Predictors of Response to Intravitreal Anti–Vascular Endothelial Growth Factor Treatment of Age-Related Macular Degeneration
Purpose To identify factors that influence visual and anatomic response to treatment with intravitreal anti–vascular endothelial growth factor (VEGF) for neovascular age-related macular degeneration (AMD). Design Observational cohort study. Methods Seventy-two patients were included in this study. B...
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description | Purpose To identify factors that influence visual and anatomic response to treatment with intravitreal anti–vascular endothelial growth factor (VEGF) for neovascular age-related macular degeneration (AMD). Design Observational cohort study. Methods Seventy-two patients were included in this study. Best-corrected Snellen visual acuity (VA) and central foveal thickness measured on optical coherence tomography (OCT) at time of treatment and post-treatment follow-up visits were recorded. Associations between demographic, behavioral, and genetic risk factors and the 2 outcomes were analyzed using mixed-effects linear regression models. Two loci in complement factor H ( CFH ) were included in a risk score to determine the association between CFH risk and improvement in VA and central foveal thickness. Results There was a small improvement in VA following anti-VEGF treatment (mean: 3.7 ± 3.0 letters), which was not statistically significant. Significant improvement in VA was observed for the nonrisk CFH Y402H genotype ( P < .001) and for a low CFH risk score ( P = .019). Regarding the outcome of change in central foveal thickness, improvement was noted in all genotype groups, but reduction after treatment was significantly higher in the low CFH risk score group ( P = .033). A significant improvement in mean VA was seen among smokers ( P < .001), but this relationship was not observed for central foveal thickness. Conclusion After anti-VEGF therapy, significant improvement in VA was observed for low-risk CFH genotypes and subjects with a low risk score. There was a statistically significant reduction in central foveal thickness overall, and subjects with a low CFH risk score improved more than the high-risk group. |
doi_str_mv | 10.1016/j.ajo.2015.11.033 |
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Design Observational cohort study. Methods Seventy-two patients were included in this study. Best-corrected Snellen visual acuity (VA) and central foveal thickness measured on optical coherence tomography (OCT) at time of treatment and post-treatment follow-up visits were recorded. Associations between demographic, behavioral, and genetic risk factors and the 2 outcomes were analyzed using mixed-effects linear regression models. Two loci in complement factor H ( CFH ) were included in a risk score to determine the association between CFH risk and improvement in VA and central foveal thickness. Results There was a small improvement in VA following anti-VEGF treatment (mean: 3.7 ± 3.0 letters), which was not statistically significant. Significant improvement in VA was observed for the nonrisk CFH Y402H genotype ( P < .001) and for a low CFH risk score ( P = .019). Regarding the outcome of change in central foveal thickness, improvement was noted in all genotype groups, but reduction after treatment was significantly higher in the low CFH risk score group ( P = .033). A significant improvement in mean VA was seen among smokers ( P < .001), but this relationship was not observed for central foveal thickness. Conclusion After anti-VEGF therapy, significant improvement in VA was observed for low-risk CFH genotypes and subjects with a low risk score. There was a statistically significant reduction in central foveal thickness overall, and subjects with a low CFH risk score improved more than the high-risk group.</description><identifier>ISSN: 0002-9394</identifier><identifier>EISSN: 1879-1891</identifier><identifier>DOI: 10.1016/j.ajo.2015.11.033</identifier><identifier>PMID: 26705092</identifier><identifier>CODEN: AJOPAA</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Age ; Aged ; Aged, 80 and over ; Angiogenesis Inhibitors - therapeutic use ; Bevacizumab - therapeutic use ; Choroidal Neovascularization - drug therapy ; Choroidal Neovascularization - genetics ; Choroidal Neovascularization - physiopathology ; Cohort Studies ; Complement Factor H - genetics ; Female ; Genotype ; Humans ; Intravitreal Injections ; Macular degeneration ; Male ; Middle Aged ; Ophthalmology ; Polymorphism, Single Nucleotide ; Ranibizumab - therapeutic use ; Retina - pathology ; Retrospective Studies ; Risk Factors ; Studies ; Tomography ; Tomography, Optical Coherence ; Treatment Outcome ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - antagonists & inhibitors ; Visual Acuity - physiology ; Wet Macular Degeneration - drug therapy ; Wet Macular Degeneration - genetics ; Wet Macular Degeneration - physiopathology</subject><ispartof>American journal of ophthalmology, 2016-03, Vol.163, p.154-166.e8</ispartof><rights>Elsevier Inc.</rights><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Mar 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c604t-fe6831fe0da401ad0cf4a4023a7183d5ecabc69e5ee05febbe824fd492985b233</citedby><cites>FETCH-LOGICAL-c604t-fe6831fe0da401ad0cf4a4023a7183d5ecabc69e5ee05febbe824fd492985b233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ajo.2015.11.033$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26705092$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shah, Anjali R</creatorcontrib><creatorcontrib>Williams, Steven</creatorcontrib><creatorcontrib>Baumal, Caroline R</creatorcontrib><creatorcontrib>Rosner, Bernard</creatorcontrib><creatorcontrib>Duker, Jay S</creatorcontrib><creatorcontrib>Seddon, Johanna M</creatorcontrib><title>Predictors of Response to Intravitreal Anti–Vascular Endothelial Growth Factor Treatment of Age-Related Macular Degeneration</title><title>American journal of ophthalmology</title><addtitle>Am J Ophthalmol</addtitle><description>Purpose To identify factors that influence visual and anatomic response to treatment with intravitreal anti–vascular endothelial growth factor (VEGF) for neovascular age-related macular degeneration (AMD). Design Observational cohort study. Methods Seventy-two patients were included in this study. Best-corrected Snellen visual acuity (VA) and central foveal thickness measured on optical coherence tomography (OCT) at time of treatment and post-treatment follow-up visits were recorded. Associations between demographic, behavioral, and genetic risk factors and the 2 outcomes were analyzed using mixed-effects linear regression models. Two loci in complement factor H ( CFH ) were included in a risk score to determine the association between CFH risk and improvement in VA and central foveal thickness. Results There was a small improvement in VA following anti-VEGF treatment (mean: 3.7 ± 3.0 letters), which was not statistically significant. Significant improvement in VA was observed for the nonrisk CFH Y402H genotype ( P < .001) and for a low CFH risk score ( P = .019). Regarding the outcome of change in central foveal thickness, improvement was noted in all genotype groups, but reduction after treatment was significantly higher in the low CFH risk score group ( P = .033). A significant improvement in mean VA was seen among smokers ( P < .001), but this relationship was not observed for central foveal thickness. Conclusion After anti-VEGF therapy, significant improvement in VA was observed for low-risk CFH genotypes and subjects with a low risk score. There was a statistically significant reduction in central foveal thickness overall, and subjects with a low CFH risk score improved more than the high-risk group.</description><subject>Age</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Angiogenesis Inhibitors - therapeutic use</subject><subject>Bevacizumab - therapeutic use</subject><subject>Choroidal Neovascularization - drug therapy</subject><subject>Choroidal Neovascularization - genetics</subject><subject>Choroidal Neovascularization - physiopathology</subject><subject>Cohort Studies</subject><subject>Complement Factor H - genetics</subject><subject>Female</subject><subject>Genotype</subject><subject>Humans</subject><subject>Intravitreal Injections</subject><subject>Macular degeneration</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Ophthalmology</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Ranibizumab - therapeutic use</subject><subject>Retina - pathology</subject><subject>Retrospective Studies</subject><subject>Risk Factors</subject><subject>Studies</subject><subject>Tomography</subject><subject>Tomography, Optical Coherence</subject><subject>Treatment Outcome</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - antagonists & inhibitors</subject><subject>Visual Acuity - physiology</subject><subject>Wet Macular Degeneration - drug therapy</subject><subject>Wet Macular Degeneration - genetics</subject><subject>Wet Macular Degeneration - physiopathology</subject><issn>0002-9394</issn><issn>1879-1891</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9ksFu1DAQhi0EokvhAbigSFy4JLXjOImFVGlV2lKpCFQKV8txJrtevPZiO4t6QbwDb8iT1NEuBXrg5LHmm1_-_Q9CzwkuCCb10aqQK1eUmLCCkAJT-gDNSNvwnLScPEQzjHGZc8qrA_QkhFW61k3VPEYHZd1ghnk5Q98_eOi1is6HzA3ZFYSNswGy6LILG73c6uhBmmxuo_714-dnGdRopM9Obe_iEoxOvXPvvsVldiYnmew68XENNk568wXkV2BkhD57J3ejb2ABFryM2tmn6NEgTYBn-_MQfTo7vT55m1--P784mV_mqsZVzAeoW0oGwL2sMJE9VkOVqpLKhrS0Z6Bkp2oODACzAboO2rIa-oqXvGVdSekhOt7pbsZuDb2CyZsRG6_X0t8IJ7X4t2P1UizcVtQ15oThJPBqL-Dd1xFCFGsdFBgjLbgxCNLULWN1xXlCX95DV270NtnbUymHJlFkRynvQvAw3D2GYDGlK1YipSumdAUhIqWbZl787eJu4necCXi9AyD95VaDF0FpsCpF7EFF0Tv9X_nje9PKaKuVNF_gBsIfFyKUAouP03pN20UYTWXb0lsUC83_</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Shah, Anjali R</creator><creator>Williams, Steven</creator><creator>Baumal, Caroline R</creator><creator>Rosner, Bernard</creator><creator>Duker, Jay S</creator><creator>Seddon, Johanna M</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160301</creationdate><title>Predictors of Response to Intravitreal Anti–Vascular Endothelial Growth Factor Treatment of Age-Related Macular Degeneration</title><author>Shah, Anjali R ; Williams, Steven ; Baumal, Caroline R ; Rosner, Bernard ; Duker, Jay S ; Seddon, Johanna M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c604t-fe6831fe0da401ad0cf4a4023a7183d5ecabc69e5ee05febbe824fd492985b233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Age</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Angiogenesis Inhibitors - therapeutic use</topic><topic>Bevacizumab - therapeutic use</topic><topic>Choroidal Neovascularization - drug therapy</topic><topic>Choroidal Neovascularization - genetics</topic><topic>Choroidal Neovascularization - physiopathology</topic><topic>Cohort Studies</topic><topic>Complement Factor H - genetics</topic><topic>Female</topic><topic>Genotype</topic><topic>Humans</topic><topic>Intravitreal Injections</topic><topic>Macular degeneration</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Ophthalmology</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Ranibizumab - therapeutic use</topic><topic>Retina - pathology</topic><topic>Retrospective Studies</topic><topic>Risk Factors</topic><topic>Studies</topic><topic>Tomography</topic><topic>Tomography, Optical Coherence</topic><topic>Treatment Outcome</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - antagonists & inhibitors</topic><topic>Visual Acuity - physiology</topic><topic>Wet Macular Degeneration - drug therapy</topic><topic>Wet Macular Degeneration - genetics</topic><topic>Wet Macular Degeneration - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shah, Anjali R</creatorcontrib><creatorcontrib>Williams, Steven</creatorcontrib><creatorcontrib>Baumal, Caroline R</creatorcontrib><creatorcontrib>Rosner, Bernard</creatorcontrib><creatorcontrib>Duker, Jay S</creatorcontrib><creatorcontrib>Seddon, Johanna M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of ophthalmology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shah, Anjali R</au><au>Williams, Steven</au><au>Baumal, Caroline R</au><au>Rosner, Bernard</au><au>Duker, Jay S</au><au>Seddon, Johanna M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Predictors of Response to Intravitreal Anti–Vascular Endothelial Growth Factor Treatment of Age-Related Macular Degeneration</atitle><jtitle>American journal of ophthalmology</jtitle><addtitle>Am J Ophthalmol</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>163</volume><spage>154</spage><epage>166.e8</epage><pages>154-166.e8</pages><issn>0002-9394</issn><eissn>1879-1891</eissn><coden>AJOPAA</coden><abstract>Purpose To identify factors that influence visual and anatomic response to treatment with intravitreal anti–vascular endothelial growth factor (VEGF) for neovascular age-related macular degeneration (AMD). Design Observational cohort study. Methods Seventy-two patients were included in this study. Best-corrected Snellen visual acuity (VA) and central foveal thickness measured on optical coherence tomography (OCT) at time of treatment and post-treatment follow-up visits were recorded. Associations between demographic, behavioral, and genetic risk factors and the 2 outcomes were analyzed using mixed-effects linear regression models. Two loci in complement factor H ( CFH ) were included in a risk score to determine the association between CFH risk and improvement in VA and central foveal thickness. Results There was a small improvement in VA following anti-VEGF treatment (mean: 3.7 ± 3.0 letters), which was not statistically significant. Significant improvement in VA was observed for the nonrisk CFH Y402H genotype ( P < .001) and for a low CFH risk score ( P = .019). Regarding the outcome of change in central foveal thickness, improvement was noted in all genotype groups, but reduction after treatment was significantly higher in the low CFH risk score group ( P = .033). A significant improvement in mean VA was seen among smokers ( P < .001), but this relationship was not observed for central foveal thickness. Conclusion After anti-VEGF therapy, significant improvement in VA was observed for low-risk CFH genotypes and subjects with a low risk score. There was a statistically significant reduction in central foveal thickness overall, and subjects with a low CFH risk score improved more than the high-risk group.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26705092</pmid><doi>10.1016/j.ajo.2015.11.033</doi><oa>free_for_read</oa></addata></record> |
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subjects | Age Aged Aged, 80 and over Angiogenesis Inhibitors - therapeutic use Bevacizumab - therapeutic use Choroidal Neovascularization - drug therapy Choroidal Neovascularization - genetics Choroidal Neovascularization - physiopathology Cohort Studies Complement Factor H - genetics Female Genotype Humans Intravitreal Injections Macular degeneration Male Middle Aged Ophthalmology Polymorphism, Single Nucleotide Ranibizumab - therapeutic use Retina - pathology Retrospective Studies Risk Factors Studies Tomography Tomography, Optical Coherence Treatment Outcome Vascular endothelial growth factor Vascular Endothelial Growth Factor A - antagonists & inhibitors Visual Acuity - physiology Wet Macular Degeneration - drug therapy Wet Macular Degeneration - genetics Wet Macular Degeneration - physiopathology |
title | Predictors of Response to Intravitreal Anti–Vascular Endothelial Growth Factor Treatment of Age-Related Macular Degeneration |
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