Prevalence, Demographics, and Treatment Characteristics of Visual Impairment due to Diabetic Macular Edema in a Representative Canadian Cohort

Petrella, Robert J.; Blouin, Julie; Davies, Brian W.; Barbeau, M

doi:10.1155/2012/159167

Cited by 27 publications

(26 citation statements)

References 11 publications

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“…Based on various population estimates, DME affects between 3% and 16% of all diabetic adults 5,6. DME is debilitating because it may lead to progressive vision loss, negatively affecting the patient’s quality of life 4,7.…”

Section: Introductionmentioning

confidence: 99%

Comorbidity and health care visit burden in working-age commercially insured patients with diabetic macular edema

Kiss

Chandwani²,

Cole³

et al. 2016

OPTH

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PurposeTo examine the comorbidity profile and update estimates of health care resource utilization for commercially insured, working-age adults with diabetic macular edema (DME) relative to a matched comparison group of diabetic adults without DME. Additional comparisons were made in the subgroup of pseudophakic patients.Patients and methodsA retrospective matched-cohort study of commercially insured diabetic adults aged 18–63 years was conducted using medical and outpatient pharmacy claims (July 1, 2008–June 30, 2013). Outcomes included diabetes-related and ocular comorbidities and health care resource utilization (any health care visit days, outpatient visit days, inpatient visit days, emergency room visits, eye care-related visit days, unique medications) in the 12-month post-index period.ResultsAll diabetes-related and ocular comorbidities were significantly more prevalent in DME cases versus non-DME controls (P<0.05). A significantly greater proportion of DME cases utilized eye care-related visits compared with non-DME controls (P<0.001). DME cases had almost twice the mean number of total health care visit days compared to non-DME controls (28.6 vs 16.9 days, P<0.001), with a minority of visit days being eye care-related (mean 5.1 vs 1.5 days, P<0.001). Similar trends were observed in pseudophakic cohorts.ConclusionThis working-age DME population experienced a mean of 29 health care visit days per year. Eye care-related visit days were a minority of the overall visit burden (mean 5 days) emphasizing the trade-offs DME patients face between managing DME and their overall diabetic disease. Insights into the complex comorbidity profile and health care needs of diabetic patients with DME will better inform treatment decisions and help optimize disease management.

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Section: Introductionmentioning

confidence: 99%

Comorbidity and health care visit burden in working-age commercially insured patients with diabetic macular edema

Kiss

Chandwani²,

Cole³

et al. 2016

OPTH

View full text Add to dashboard Cite

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“…1 Diabetic macular edema (DME) is the most frequent cause of vision loss in diabetic retinopathy. 2 Recently, anti-VEGF therapy has been established as a first-line therapy for DME. The overall efficacy of anti-VEGF therapy for both anatomic and functional improvement has been established in multiple studies.…”

Section: Introductionmentioning

confidence: 99%

Optical Coherence Tomography Features in Diabetic Macular Edema and the Impact on Anti-VEGF Response

Itoh¹,

Petkovsek²,

Singh³

et al. 2016

Ophthalmic Surg Lasers Imaging Retina

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Purpose To assess the relationship between SDOCT features and functional outcomes for diabetic macular edema (DME) undergoing treatment with intravitreal bevacizumab. Methods IRB-approved retrospective consecutive case series of eyes receiving intravitreal bevacizumab (1.25 mg) for DME. SDOCT features were evaluated and correlated with functional response to anti-VEGF therapy. Results One hundred fifty-nine eyes of 159 subjects were included in this study. Mean visual acuity improved from 20/76 to 20/58. The proportion of eyes with 20/40 or greater visual acuity increased with treatment (35% at initial visit, 51% at final visit). SDOCT factors that were associated with functional outcomes to anti-VEGF therapy include ellipsoid zone integrity and severity of intraretinal fluid. Conclusions SDOCT features appear to provide important markers for functional response to anti-VEGF therapy in DME.

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“…Additionally, vascular permeability is increased and the blood-retinal barrier (BRB) is disrupted resulting in leakage of fluid into the retinal tissue. In diabetes, this may result in the development of diabetic macular edema, a leading cause of visual loss in diabetes [10]. Although various cells in the retina can be adversely affected by hypoxia, this review focuses on the death of the RGCs in hypoxia.…”

Section: Introductionmentioning

confidence: 99%

Cellular and Molecular Mechanisms of Retinal Ganglion Cell Death in Hypoxic-Ischemic Injuries

Kaur¹,

Rathnasamy²,

Foulds³

et al. 2015

J Neurol Exp Neurosci

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Loss of retinal ganglion cells (RGCs) occurs in retinal degenerative diseases, such as glaucoma, age-related macular degeneration, diabetic retinopathy, central retinal artery occlusion and ischemic central retinal vein thrombosis in adults and in retinopathy of prematurity in infants. A critical role of hypoxia, which underlies most of the above disorders, has been reported in causing RGC death. Disruption of blood-retinal barrier (BRB) occurs due to increased production of vascular endothelial growth factor and nitric oxide in response to hypoxia resulting in extravasation of serum derived substances and retinal edema and this may be one of important factors mediating RGC death. Activation of microglial cells in response to hypoxia and subsequent increased release of proinflammatory cytokines by them such as tumor-necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) target the TNF-receptor 1 and IL-receptor 1 on RGCs. Excess release of glutamate in retinal tissue under hypoxia activates the ionotropic glutamate receptors causing excitotoxicity through increased influx of calcium into the RGCs. Increased production of TNF-α, IL-1β and enhanced intracellular calcium results in RGC death through activating several pathways such as caspase signaling, mitochondrial dysfunction and oxidative stress. In our investigations, melatonin, an antioxidant, was shown to reduce RGC death in the adult and neonatal hypoxic retina, through suppression of TNF-α, IL-1β and glutamate levels as well as oxidative stress. Moreover, the function and structure of BRB was well preserved in these animals along with reduction in retinal edema. In view of our observations, we suggest that melatonin could be considered as a therapeutic agent to reduce RGC death in various retinal pathologies, in addition to other potential drugs/molecules of therapeutic interest that could render protection to RGCs. However, future in-depth research on the effects of melatonin on the retina under hypoxic conditions needs to be undertaken to explore its full potential in preventing/ameliorating RGC death. Factors Mediating RGC DeathSeveral factors induced or upregulated by hypoxia may be involved in causing RGC death. These factors include, among others, disruption of the blood-retinal barrier, activation of microglial cells and the accompanying enhanced release of inflammatory cytokines and excess release and accumulation of glutamate in the retinal tissues. Hypoxia and the blood-retinal barrierThe BRB regulates the passage of molecules from blood into the retina [11,12]. It consists of an inner BRB formed by the tight junctions (TJ) between capillary endothelial cells and an outer barrier formed by TJ between retinal pigment epithelial cells [12][13][14][15][16]. The TJ are made up of transmembrane proteins such as occludin, claudin-5 and cytoplasmic proteins such as zona occludens (ZO)-1 that are structurally and functionally important for maintaining the integrity of the BRB. The proper functioning of the inner BRB also requires the collective co...

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Prevalence, Demographics, and Treatment Characteristics of Visual Impairment due to Diabetic Macular Edema in a Representative Canadian Cohort

Cited by 27 publications

References 11 publications

Comorbidity and health care visit burden in working-age commercially insured patients with diabetic macular edema

Comorbidity and health care visit burden in working-age commercially insured patients with diabetic macular edema

Optical Coherence Tomography Features in Diabetic Macular Edema and the Impact on Anti-VEGF Response

Cellular and Molecular Mechanisms of Retinal Ganglion Cell Death in Hypoxic-Ischemic Injuries

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