Higher Numbers of Hyperreflective Foci Seen in the Vitreous on Spectral-Domain Optical Coherence Tomographic Images in Eyes with More Severe Diabetic Retinopathy

Mizukami, Takahiro; Hotta, Yosuke; Katai, Naomichi

doi:10.1159/000473886

Cited by 13 publications

(11 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Pronounced vessel dilation and beading, both of which were prominent in cytokine-treated NOD mice, are characteristic signs of pericyte loss, endothelial cell death, and BRB breakdown [ 30 ]. Vitreous HRF, also known as vitreous inflammatory cells, have been reported in patients with severe proliferative DR [ 31 , 32 ], and in animal models of ischemic optic neuropathy, these HRF are thought to be macrophages [ 33 ]. Authors of these studies, and others, believe that the presence of HRF within the vitreous reflects the infiltration of immune cells that contribute to vascular breakdown and endothelial cell damage [ 32 , 34 ].…”

Section: Discussionmentioning

confidence: 99%

Intravitreal pro-inflammatory cytokines in non-obese diabetic mice: Modelling signs of diabetic retinopathy

et al. 2018

View full text Add to dashboard Cite

Diabetic retinopathy is a vascular disease of the retina characterised by hyperglycaemic and inflammatory processes. Most animal models of diabetic retinopathy are hyperglycaemia-only models that do not account for the significant role that inflammation plays in the development of the disease. In the present study, we present data on the establishment of a new animal model of diabetic retinopathy that incorporates both hyperglycaemia and inflammation. We hypothesized that inflammation may trigger and worsen the development of diabetic retinopathy in a hyperglycaemic environment. Pro-inflammatory cytokines, IL-1β and TNF-α, were therefore injected into the vitreous of non-obese diabetic (NOD) mice. CD1 mice were used as same genetic background controls. Fundus and optical coherence tomography images were obtained before (day 0) as well as on days 2 and 7 after intravitreal cytokine injection to assess vessel dilation and beading, retinal and vitreous hyper-reflective foci and retinal thickness. Astrogliosis and microgliosis were assessed using immunohistochemistry. Results showed that intravitreal cytokines induced vessel dilation, beading, severe vitreous hyper-reflective foci, retinal oedema, increased astrogliosis and microglia upregulation in diabetic NOD mice. Intravitreal injection of inflammatory cytokines into the eyes of diabetic mice therefore appears to provide a new model of diabetic retinopathy that could be used for the study of disease progression and treatment strategies.

show abstract

Section: Discussionmentioning

confidence: 99%

Intravitreal pro-inflammatory cytokines in non-obese diabetic mice: Modelling signs of diabetic retinopathy

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Hyperreflective foci identified on SD-OCT imaging have been observed in patients with age-related macular degeneration, 26 diabetic retinopathy, 27,28 and RP. 29,30 The foci in age-related macular degeneration and diabetic retinopathy are believed to reflect macrophages, migrating RPE cells, and extravasated lipoproteins.…”

Section: Discussionmentioning

confidence: 99%

Disease Progression in Patients with Autosomal Dominant Retinitis Pigmentosa due to a Mutation in Inosine Monophosphate Dehydrogenase 1 (IMPDH1)

Bennett

Klein

John

et al. 2020

Trans. Vis. Sci. Tech.

View full text Add to dashboard Cite

Mutations in the inosine monophosphate dehydrogenase 1 (IMPDH1) gene are a common cause of inherited retinal degeneration (IRD). Due to species-and tissuedependent expression of IMPDH1, there are no appropriate models of human IMPDH1 disease. Therefore, a limited understanding remains of disease expression and rates of progression for IMPDH1-related IRD. Methods: We evaluated semiautomated kinetic and chromatic static perimetry, spectral-domain optical coherence tomography (SD-OCT), and ultra-wide field fundus images with autofluorescence in a cohort of 12 patients (ages 11-58 at first visit). Ten patients had longitudinal data for which rates of progression were estimated. Results: Visual acuities were relatively stable over time and the photoreceptors within the central retina remained intact. Perifoveal photoreceptor loss measured over a period of years coincided with visual fields, which were constricted and progressed over time in all patients. Rod sensitivity showed a similar pattern of defect to that of the kinetic perimetry and the autofluorescence ultra-wide field imaging. Full-field electroretinograms were severely reduced and the dark-adapted rod and mixed responses were extinguished at earlier visits than the light-adapted cone responses. Conclusions: There was variability in disease severity at the first visit, but results show that the peripheral retina is more susceptible to the deleterious consequences of an IMPDH1 mutation. Given the pattern of degeneration and the alternatively spliced isoforms of IMPDH1, potential interventions may consider targeting the periphery early in disease, modulating transcript expression, and/or preserving central vision at late stages of the disease. Translational Relevance: These results inform clinical prognosis and offer evidence strategies toward therapeutic intervention.

show abstract

“…125 DME-related cell damage and attraction of scavenger cells to the retina may be a plausible source of IL-6. 126 Vitreous hyperreflective foci have been described in eyes with severe DR. 127 Based on the previous findings that patients with proliferative diabetic retinopathy (PDR) had an increased number of T lymphocytes in the vitreous, 128 it has been hypothesized that vitreous hyperreflective foci correspond to inflammatory cells. Similarly, hyperreflective macrophage-like cells (MLCs) have been recently described on averaged 3-µm OCT en face slabs located above the inner limiting membrane surface.…”

Section: Imaging Biomarkers Of Inflammationmentioning

confidence: 99%

The role of inflammation and neurodegeneration in diabetic macular edema

et al. 2021

View full text Add to dashboard Cite

The pathogenesis of diabetic macular edema (DME) is complex. Persistently high blood glucose activates multiple cellular pathways and induces inflammation, oxidation stress, and vascular dysfunction. Retinal ganglion cells, macroglial and microglial cells, endothelial cells, pericytes, and retinal pigment epithelium cells are involved. Neurodegeneration, characterized by dysfunction or apoptotic loss of retinal neurons, occurs early and independently from the vascular alterations. Despite the increasing knowledge on the pathways involved in DME, only limited therapeutic strategies are available. Besides antiangiogenic drugs and intravitreal corticosteroids, alternative therapeutic options tackling inflammation, oxidative stress, and neurodegeneration have been considered, but none of them has been currently approved.

show abstract

Higher Numbers of Hyperreflective Foci Seen in the Vitreous on Spectral-Domain Optical Coherence Tomographic Images in Eyes with More Severe Diabetic Retinopathy

Cited by 13 publications

References 24 publications

Intravitreal pro-inflammatory cytokines in non-obese diabetic mice: Modelling signs of diabetic retinopathy

Intravitreal pro-inflammatory cytokines in non-obese diabetic mice: Modelling signs of diabetic retinopathy

Disease Progression in Patients with Autosomal Dominant Retinitis Pigmentosa due to a Mutation in Inosine Monophosphate Dehydrogenase 1 (IMPDH1)

The role of inflammation and neurodegeneration in diabetic macular edema

Contact Info

Product

Resources

About