Genetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic population

Age-related macular degeneration (AMD) is the leading cause of visual impairment in patients over 55 years. Currently, the most common therapies for neovascular AMD (nAMD) are intravitreal antiangiogenics. Studies suggest that genetic factors influence on antiangiogenics therapy outcomes. The purpos...

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Tipo de recurso:
Fecha de publicación:
2019
Institución:
Universidad del Rosario
Repositorio:
Repositorio EdocUR - U. Rosario
Idioma:
eng
OAI Identifier:
oai:repository.urosario.edu.co:10336/23364
Acceso en línea:
https://doi.org/10.4103/tjo.tjo_72_19
https://repository.urosario.edu.co/handle/10336/23364
Palabra clave:
Angiogenesis inhibitors
Hispanic Americans
Macular degeneration
Polymorphism
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spelling 65835231-3f4b-4f2f-91eb-b382dddebc11-1e49020d5-9478-4cf8-8b40-00612e5d5a5f-16b752734-7b0a-4027-8bed-03ce64ddcbde-1e2fac31d-383e-45d4-bd1d-ac69caceeb7a-1a9725f07-a013-47c5-a7ab-68888e1b2c57-1ba748577-bb0f-4e5f-8736-b40c337cb8c3-1d8c1ebf7-c731-45e6-9395-74ff3da0f778-12020-05-26T00:01:25Z2020-05-26T00:01:25Z2019Age-related macular degeneration (AMD) is the leading cause of visual impairment in patients over 55 years. Currently, the most common therapies for neovascular AMD (nAMD) are intravitreal antiangiogenics. Studies suggest that genetic factors influence on antiangiogenics therapy outcomes. The purpose of this work was to establish the association between complement factor H (CFH) (Y402H), age-related maculopathy susceptibility 2 (ARMS2) (A69S), and high-temperature requirement factor A1 (HTRA1) (rs11200638) polymorphisms and the response to treatment with ranibizumab in patients with nAMD. METHODS: A cross-sectional study with 61 eyes with nAMD treated with ranibizumab was performed. Association between polymorphisms from CFH, ARMS2, and HTRA1 with the response to treatment was established. RESULTS: The mean age of patients was 76.6 (51-91) years. Only 37.7% of patients had a functional response and 26.2% had an anatomic response. TT polymorphism Y402H from CFH gene was associated with an increased likelihood of functional response to treatment. Otherwise, there was not a statistically significant association between anatomic and functional response to gene polymorphisms rs11200638 from HTRA1 and rs10490924 from ARMS 2. CONCLUSIONS: This study suggests that the response to intravitreal antiangiogenic therapy with ranibizumab was not associated to main polymorphisms from genes HTRA1 and ARMS2. However, it was found that the response to treatment differed according to CFH genotype, suggesting that further investigations are needed to establish if patients with the CC and TC genotype may need to be monitored more closely for disease recurrence than the TT genotype. © 2019 Taiwan J Ophthalmolapplication/pdfhttps://doi.org/10.4103/tjo.tjo_72_192211505622115072https://repository.urosario.edu.co/handle/10336/23364engWolters Kluwer Medknow Publications248No. 4243Taiwan Journal of OphthalmologyVol. 9Taiwan Journal of Ophthalmology, ISSN:22115056, 22115072, Vol.9, No.4 (2019); pp. 243-248https://www.scopus.com/inward/record.uri?eid=2-s2.0-85076821403&doi=10.4103%2ftjo.tjo_72_19&partnerID=40&md5=29a50709a6b9063a5aa2a0a40520a4f0Abierto (Texto Completo)http://purl.org/coar/access_right/c_abf2instname:Universidad del Rosarioreponame:Repositorio Institucional EdocURAngiogenesis inhibitorsHispanic AmericansMacular degenerationPolymorphismGenetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic populationarticleArtículohttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_6501Rodríguez, Francisco JoseRios, Hernan AndresAguilar, María CamilaRosenstiehl, Shirley MargaritaGelvez, NancyLopez, GreizyTamayo, Martha LORIGINALTaiwanJOphthalmol94243-559071_153147.pdfapplication/pdf531847https://repository.urosario.edu.co/bitstreams/8c43cbcd-5760-4bbe-a406-8ebdc1c25b24/download66b74f37e7cc75ac327402d5b67aa5cfMD51TEXTTaiwanJOphthalmol94243-559071_153147.pdf.txtTaiwanJOphthalmol94243-559071_153147.pdf.txtExtracted texttext/plain27305https://repository.urosario.edu.co/bitstreams/2733816c-7d4d-49b5-a68a-793dd54cd357/download5e3399596bc2c93a0e296c590a3a238eMD52THUMBNAILTaiwanJOphthalmol94243-559071_153147.pdf.jpgTaiwanJOphthalmol94243-559071_153147.pdf.jpgGenerated Thumbnailimage/jpeg4789https://repository.urosario.edu.co/bitstreams/a510a7e3-433e-45c2-a03c-570513bf3b3d/download534dc3b1eb1b38c310085143b5e3ea0aMD5310336/23364oai:repository.urosario.edu.co:10336/233642022-05-02 07:37:21.468066https://repository.urosario.edu.coRepositorio institucional EdocURedocur@urosario.edu.co
dc.title.spa.fl_str_mv Genetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic population
title Genetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic population
spellingShingle Genetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic population
Angiogenesis inhibitors
Hispanic Americans
Macular degeneration
Polymorphism
title_short Genetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic population
title_full Genetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic population
title_fullStr Genetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic population
title_full_unstemmed Genetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic population
title_sort Genetic association with intravitreal ranibizumab response for neovascular age-related macular degeneration in Hispanic population
dc.subject.keyword.spa.fl_str_mv Angiogenesis inhibitors
Hispanic Americans
Macular degeneration
Polymorphism
topic Angiogenesis inhibitors
Hispanic Americans
Macular degeneration
Polymorphism
description Age-related macular degeneration (AMD) is the leading cause of visual impairment in patients over 55 years. Currently, the most common therapies for neovascular AMD (nAMD) are intravitreal antiangiogenics. Studies suggest that genetic factors influence on antiangiogenics therapy outcomes. The purpose of this work was to establish the association between complement factor H (CFH) (Y402H), age-related maculopathy susceptibility 2 (ARMS2) (A69S), and high-temperature requirement factor A1 (HTRA1) (rs11200638) polymorphisms and the response to treatment with ranibizumab in patients with nAMD. METHODS: A cross-sectional study with 61 eyes with nAMD treated with ranibizumab was performed. Association between polymorphisms from CFH, ARMS2, and HTRA1 with the response to treatment was established. RESULTS: The mean age of patients was 76.6 (51-91) years. Only 37.7% of patients had a functional response and 26.2% had an anatomic response. TT polymorphism Y402H from CFH gene was associated with an increased likelihood of functional response to treatment. Otherwise, there was not a statistically significant association between anatomic and functional response to gene polymorphisms rs11200638 from HTRA1 and rs10490924 from ARMS 2. CONCLUSIONS: This study suggests that the response to intravitreal antiangiogenic therapy with ranibizumab was not associated to main polymorphisms from genes HTRA1 and ARMS2. However, it was found that the response to treatment differed according to CFH genotype, suggesting that further investigations are needed to establish if patients with the CC and TC genotype may need to be monitored more closely for disease recurrence than the TT genotype. © 2019 Taiwan J Ophthalmol
publishDate 2019
dc.date.created.spa.fl_str_mv 2019
dc.date.accessioned.none.fl_str_mv 2020-05-26T00:01:25Z
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dc.identifier.issn.none.fl_str_mv 22115056
22115072
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dc.relation.citationTitle.none.fl_str_mv Taiwan Journal of Ophthalmology
dc.relation.citationVolume.none.fl_str_mv Vol. 9
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