Visual complications in diabetes mellitus: beyond retinopathy

Khan, Adnan; Petropoulos, Ioannis N.; Ponirakis, Georgios; Malik, Rayaz A.

doi:10.1111/dme.13296

Cited by 72 publications

(55 citation statements)

References 58 publications

(86 reference statements)

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“…Diabetes mellitus is often associated with progressive loss of vision and is one of the fastest-growing health problems in the world 1 , 2 . The loss of vision is more likely to occur in people with type 2 diabetes than in older adults without type 2 diabetes 3 , 4 . This has been explained based on the presence of proliferative diabetic retinopathy and clinically significant macular edema.…”

Section: Introductionmentioning

confidence: 99%

Prevalence and causes of low vision and blindness in a Chinese population with type 2 diabetes: the Dongguan Eye Study

Cui

Zhang

et al. 2017

Sci Rep

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To assess the prevalence and causes of low vision and blindness in type 2 diabetes patients, a population-based cross-sectional study including 8952 rural-dwelling residents aged 40 years or older from Hengli Town in Southern China was conducted. Participants underwent standard interviews, physical measurements, laboratory tests, and comprehensive eye examinations. Low vision and blindness were defined based on WHO criteria. Visual acuity data were available for 1348 (89.9%) of the 1500 subjects with type 2 diabetes. Age-standardized prevalence of bilateral low vision and blindness assessed in the better-seeing eye was 2.9% (95% confidence interval [CI]: 2.0–3.8) and 0.7% (95% CI: 0.2–1.1) based on best-corrected visual acuity (BCVA). Cataracts were the primary cause of low vision and blindness. Visual impairment was associated with age (odds ratio [OR]: 3.73, 95% CI: 2.39–5.83), education level (OR: 3.21, 95% CI: 1.63–6.29), duration of diabetes (OR: 1.14, 95% CI: 1.04–1.25) and body mass index (OR: 0.86, 95% CI: 0.77–0.95). Our data suggest that approximately 70% of visual impairment in this diabetic population could be eliminated with appropriate cataract surgery or spectacle correction. Greater consideration should be given to older type 2 diabetes patients with a level of lower education.

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Section: Introductionmentioning

confidence: 99%

Prevalence and causes of low vision and blindness in a Chinese population with type 2 diabetes: the Dongguan Eye Study

Cui

Zhang

et al. 2017

Sci Rep

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“…T he most common eye complication of diabetes is retinopathy; however, several additional complications including cataract, glaucoma, refractive alterations, and dry eye contribute to the morbidity of diabetic eye disease. 1,2 Indeed, dry eye has a reported prevalence of~54.3% and is associated with an increased risk of epithelial defects and corneal ulcers in patients with diabetes. [3][4][5] Diabetic keratopathy can manifest as recurrent corneal erosions, ulceration, and delayed wound healing after surgery, 6 superficial punctate keratopathy, and neurotrophic keratitis.…”

mentioning

confidence: 99%

No Relation Between the Severity of Corneal Nerve, Epithelial, and Keratocyte Cell Morphology With Measures of Dry Eye Disease in Type 1 Diabetes

Ferdousi

Petropoulos

Kalteniece

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Patients with diabetes have a propensity to develop dry eye symptoms (DES), with reduced tear secretion and corneal sensitivity. The underlying pathologic basis of DES was explored in patients with Type 1 diabetes. METHODS. Forty-two patients with Type 1 diabetes mellitus (T1DM) (age: 49.21 6 2.53 years, duration of diabetes: 29.98 6 2.64 years) and 25 control subjects (age: 48.70 6 2.84 years) underwent assessment of DES using a validated dry eye questionnaire, and tear stability and tear production were assessed using tear breakup time (TBUT) and Schirmer's test, respectively. Corneal confocal microscopy was undertaken to quantify corneal nerve fiber density (CNFD), branch density (CNBD), fiber length (CNFL), keratocyte density (KD), and corneal epithelial basal cell (CEBC) density and area. RESULTS. The prevalence of DES was significantly higher (P ¼ 0.03), and TBUT (P ¼ 0.006), corneal sensation (P < 0.0001), CNFD (P ¼ 0.001), CNBD (P ¼ 0.001), CNFL (P ¼ 0.003), and KD (P ¼ 0.04) were significantly lower in patients with T1DM compared to control subjects. However, these measures did not differ significantly between T1DM patients with and without dry eye. There was no correlation between DES and TBUT or corneal nerve keratocyte and CEBC morphology. CONCLUSIONS. DES and TBUT are significantly increased in patients with T1DM, but are not related to corneal nerve, basal epithelial, or keratocyte cell morphology.

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“…During that time, GLP-1R agonists have demonstrated a favorable safety profile in the long-term treatment of type 2 diabetes mellitus (Aroda, 2018). Diabetes is a known risk factor in glaucoma (Khan et al, 2016), and GLP-1R's wide usage in diabetes treatment presents an opportunity to retrospectively evaluate its effects among patients with glaucoma and type 2 diabetes in a large scale observational study. The findings of that study could provide evidence as to whether existing GLP-1R agonists reduce glaucoma incidence or progression among patients with diabetes.…”

Section: Discussionmentioning

confidence: 99%

GLP-1R agonist NLY01 reduces retinal inflammation, astrocyte reactivity, and retinal ganglion cell death secondary to ocular hypertension

Sterling

Adetunji

Guttha

et al. 2020

Preprint

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Glaucoma is the leading cause of irreversible blindness worldwide and is characterized by the death of retinal ganglion cells. Reduction of intraocular pressure (IOP) is the only therapeutic mechanism available to slow disease progression. However, glaucoma can continue to progress despite normalization of IOP. New treatments are needed to reduce vision loss and improve outcomes for patients who have exhausted existing therapeutic avenues. Recent studies have implicated neuroinflammation in the pathogenesis of neurodegenerative diseases of both the retina and the brain, including glaucoma and Parkinson's disease. Pro-inflammatory A1 astrocytes contribute to neuronal cell death in multiple disease processes and have been targeted therapeutically in mouse models of Parkinson's disease. Microglial release of pro-inflammatory cytokines C1q, IL-1α, and TNF-α is sufficient to drive the formation of A1 astrocytes. The role of A1 astrocytes in glaucoma pathogenesis has not been explored. Using a mouse model of glaucoma, we demonstrated that IOP elevation was sufficient to trigger production of C1q, IL-1α, and TNF-α by infiltrating macrophages followed by resident microglia. These three cytokines drove the formation of A1 astrocytes in the retina. Furthermore, cytokine production and A1 astrocyte transformation persisted following IOP normalization. Ablation of this pathway, by either genetic deletions of C1q, IL-1α, and TNF-α, or treatment with glucagon-like peptide-1 receptor agonist NLY01, reduced A1 astrocyte transformation and RGC death. Together, these results highlight a new neuroinflammatory mechanism behind glaucomatous neurodegeneration that can be therapeutically targeted by NLY01 administration.

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Visual complications in diabetes mellitus: beyond retinopathy

Cited by 72 publications

References 58 publications

Prevalence and causes of low vision and blindness in a Chinese population with type 2 diabetes: the Dongguan Eye Study

Prevalence and causes of low vision and blindness in a Chinese population with type 2 diabetes: the Dongguan Eye Study

No Relation Between the Severity of Corneal Nerve, Epithelial, and Keratocyte Cell Morphology With Measures of Dry Eye Disease in Type 1 Diabetes

GLP-1R agonist NLY01 reduces retinal inflammation, astrocyte reactivity, and retinal ganglion cell death secondary to ocular hypertension

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