Retinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriers
Autor(a) principal: | |
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Data de Publicação: | 2012 |
Outros Autores: | , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/handle/11600/35437 http://dx.doi.org/10.5301/ejo.5000154 |
Resumo: | PURPOSE. Recent investigations suggested that unaffected carriers of Leber hereditary optic neuropathy (LHON) may show subclinical visual alterations. Structural changes have also been detected by optical coherence tomography (007), which revealed a temporal thickening of the retinal nerve fiber layer (RNFL). These changes may reflect compensatory effects such as mitochondria accumulation within the RNFL axons. This study aimed to investigate whether the RNFL of LHON carriers shows greater than expected thickness variations, which may reflect transient subclinical changes, over the course of years.METHODS. Using Stratus OCT, the RNFL thickness was measured yearly from 2005 to 2008 in 24 Brazilian LHON carriers, all with homoplasmic 11778/ND4 mtDNA mutation. An Italian sample of 20 healthy subjects served as a control. Data were compared also to a previously published sample (n=59) of glaucomatous eyes.RESULTS. the LHON carriers showed test-retest standard deviations that were larger than normal controls in the temporal (p=0.004), superior (p<0.0001), and inferior quadrants (p=0.019). Compared to the glaucoma cases, no statistical differences were observed.CONCLUSIONS. the RNFL thickness in LHON carriers, when measured at different time points, has higher variability than in normal subjects. Transitory RNFL swelling may be caused either by compensatory mechanisms (increased mitochondrial biogenesis) or by axonal stasis preceding decompensation of retinal ganglion cells. in both situations, these changes may represent the origin of the visual alterations previously detected in LHON carriers. Alternatively, increased variability of RNFL thickness may be influenced by the LHON microangiopathy, as retinal blood vessels contribute to the OCT RNFL thickness measurements. |
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Barboni, PieroSavini, GiacomoFeuer, William J.Budenz, Donald L.Carbonelli, MicheleChicani, Filipe [UNIFESP]Ramos, Carolina do Val Ferreira [UNIFESP]Salomão, Solange Rios [UNIFESP]De Negri, AnnamariaParisi, VincenzoCarelli, ValerioSadun, Alfredo A.Studio Oculist dAzeglioUniv BolognaIRCCSUniv MiamiUniv So CalifUniversidade Federal de São Paulo (UNIFESP)Azienda San Camillo Forlanini2016-01-24T14:27:55Z2016-01-24T14:27:55Z2012-11-01European Journal of Ophthalmology. Milan: Wichtig Editore, v. 22, n. 6, p. 985-991, 2012.1120-6721http://repositorio.unifesp.br/handle/11600/35437http://dx.doi.org/10.5301/ejo.500015410.5301/ejo.5000154WOS:000312043200017PURPOSE. Recent investigations suggested that unaffected carriers of Leber hereditary optic neuropathy (LHON) may show subclinical visual alterations. Structural changes have also been detected by optical coherence tomography (007), which revealed a temporal thickening of the retinal nerve fiber layer (RNFL). These changes may reflect compensatory effects such as mitochondria accumulation within the RNFL axons. This study aimed to investigate whether the RNFL of LHON carriers shows greater than expected thickness variations, which may reflect transient subclinical changes, over the course of years.METHODS. Using Stratus OCT, the RNFL thickness was measured yearly from 2005 to 2008 in 24 Brazilian LHON carriers, all with homoplasmic 11778/ND4 mtDNA mutation. An Italian sample of 20 healthy subjects served as a control. Data were compared also to a previously published sample (n=59) of glaucomatous eyes.RESULTS. the LHON carriers showed test-retest standard deviations that were larger than normal controls in the temporal (p=0.004), superior (p<0.0001), and inferior quadrants (p=0.019). Compared to the glaucoma cases, no statistical differences were observed.CONCLUSIONS. the RNFL thickness in LHON carriers, when measured at different time points, has higher variability than in normal subjects. Transitory RNFL swelling may be caused either by compensatory mechanisms (increased mitochondrial biogenesis) or by axonal stasis preceding decompensation of retinal ganglion cells. in both situations, these changes may represent the origin of the visual alterations previously detected in LHON carriers. Alternatively, increased variability of RNFL thickness may be influenced by the LHON microangiopathy, as retinal blood vessels contribute to the OCT RNFL thickness measurements.Studio Oculist dAzeglio, I-40123 Bologna, ItalyUniv Bologna, Dipartimento Sci Neurol, Bologna, ItalyIRCCS, Fdn GB Bietti, Rome, ItalyUniv Miami, Miller Sch Med, Bascom Palmer Eye Inst, Dept Ophthalmol, Miami, FL 33136 USAUniv So Calif, Keck Sch Med, Dept Ophthalmol, Los Angeles, CA 90033 USAUniv So Calif, Keck Sch Med, Doheny Eye Inst, Los Angeles, CA 90033 USAUniversidade Federal de São Paulo, Dept Ophthalmol, UNIFESP, São Paulo, BrazilAzienda San Camillo Forlanini, Rome, ItalyUniversidade Federal de São Paulo, Dept Ophthalmol, UNIFESP, São Paulo, BrazilWeb of Science985-991engWichtig EditoreEuropean Journal of OphthalmologyLeber hereditary optic neuropathyRetinal nerve fiber layer thicknessRetinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriersinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/354372022-02-07 21:50:20.449metadata only accessoai:repositorio.unifesp.br:11600/35437Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-02-08T00:50:20Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Retinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriers |
title |
Retinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriers |
spellingShingle |
Retinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriers Barboni, Piero Leber hereditary optic neuropathy Retinal nerve fiber layer thickness |
title_short |
Retinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriers |
title_full |
Retinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriers |
title_fullStr |
Retinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriers |
title_full_unstemmed |
Retinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriers |
title_sort |
Retinal nerve fiber layer thickness variability in Leber hereditary optic neuropathy carriers |
author |
Barboni, Piero |
author_facet |
Barboni, Piero Savini, Giacomo Feuer, William J. Budenz, Donald L. Carbonelli, Michele Chicani, Filipe [UNIFESP] Ramos, Carolina do Val Ferreira [UNIFESP] Salomão, Solange Rios [UNIFESP] De Negri, Annamaria Parisi, Vincenzo Carelli, Valerio Sadun, Alfredo A. |
author_role |
author |
author2 |
Savini, Giacomo Feuer, William J. Budenz, Donald L. Carbonelli, Michele Chicani, Filipe [UNIFESP] Ramos, Carolina do Val Ferreira [UNIFESP] Salomão, Solange Rios [UNIFESP] De Negri, Annamaria Parisi, Vincenzo Carelli, Valerio Sadun, Alfredo A. |
author2_role |
author author author author author author author author author author author |
dc.contributor.institution.none.fl_str_mv |
Studio Oculist dAzeglio Univ Bologna IRCCS Univ Miami Univ So Calif Universidade Federal de São Paulo (UNIFESP) Azienda San Camillo Forlanini |
dc.contributor.author.fl_str_mv |
Barboni, Piero Savini, Giacomo Feuer, William J. Budenz, Donald L. Carbonelli, Michele Chicani, Filipe [UNIFESP] Ramos, Carolina do Val Ferreira [UNIFESP] Salomão, Solange Rios [UNIFESP] De Negri, Annamaria Parisi, Vincenzo Carelli, Valerio Sadun, Alfredo A. |
dc.subject.eng.fl_str_mv |
Leber hereditary optic neuropathy Retinal nerve fiber layer thickness |
topic |
Leber hereditary optic neuropathy Retinal nerve fiber layer thickness |
description |
PURPOSE. Recent investigations suggested that unaffected carriers of Leber hereditary optic neuropathy (LHON) may show subclinical visual alterations. Structural changes have also been detected by optical coherence tomography (007), which revealed a temporal thickening of the retinal nerve fiber layer (RNFL). These changes may reflect compensatory effects such as mitochondria accumulation within the RNFL axons. This study aimed to investigate whether the RNFL of LHON carriers shows greater than expected thickness variations, which may reflect transient subclinical changes, over the course of years.METHODS. Using Stratus OCT, the RNFL thickness was measured yearly from 2005 to 2008 in 24 Brazilian LHON carriers, all with homoplasmic 11778/ND4 mtDNA mutation. An Italian sample of 20 healthy subjects served as a control. Data were compared also to a previously published sample (n=59) of glaucomatous eyes.RESULTS. the LHON carriers showed test-retest standard deviations that were larger than normal controls in the temporal (p=0.004), superior (p<0.0001), and inferior quadrants (p=0.019). Compared to the glaucoma cases, no statistical differences were observed.CONCLUSIONS. the RNFL thickness in LHON carriers, when measured at different time points, has higher variability than in normal subjects. Transitory RNFL swelling may be caused either by compensatory mechanisms (increased mitochondrial biogenesis) or by axonal stasis preceding decompensation of retinal ganglion cells. in both situations, these changes may represent the origin of the visual alterations previously detected in LHON carriers. Alternatively, increased variability of RNFL thickness may be influenced by the LHON microangiopathy, as retinal blood vessels contribute to the OCT RNFL thickness measurements. |
publishDate |
2012 |
dc.date.issued.fl_str_mv |
2012-11-01 |
dc.date.accessioned.fl_str_mv |
2016-01-24T14:27:55Z |
dc.date.available.fl_str_mv |
2016-01-24T14:27:55Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
European Journal of Ophthalmology. Milan: Wichtig Editore, v. 22, n. 6, p. 985-991, 2012. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/handle/11600/35437 http://dx.doi.org/10.5301/ejo.5000154 |
dc.identifier.issn.none.fl_str_mv |
1120-6721 |
dc.identifier.doi.none.fl_str_mv |
10.5301/ejo.5000154 |
dc.identifier.wos.none.fl_str_mv |
WOS:000312043200017 |
identifier_str_mv |
European Journal of Ophthalmology. Milan: Wichtig Editore, v. 22, n. 6, p. 985-991, 2012. 1120-6721 10.5301/ejo.5000154 WOS:000312043200017 |
url |
http://repositorio.unifesp.br/handle/11600/35437 http://dx.doi.org/10.5301/ejo.5000154 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
European Journal of Ophthalmology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
985-991 |
dc.publisher.none.fl_str_mv |
Wichtig Editore |
publisher.none.fl_str_mv |
Wichtig Editore |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1802764145896980480 |