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Association between neurodegeneration and macular perfusion in the progression of diabetic retinopathy: a 3-year longitudinal study

dc.contributor.authorMarques, Inês P.
dc.contributor.authorFerreira, Sónia
dc.contributor.authorSantos, Torcato
dc.contributor.authorMadeira, Maria H.
dc.contributor.authorSantos, Ana Rita
dc.contributor.authorMendes, Luís
dc.contributor.authorLobo, Conceição
dc.contributor.authorCunha-Vaz, José
dc.date.accessioned2022-12-13T18:11:08Z
dc.date.available2022-12-13T18:11:08Z
dc.date.issued2022-08
dc.description.abstractThe aim of this study was to explore the relation between retinal neurodegenerative changes and vessel closure (VC) in individuals with nonproliferative diabetic retinopathy (NPDR) in a follow-up period of 3 years. This is a 3-year prospective longitudinal study with four annual visits. This study involved 74 individuals with type 2 diabetes, NPDR, and Early Treatment Diabetic Retinopathy Study grades from 10 to 47, one eye/person. An age-matched healthy control population of 84 eyes was used as control group. Participants were annually examined by color fundus photography, spectral domain-optical coherence tomography (SD-OCT) and OCT-angiography (OCTA). VC was assessed by OCTA vessel density maps. SD-OCT segmentations were performed to access central retinal thickness (CRT) and retinal neurodegeneration considered as thinning of the ganglion cell plus inner plexiform layer (GCL + IPL). Results: Type 2 diabetic individuals presented significantly higher CRT (p = 0.001), GCL + IPL thinning (p = 0.042), and decreased vessel density at the superficial capillary plexus (p < 0.001) and full retina (FR) (p = 0.001). When looking at changes occurring over the 3-year period of follow-up (Table 2), there were statistically significant decreases in GCL + IPL thickness (−0.438 μm/year; p = 0.038), foveal avascular zone circularity (−0.009; p = 0.047), and vessel density in superficial capillary plexus (−0.172 mm−1/year; p < 0.001), deep capillary plexus (DCP) (−0.350 mm−1/year; p < 0.001), and FR (−0.182 mm−1/year; p < 0.001). A statistically significant association was identified between GCL + IPL thinning and decrease in DCP vessel density (β = 0.196 [95% confidence interval: 0.037, 0.355], z = 2.410, p = 0.016), after controlling for age, gender, diabetes duration, hemoglobin A1c level, and CRT. Retinal neurodegenerative changes show a steady progression during a 3-year period of follow-up in eyes with NPDR and appear to be directly associated with progression in decreased vessel density including vascular closure through preferential involvement of the DCP. Our findings provide evidence that retinal neuropathy is linked with microvascular changes occurring in diabetic patients.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationMarques, I. P., Ferreira, S., Santos, T., Madeira, M. H., Santos, A. R., Mendes, L., Lobo, C., & Cunha-Vaz, J. (2022). Association between Neurodegeneration and Macular Perfusion in the Progression of Diabetic Retinopathy: A 3-Year Longitudinal Study. Ophthalmologica, 245(4), 335–341. https://doi.org/10.1159/000522527pt_PT
dc.identifier.doihttps://doi.org/10.1159/000522527pt_PT
dc.identifier.issn0030-3755
dc.identifier.issn1423-0267
dc.identifier.urihttp://hdl.handle.net/10400.22/21189
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherKargerpt_PT
dc.relation.publisherversionhttps://www.karger.com/Article/FullText/522527pt_PT
dc.subjectDiabetespt_PT
dc.subjectRetinopathypt_PT
dc.subjectNeurodegenerationpt_PT
dc.subjectVessel closurept_PT
dc.subjectProgressionpt_PT
dc.titleAssociation between neurodegeneration and macular perfusion in the progression of diabetic retinopathy: a 3-year longitudinal studypt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage341pt_PT
oaire.citation.startPage335pt_PT
oaire.citation.titleOphthalmologicapt_PT
oaire.citation.volume245pt_PT
person.familyNameSantos
person.givenNameAna Rita
person.identifier.ciencia-id0911-4138-0C3A
person.identifier.orcid0000-0003-0139-0285
rcaap.rightsclosedAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationd71931b8-d869-4334-993c-ba14ad713f01
relation.isAuthorOfPublication.latestForDiscoveryd71931b8-d869-4334-993c-ba14ad713f01

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