Retinal Ganglion Cell Loss in Children With Type 1 Diabetes Mellitus Without Diabetic Retinopathy

Kartı, Ömer; Nalbantoğlu, Özlem; Abali, Saygın; Ayhan, Zi̇ya; Tunç, Selma; Küsbeci, Tuncay; Özkan, Behzat

doi:10.3928/23258160-20170601-05

Cited by 27 publications

(39 citation statements)

References 19 publications

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“…Changes in inner retinal structure before the development of DR Due to advancements in in vivo spectral-domain optical coherence tomography (SD-OCT) imaging of the retina (Jaffe & Caprioli, 2004), retinal layer thickness can be measured in vivo in diabetic humans and animal models at similar stages of diabetes as the retinal and visual activity measurements described above. In humans with diabetes but no DR, OCT measurements in vivo have shown smaller total retinal thickness (Bronson-Castain et al, 2012;Chen et al, 2016), retinal nerve fiber layer (RNFL) (Lopes de Faria et al, 2002;Verma et al, 2012;Gundogan et al, 2016), ganglion cell layer (GCL) (Van Dijk et al, 2010), and inner retina (Karti et al, 2017). Other studies have not found retinal thinning (Park et al, 2011;Dhamdhere et al, 2012), suggesting that this is something that develops over the course of diabetes (Pinilla et al, 2020).…”

Section: Changes In In Vivo Inner Retinal Activity Before the Developmentioning

confidence: 99%

The effects of early diabetes on inner retinal neurons

Eggers

Carreon

2020

Vis Neurosci

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Diabetic retinopathy is now well understood as a neurovascular disease. Significant deficits early in diabetes are found in the inner retina that consists of bipolar cells that receive inputs from rod and cone photoreceptors, ganglion cells that receive inputs from bipolar cells, and amacrine cells that modulate these connections. These functional deficits can be measured in vivo in diabetic humans and animal models using the electroretinogram (ERG) and behavioral visual testing. Early effects of diabetes on both the human and animal model ERGs are changes to the oscillatory potentials that suggest dysfunctional communication between amacrine cells and bipolar cells as well as ERG measures that suggest ganglion cell dysfunction. These are coupled with changes in contrast sensitivity that suggest inner retinal changes. Mechanistic in vitro neuronal studies have suggested that these inner retinal changes are due to decreased inhibition in the retina, potentially due to decreased gamma aminobutyric acid (GABA) release, increased glutamate release, and increased excitation of retinal ganglion cells. Inner retinal deficits in dopamine levels have also been observed that can be reversed to limit inner retinal damage. Inner retinal targets present a promising new avenue for therapies for early-stage diabetic eye disease.

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Section: Changes In In Vivo Inner Retinal Activity Before the Developmentioning

confidence: 99%

The effects of early diabetes on inner retinal neurons

Eggers

Carreon

2020

Vis Neurosci

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“…1 Microvascular complications can occur in young people with T1DM, [2][3][4] and diabetic retinopathy (DR) is considered to be the earliest and most common complication. 5,6 Optical coherence tomography (OCT) has shown reduced thickness of the retinal nerve fiber and ganglion cell layers in children with T1DM without retinopathy, which is suggestive of early neuronal damage. [6][7][8] Furthermore, in vivo corneal confocal microscopy (IVCCM), a rapid noninvasive ophthalmic imaging technique has also been shown to identify early corneal cellular and nerve fiber pathology in children and adolescents with T1DM, 9 adults with T1DM without neuropathy, 10 or retinopathy or microalbuminuria.…”

mentioning

confidence: 99%

“…5,6 Optical coherence tomography (OCT) has shown reduced thickness of the retinal nerve fiber and ganglion cell layers in children with T1DM without retinopathy, which is suggestive of early neuronal damage. [6][7][8] Furthermore, in vivo corneal confocal microscopy (IVCCM), a rapid noninvasive ophthalmic imaging technique has also been shown to identify early corneal cellular and nerve fiber pathology in children and adolescents with T1DM, 9 adults with T1DM without neuropathy, 10 or retinopathy or microalbuminuria. 11 Furthermore, reduced corneal nerve fiber length predicts the development of clinical diabetic neuropathy 12 and the development or worsening of retinopathy.…”

mentioning

confidence: 99%

Longitudinal Changes in Corneal Cell and Nerve Fiber Morphology in Young Patients with Type 1 Diabetes with and without Diabetic Retinopathy: A 2-Year Follow-up Study

Deák

Szalai

Tóth

et al. 2019

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. We have previously used in vivo corneal confocal microscopy (IVCCM) to demonstrate significant alterations in the corneal epithelial cells, stromal keratocytes, and subbasal nerves in young patients with type 1 diabetes mellitis (T1DM), especially those with diabetic retinopathy (DR). We have evaluated the change in corneal cellular and subbasal nerve morphology over 2 years in young patients with T1DM with or without DR. METHODS. A total of 19 patients with T1DM, without (n ¼ 12) and with (n ¼ 7) DR and 19 ageand sex-matched healthy control subjects underwent quantification of corneal cellular and subbasal nerve plexus morphology by using IVCCM at baseline and after 2 years. RESULTS. There was no significant change in corneal basal epithelial, posterior stromal keratocyte, or endothelial cell densities over 2 years. However, there was a significant reduction in corneal nerve branch (P ¼ 0.03) and total nerve branch density (P ¼ 0.04) in patients without DR and a significant reduction in corneal nerve fibre density (P ¼ 0.004) in those with DR. CONCLUSIONS. IVCCM can detect a progressive loss of corneal nerve fibers in young patients with T1DM and may allow the identification of individuals at risk of neuropathy progression for more active risk factor reduction.

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“…Another recently published study confirmed these results, in part; however, it was assessing macular RNFL and GCL-IPL thickness in children with T1DM. Here, the GCL-IPL thickness was lower in all quadrants except the superior nasal quadrant in DM, while macular RNFL thickness showed no change [29].…”

Section: Studies Employing Sd-oct In Early Drmentioning

confidence: 75%

The Use of Optical Coherence Tomography for the Detection of Early Diabetic Retinopathy

Somfai

Gerding

DeBuc

2018

Klin Monatsbl Augenheilkd

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Diabetic retinopathy (DR) is one of the leading causes of vision loss globally with a severe burden on all societies due to its high treatment and rehabilitation costs. The early diagnosis of DR may provide preventive steps (including retinal laser therapy and tight carbohydrate, blood pressure, and cholesterol control) that could in turn help to avoid progression of the pathology with the resultant vision loss. Optical coherence tomography (OCT) enables the in vivo structural imaging of the retina, providing both qualitative (structure) and quantitative (thickness) information. In the past decades, extensive OCT research has been done in the field of DR. In the present review, we are focusing on those that were aiming at detection of the earliest retinal changes before DR could be diagnosed funduscopically. The latest, widely available technology of spectral-domain (SD-)OCT comes with a fast and reliable retinal imaging, which, together with the most recent developments in image processing and artificial intelligence, holds the promise of developing a quick and efficient, state-of-the-art screening tool for DR.

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Retinal Ganglion Cell Loss in Children With Type 1 Diabetes Mellitus Without Diabetic Retinopathy

Cited by 27 publications

References 19 publications

The effects of early diabetes on inner retinal neurons

The effects of early diabetes on inner retinal neurons

Longitudinal Changes in Corneal Cell and Nerve Fiber Morphology in Young Patients with Type 1 Diabetes with and without Diabetic Retinopathy: A 2-Year Follow-up Study

The Use of Optical Coherence Tomography for the Detection of Early Diabetic Retinopathy

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