cellular Pathways with Sub-Phenotypes in Age-Related Macular Degeneration.
[So] Source:Ophthalmology;125(3):398-406, 2018 Mar.
[Is] ISSN:1549-4713
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: To investigate the association of rare predicted loss-of-function (pLoF) variants within age-related macular degeneration (AMD) risk loci and AMD sub-phenotypes. DESIGN: Case-control study. PARTICIPANTS: Participants of AREDS, AREDS2, and Michigan Genomics Initiative. METHODS: Whole genome sequencing data were analyzed for rare pLoF variants (frequency <0.1%) in the regions of previously identified 52 independent risk variants known to be associated with AMD. Frequency of the rare pLoF variants in cases with intermediate or advanced AMD was compared with controls. Variants were assigned to the complement, extracellular matrix (ECM), lipid, cell survival, immune system, metabolism, or unknown/other pathway. Associations of rare pLoF variant pathways with AMD sub-phenotypes were analyzed using logistic and linear regression, and Cox proportional hazards models. MAIN OUTCOME MEASURES: Differences in rare pLoF variant pathway burden and association of rare pLoF variant pathways with sub-phenotypes within the population with AMD were evaluated. RESULTS: Rare pLoF variants were found in 298 of 1689 cases (17.6%) and 237 of 1518 controls (15.6%) (odds ratio [OR], 1.11; 95% confidence interval [CI], 0.91-1.36; P = 0.310). An enrichment of rare pLoF variants in the complement pathway in cases versus controls (OR, 2.94; 95% CI, 1.49-5.79; P = 0.002) was observed. Within cases, associations between all rare pLoF variants and choroidal neovascularization (CNV) (OR, 1.34; 95% CI, 1.04-1.73; P = 0.023), calcified drusen (OR, 1.33; 95% CI, 1.04-1.72; P = 0.025), higher scores on the AREDS Extended AMD Severity Scale (Standardized Coefficient Beta (ß)=0.346 [0.086-0.605], P = 0.009), and progression to advanced disease (hazard ratio, 1.25; 95% CI, 1.01-1.55; P = 0.042) were observed. At the pathway level, there were associations between the complement pathway and geographic atrophy (GA) (OR, 2.17; 95% CI, 1.12-4.24; P = 0.023), the complement pathway and calcified drusen (OR, 3.75; 95% CI, 1.79-7.86; P < 0.001), and the ECM pathway and more severe levels in the AREDS Extended AMD Severity Scale (ß = 0.62; 95% CI, 0.04-1.20; P = 0.035). CONCLUSIONS: Rare pLoF variants are associated with disease progression. Variants in the complement pathway modify the clinical course of AMD and increase the risk of developing specific sub-phenotypes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review

  2 / 1452 MEDLINE  
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[PMID]: 29506321
[Au] Autor:Denniss J; Astle AT
[Ad] Address:Visual Neuroscience Group, School of Psychology, University of Nottingham, Nottingham, UK.
[Ti] Title:Modified images reflecting effects of age-related macular degeneration on perception of everyday scenes.
[So] Source:Clin Exp Optom;, 2018 Mar 05.
[Is] ISSN:1444-0938
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:BACKGROUND: Depictions of vision with age-related macular degeneration (AMD) in public information material typically show a central region of absolute vision loss. Patients with early and moderate disease frequently do not report this. We aimed to measure how a group of people with AMD perceive everyday scenes in order to produce accurate depictions. METHODS: We report on six people aged 65-82 years with monocular AMD (visual acuity +0.04 to +1.64 logMAR) and normal vision in the fellow eye. Participants viewed four images monocularly, alternating between eyes. The image was digitally altered to approximate participants' descriptions of their perception with the affected eye. The altered image was viewed with the unaffected eye, and compared with the original image viewed with the affected eye. This was repeated iteratively until a perceptual match was achieved between the modified image/unaffected eye and the original image/affected eye. RESULTS: For five AMD participants with visual acuity +0.04 to +0.50 logMAR the modified images did not resemble those in current public information material. Image modifications required to achieve perceptual similarity with the affected eyes included localised distortion, contrast reduction and blur. Widespread colour desaturation was also required in some cases. One participant with advanced geographic atrophy reported an absolute positive scotoma, similar to existing depictions. CONCLUSIONS: Vision in people with AMD may not conform to the common depiction of a central region of absolute vision loss. The accurate representations of AMD patients' vision produced in this study will enable better understanding of the visual consequences of AMD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[St] Status:Publisher
[do] DOI:10.1111/cxo.12672

  3 / 1452 MEDLINE  
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[PMID]: 29351793
[Au] Autor:Jiang Y; Brenner JE; Foster WJ
[Ad] Address:Department of Ophthalmology, Temple University, 3401 N Broad Street, 6th Floor Parkinson Pavilion, Philadelphia, PA, 19140, USA.
[Ti] Title:Retinal complications of gout: a case report and review of the literature.
[So] Source:BMC Ophthalmol;18(1):11, 2018 Jan 19.
[Is] ISSN:1471-2415
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: There have been few reported findings of posterior segment complications of gout. While exudative lesions, an increased risk of macular degeneration, and vascular occlusions have been previously reported, to our knowledge, refractile macular lesions have not been reported in a patient with chronic uncontrolled gout. CASE PRESENTATION: Highly refractile, crystal-like lesions were found in the macula of a 62 year old male patient with chronically uncontrolled gout. The lesions appeared at the termination of retinal arterioles and were located at the level of the retinal pigment epithelium. The lesions did not stain with fluorescein and were associated with larger areas geographic atrophy. Review of the patient's blood tests revealed well-controlled vasculopathic risk factors. Fundus appearance and best-corrected visual acuity remained stable over 12 months of follow-up during which the uric acid levels were well controlled. CONCLUSION: Retinopathy may be associated with chronically uncontrolled gout and patients with visual complaints should undergo a dilated examination in addition to the typical anterior segment slit-lamp exam.
[Mh] MeSH terms primary: Anterior Eye Segment/diagnostic imaging
Gout/complications
Macula Lutea/diagnostic imaging
Retinal Diseases/etiology
Retinal Vessels/diagnostic imaging
[Mh] MeSH terms secundary: Fluorescein Angiography/methods
Fundus Oculi
Gout/blood
Humans
Male
Middle Aged
Retinal Diseases/diagnosis
Tomography, Optical Coherence/methods
Uric Acid/blood
Visual Acuity
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:268B43MJ25 (Uric Acid)
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:IM
[Da] Date of entry for processing:180121
[St] Status:MEDLINE
[do] DOI:10.1186/s12886-018-0669-6

  4 / 1452 MEDLINE  
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[PMID]: 29484559
[Au] Autor:Taylor DJ; Smith ND; Binns AM; Crabb DP
[Ad] Address:Division of Optometry and Visual Science, School of Health Sciences, City, University of London, Northampton Square, London, EC1V 0HB, UK.
[Ti] Title:The effect of non-neovascular age-related macular degeneration on face recognition performance.
[So] Source:Graefes Arch Clin Exp Ophthalmol;, 2018 Feb 27.
[Is] ISSN:1435-702X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:PURPOSE: There is a well-established research base surrounding face recognition in patients with age-related macular degeneration (AMD). However, much of this existing research does not differentiate between results obtained for 'wet' AMD and 'dry' AMD. Here, we test the hypothesis that face recognition performance is worse in patients with dry AMD compared with visually healthy peers. METHODS: Patients (>60 years of age, logMAR binocular visual acuity 0.7 or better) with dry AMD of varying severity and visually healthy age-related peers (controls) completed a modified version of the Cambridge Face Memory Test (CFMT). Percentage of correctly identified faces was used as an outcome measure for performance for each participant. A 90% normative reference limit was generated from the distribution of CFMT scores recorded in the visually healthy controls. Scores for AMD participants were then specifically compared to this limit, and comparisons between average scores in the AMD severity groups were investigated. RESULTS: Thirty patients (median [interquartile range] age of 76 [70, 79] years) and 34 controls (median age of 70 [64, 75] years) were examined. Four, seventeen and nine patients were classified as having early, intermediate and late AMD (geographic atrophy) respectively. Five (17%) patients recorded a face recognition performance worse than the 90% limit (Fisher's exact test, p = 0.46) set by controls; four of these had geographic atrophy. Patients with geographic atrophy identified fewer faces on average (±SD) (61% ± 22%) than those with early and intermediate AMD (75 ± 11%) and controls (74% ± 11%). CONCLUSIONS: People with dry AMD may not suffer from problems with face recognition until the disease is in its later stages; those with late AMD (geographic atrophy) are likely to have difficulty recognising faces. The results from this study should influence the management and expectations of patients with dry AMD in both community practice and hospital clinics.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:Publisher
[do] DOI:10.1007/s00417-017-3879-3

  5 / 1452 MEDLINE  
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[PMID]: 29346644
[Au] Autor:Yan Q; Ding Y; Liu Y; Sun T; Fritsche LG; Clemons T; Ratnapriya R; Klein ML; Cook RJ; Liu Y; Fan R; Wei L; Abecasis GR; Swaroop A; Chew EY; Weeks DE; Chen W; AREDS2 Research Group
[Ad] Address:Division of Pulmonary Medicine, Allergy and Immunology, Department of Pediatrics, Children's Hospital of Pittsburgh of UPMC University of Pittsburgh, Pittsburgh, PA 15224, USA.
[Ti] Title:Genome-wide analysis of disease progression in age-related macular degeneration.
[So] Source:Hum Mol Genet;27(5):929-940, 2018 Mar 01.
[Is] ISSN:1460-2083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Family- and population-based genetic studies have successfully identified multiple disease-susceptibility loci for Age-related macular degeneration (AMD), one of the first batch and most successful examples of genome-wide association study. However, most genetic studies to date have focused on case-control studies of late AMD (choroidal neovascularization or geographic atrophy). The genetic influences on disease progression are largely unexplored. We assembled unique resources to perform a genome-wide bivariate time-to-event analysis to test for association of time-to-late-AMD with ∼9 million variants on 2721 Caucasians from a large multi-center randomized clinical trial, the Age-Related Eye Disease Study. To our knowledge, this is the first genome-wide association study of disease progression (bivariate survival outcome) in AMD genetic studies, thus providing novel insights to AMD genetics. We used a robust Cox proportional hazards model to appropriately account for between-eye correlation when analyzing the progression time in the two eyes of each participant. We identified four previously reported susceptibility loci showing genome-wide significant association with AMD progression: ARMS2-HTRA1 (P = 8.1 × 10-43), CFH (P = 3.5 × 10-37), C2-CFB-SKIV2L (P = 8.1 × 10-10) and C3 (P = 1.2 × 10-9). Furthermore, we detected association of rs58978565 near TNR (P = 2.3 × 10-8), rs28368872 near ATF7IP2 (P = 2.9 × 10-8) and rs142450006 near MMP9 (P = 0.0006) with progression to choroidal neovascularization but not geographic atrophy. Secondary analysis limited to 34 reported risk variants revealed that LIPC and CTRB2-CTRB1 were also associated with AMD progression (P < 0.0015). Our genome-wide analysis thus expands the genetics in both development and progression of AMD and should assist in early identification of high risk individuals.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[St] Status:In-Data-Review
[do] DOI:10.1093/hmg/ddy002

  6 / 1452 MEDLINE  
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[PMID]: 29443034
[Au] Autor:Petrus-Reurer S; Bartuma H; Aronsson M; Westman S; Lanner F; Kvanta A
[Ad] Address:Clinical Neuroscience, Section for Ophtalmology and Vision, Karolinska Institutet; Clinical Sciences, Intervention and Technology, Division of Obstetrics and Gynecology, Karolinska Institutet; sandra.petrus-reurer@ki.se.
[Ti] Title:Subretinal Transplantation of Human Embryonic Stem Cell Derived-retinal Pigment Epithelial Cells into a Large-eyed Model of Geographic Atrophy.
[So] Source:J Vis Exp;(131), 2018 Jan 22.
[Is] ISSN:1940-087X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Geographic atrophy (GA), the late stage of dry age-related macular degeneration is characterized by loss of the retinal pigment epithelial (RPE) layer, which leads to subsequent degeneration of vital retinal structures (e.g., photoreceptors) causing severe vision impairment. Similarly, RPE-loss and decrease in visual acuity is seen in long-term follow up of patients with advanced wet age-related macular degeneration (AMD) receiving intravitreal anti-vascular endothelial growth factor (VEGF) treatment. Therefore, on the one hand, it is fundamental to efficiently derive RPE cells from an unlimited source that could serve as replacement therapy. On the other hand, it is important to assess the behavior and integration of the derived cells in a model of the disease entailing surgical and imaging methods as close as possible to those applied in humans. Here, we provide a detailed protocol based on our previous publications that describes the generation of a preclinical model of GA using the albino rabbit eye, for evaluation of the human embryonic stem cell derived retinal pigment epithelial cells (hESC-RPE) in a clinically relevant setting. Differentiated hESC-RPE are transplanted into naive eyes or eyes with NaIO3-induced GA-like retinal degeneration using a 25 G transvitreal pars plana technique. Evaluation of degenerated and transplanted areas is performed by multimodal high-resolution non-invasive real-time imaging.
[Pt] Publication type:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Em] Entry month:1802
[Cu] Class update date: 180214
[Lr] Last revision date:180214
[St] Status:In-Data-Review
[do] DOI:10.3791/56702

  7 / 1452 MEDLINE  
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[PMID]: 29259020
[Au] Autor:Rajendran A; Dhoble P; Sundaresan P; Saravanan V; Vashist P; Nitsch D; Smeeth L; Chakravarthy U; Ravindran RD; Fletcher AE
[Ad] Address:Aravind Eye Hospital, Madurai, Tamil Nadu, India.
[Ti] Title:Genetic risk factors for late age-related macular degeneration in India.
[So] Source:Br J Ophthalmol;, 2017 Dec 19.
[Is] ISSN:1468-2079
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND/AIMS: There are limited data from India on genetic variants influencing late age-related macular degeneration (AMD). We have previously reported associations from a population-based study in India (the India age-related eye disease study (INDEYE)) of early AMD and single nucleotide polymorphisms (SNPs) in and no association with , or . Late AMD cases were too few for meaningful analyses. We aimed to investigate SNPs for late AMD through case enrichment and extend the loci for early AMD. METHODS: Fundus images of late AMD hospital cases were independently graded by the modified Wisconsin AMD grading scheme. In total 510 cases with late AMD (14 geographic atrophy and 496 neovascular AMD (nvAMD)), 1876 with early AMD and 1176 with no signs of AMD underwent genotyping for selected SNPs. We investigated genotype and per-allele additive associations (OR and 95% CIs) with nvAMD or early AMD. Bonferroni adjusted P values are presented. RESULTS: We found associations with nvAMD for variant (rs1061170) (OR=1.99, 95% CI 1.67 to 2.37, P=10 ), (rs10490924) (OR=2.94, 95% CI 2.45 to 3.52, P=10 ), (rs547154) (OR=0.67, 95% CI 0.53 to 0.85, P=0.01), (rs1883025) (OR=0.77, 95% CI 0.65 to 0.92, P=0.04) and an SNP near (rs4711751) (OR=0.64, 95% CI 0.54 to 0.77, P=10 ). We found no associations of (rs3775291), (rs3826945), (rs1999930) or (rs10468017) or ε4 alleles with nvAMD or early AMD, nor between early AMD and rs1883025 or rs4711751. CONCLUSIONS: The major genetic determinants of nvAMD risk in India are similar to those in other ancestries, while findings for early AMD suggest potential differences in the pathophysiology of AMD development.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180214
[Lr] Last revision date:180214
[St] Status:Publisher

  8 / 1452 MEDLINE  
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[PMID]: 29433793
[Au] Autor:Calucho M; Bernal S; Alías L; March F; Venceslá A; Rodríguez-Álvarez FJ; Aller E; Fernández RM; Borrego S; Millán JM; Hernández-Chico C; Cuscó I; Fuentes-Prior P; Tizzano EF
[Ad] Address:Medicine Genetics Group, Vall d'Hebron Research Institute (VHIR), 08035 Barcelona, Spain.
[Ti] Title:Correlation between SMA type and SMN2 copy number revisited: An analysis of 625 unrelated Spanish patients and a compilation of 2834 reported cases.
[So] Source:Neuromuscul Disord;, 2018 Jan 11.
[Is] ISSN:1873-2364
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Spinal muscular atrophy (SMA) is a neuromuscular disorder caused by loss or mutations in SMN1. According to age of onset, achieved motor abilities, and life span, SMA patients are classified into type I (never sit), II (never walk unaided) or III (achieve independent walking abilities). SMN2, the highly homologous copy of SMN1, is considered the most important phenotypic modifier of the disease. Determination of SMN2 copy number is essential to establish careful genotype-phenotype correlations, predict disease evolution, and to stratify patients for clinical trials. We have determined SMN2 copy numbers in 625 unrelated Spanish SMA patients with loss or mutation of both copies of SMN1 and a clear assignation of the SMA type by clinical criteria. Furthermore, we compiled data from relevant worldwide reports that link SMN2 copy number with SMA severity published from 1999 to date (2834 patients with different ethnic and geographic backgrounds). Altogether, we have assembled a database with a total of 3459 patients to delineate more universal prognostic rules regarding the influence of SMN2 copy number on SMA phenotype. This issue is crucial in the present scenario of therapeutic advances with the perspective of SMA neonatal screening and early diagnosis to initiate treatments.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180213
[Lr] Last revision date:180213
[St] Status:Publisher

  9 / 1452 MEDLINE  
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[PMID]: 29431645
[Au] Autor:Koh S; Chen WJ; Dejneka NS; Harris IR; Lu B; Girman S; Saylor J; Wang S; Eroglu C
[Ad] Address:Department of Cell Biology, Duke University, Durham, NC27710, USA.
[Ti] Title:Subretinal Human Umbilical Tissue-Derived Cell Transplantation Preserves Retinal Synaptic Connectivity and Attenuates Müller Glial Reactivity.
[So] Source:J Neurosci;, 2018 Feb 05.
[Is] ISSN:1529-2401
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Human umbilical tissue-derived cells (hUTC or palucorcel) are currently under clinical investigation for the treatment of geographic atrophy, a late stage of macular degeneration, but how hUTC transplantation mediates vision recovery is not fully elucidated. Subretinal administration of hUTC preserves visual function in the Royal College of Surgeons (RCS) rat, a genetic model of retinal degeneration caused by loss-of-function. hUTC secrete synaptogenic and neurotrophic factors that improve the health and connectivity of the neural retina. Therefore, we investigated the progression of synapse and photoreceptor loss and whether hUTC treatment preserves photoreceptors and synaptic connectivity in the RCS rats of both sexes. We found that RCS retinas display significant deficits in synaptic development already by postnatal day 21 (P21), prior to the onset of photoreceptor degeneration. Subretinal transplantation of hUTC at P21 is necessary to rescue visual function in RCS rats, and the therapeutic effect is enhanced with repeated injections. Synaptic development defects occurred concurrently with morphological changes in Müller glia, the major perisynaptic glia in the retina. hUTC transplantation strongly diminished Müller glia reactivity and specifically protected the α2δ-1-containing retinal synapses, which are responsive to Thrombospondin (TSP) family synaptogenic proteins secreted by Müller glia. Müller glial reactivity and reduced synaptogenesis observed in RCS retinas could be recapitulated by CRISPR/Cas9-mediated loss-of- in Müller glia in wildtype rats. Taken together, our results show that hUTC-transplantation supports the health of retina at least in part by preserving the functions of Müller glial cells, revealing a previously unknown aspect of hUTC transplantation-based therapy. Despite the promising effects observed in clinical trials and preclinical studies, how subretinal hUTC transplantation mediates vision improvements is not fully known. Using a rat model of retinal degeneration, the RCS rat (lacking ), here we provide evidence that hUTC transplantation protects visual function and health by protecting photoreceptors and preserving retinal synaptic connectivity. Furthermore, we find that loss of function only in Müller glia is sufficient to impair synaptic development and cause activation of Müller glia. hUTC transplantation strongly attenuates the reactivity of Müller glia in RCS rats. These findings highlight novel cellular and molecular mechanisms within the neural retina which underlie disease mechanisms and pinpoint Müller glia as a novel cellular target for hUTC transplantation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180212
[Lr] Last revision date:180212
[St] Status:Publisher

  10 / 1452 MEDLINE  
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[PMID]: 29283981
[Au] Autor:Lynch AM; Patnaik JL; Cathcart JN; Mathias MT; Siringo FS; Lacey Echalier E; Wagner BD; Oliver SCN; Pecen PE; Olson JL; Fine SL; Palestine AG; Mandava N
[Ad] Address:Department of Ophthalmology, University of Colorado School of Medicine, Aurora, Colorado.
[Ti] Title:COLORADO AGE-RELATED MACULAR DEGENERATION REGISTRY: Design and Clinical Risk Factors of the Cohort.
[So] Source:Retina;, 2018 Jan 31.
[Is] ISSN:1539-2864
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: To study new and existing risk factors related to age-related macular degeneration (AMD) phenotypes in a Colorado cohort. METHODS: Age-related macular degeneration was categorized into early, intermediate, or advanced forms. Controls (n = 180) were patients with cataract and no AMD. Demographic and clinical data were gathered by patient interview and verified by chart review. Image data were reviewed by vitreoretinal specialists. Statistical analysis included univariable and multivariate logistic regression analysis (P < 0.05). RESULTS: Among the 456 patients with AMD, 157 (34.4%), 80 (17.6%), and 219 (48.0%) had the early/intermediate, geographic atrophy, and neovascular forms of the disease, respectively. Adjusted for age, African-American race was associated with a reduced risk of early/intermediate (adjusted odds ratio [AOR] = 0.08, confidence interval [CI] = 0.01-0.67) and neovascular AMD (AOR = 0.15, CI = 0.03-0.72). A family history of AMD was a risk factor for early/intermediate (AOR = 4.08, CI = 2.30-7.25), geographic atrophy (AOR = 8.62, CI = 3.77-19.7), and neovascular AMD (AOR = 3.76, CI = 2.16-6.56). A history of asthma was related to the early/intermediate form of AMD (AOR = 2.34, CI = 1.22-4.46). CONCLUSION: Studying AMD in specific populations may reveal novel risk factors such as our finding of a relationship between asthma history and AMD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180202
[Lr] Last revision date:180202
[St] Status:Publisher
[do] DOI:10.1097/IAE.0000000000002023


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