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Complications
Pathophysiology of Diabetic Retinopathy: The Old and the New
Sentaro Kusuhara, Yoko Fukushima, Shuntaro Ogura, Naomi Inoue, Akiyoshi Uemura
Diabetes Metab J. 2018;42(5):364-376.   Published online October 22, 2018
DOI: https://doi.org/10.4093/dmj.2018.0182
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  • 122 Crossref
AbstractAbstract PDFPubReader   

Vision loss in diabetic retinopathy (DR) is ascribed primarily to retinal vascular abnormalities—including hyperpermeability, hypoperfusion, and neoangiogenesis—that eventually lead to anatomical and functional alterations in retinal neurons and glial cells. Recent advances in retinal imaging systems using optical coherence tomography technologies and pharmacological treatments using anti-vascular endothelial growth factor drugs and corticosteroids have revolutionized the clinical management of DR. However, the cellular and molecular mechanisms underlying the pathophysiology of DR are not fully determined, largely because hyperglycemic animal models only reproduce limited aspects of subclinical and early DR. Conversely, non-diabetic mouse models that represent the hallmark vascular disorders in DR, such as pericyte deficiency and retinal ischemia, have provided clues toward an understanding of the sequential events that are responsible for vision-impairing conditions. In this review, we summarize the clinical manifestations and treatment modalities of DR, discuss current and emerging concepts with regard to the pathophysiology of DR, and introduce perspectives on the development of new drugs, emphasizing the breakdown of the blood-retina barrier and retinal neovascularization.

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Original Articles
Intravitreal Ranibizumab for Subfoveal Choroidal Neovascularization from Age-Related Macular Degeneration with Combined Severe Diabetic Retinopathy
So Young Han, Jeong Hun Bae, Jaeryung Oh, Hyeong Gon Yu, Su Jeong Song
Diabetes Metab J. 2015;39(1):46-50.   Published online February 16, 2015
DOI: https://doi.org/10.4093/dmj.2015.39.1.46
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AbstractAbstract PDFPubReader   
Background

To evaluate the efficacy of intravitreal ranibizumab for subfoveal choroidal neovascularization (CNV) from age-related macular degeneration (AMD) with combined severe diabetic retinopathy (DR).

Methods

This retrospective, interventional case series included eleven patients (mean age, 70.09 years; range, 54 to 83 years) with at least severe non-proliferative DR and subfoveal CNV secondary to AMD. Each subject was treated with intravitreal injections of 0.5 mg ranibizumab. The primary outcomes included change in best-corrected visual acuity and central subfield thickness (CST) on optical coherence tomography (OCT).

Results

The mean follow-up time was 16.7±14 months (range, 6 to 31 months). Mean visual acuity improved from 1.21±0.80 logarithm of the minimum angle of resolution (logMAR) to 1.0±0.6 logMAR (P=0.107), 0.95±0.62 logMAR (P=0.044), 1.10±0.68 logMAR (P=0.296), and 1.13±0.66 logMAR (P=0.838) at 1, 3, 6, and 12 months after injection, respectively. Eight patients (72.7%) gained or maintained vision (mean 0.32 logMAR), whereas three patients (27.3%) lost more than one line of vision (mean 0.51 logMAR). The mean OCT CST was 343.9±134.6 µm at baseline, and the mean CST at 1, 3, 6, 12 months after the injection was 367.8±172.1 (P=0.864), 346.2±246.2 (P=0.857), 342±194.1 (P=0.551), and 294.2±108.3 µm (P=0.621), respectively.

Conclusion

Intravitreal ranibizumab injection can be considered to be a therapy for the stabilization of subfoveal CNV secondary to AMD with combined severe DR. However, these patients might exhibit limited visual improvement after treatment.

Citations

Citations to this article as recorded by  
  • Comparative study of widefield swept-source optical coherence tomography angiography in eyes with concomitant age-related macular degeneration and diabetic retinopathy
    Matthew Finn, Grace Baldwin, Itika Garg, Hannah E Wescott, Thomas Koch, Filippos Vingopoulos, Rebecca Zeng, Hanna Choi, Diane Sayah, Deeba Husain, Nimesh A Patel, Leo A Kim, Joan W Miller, David M Wu, Demetrios G Vavvas, John B Miller
    British Journal of Ophthalmology.2024; 108(7): 963.     CrossRef
  • Outcomes of intravitreal anti-VEGF therapy in eyes with both neovascular age-related macular degeneration and diabetic retinopathy
    Francesco Bandello, Federico Corvi, Carlo La Spina, Lucia Benatti, Lea Querques, Vittorio Capuano, Jonathan Naysan, Xuejing Chen, David Sarraf, Maurizio Battaglia Parodi, Eric Souied, K Bailey Freund, Giuseppe Querques
    British Journal of Ophthalmology.2016; 100(12): 1611.     CrossRef
VEGF-Angiopoietin-Tie2 System in Diabetic Retinopathy.
Nan Hee Kim, Hee Young Kim, Ji A Seo, Kye Won Lee, Sin Gon Kim, Kyung Mook Choi, Sei Hyun Baik, Yoon Shin Park, Inho Jo, Dong Seop Choi
Korean Diabetes J. 2005;29(2):122-132.   Published online March 1, 2005
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AbstractAbstract PDF
BACKGROUND
Ischemia-induced neovascularization can cause the loss of vision in retinal disorders such as diabetic retinopathy. Recent studies have shown that the angiopoietin-Tie2 system is a major regulator of vascular integrity and it is involved in pathologic angiogenesis. However, its role in the pathophysiology of diabetic retinopathy is not yet known. We examined the regulation of the VEGF-angiopoietin-Tie2 system in both in vitro and in vivo studies to discover their possible role in diabetic retinopathy. METHODS: We investigated the effects of a well-known angiogenic stimulus, hypoxia(2% O2 concentration) and vascular endothelial growth factor(VEGF, 10 ng/mL) on the expression of the angiopoietin-Tie2 mRNA in bovine retinal pericytes(BRP) and bovine aortic endothelial cells(BAEC). We also examined the expressions of VEGF-angiopoietin-Tie2 mRNA in retinas of type 2 diabetic OLETF(Otsuka-Long-Evans-Tokushima-Fatty) rats at 30 and 50 weeks. We also investigated the effect of angiotensin II receptor type 1(AT1) antagonist on the VEGFangiopoietin-Tie2 expression. RESULTS: Hypoxia and VEGF treatment significantly increased angiopoietin-1(Ang1) mRNA expression in the BRPs. In contrast, the angiopoietin-2(Ang2) mRNA expression was unaltered in the BRPs treated with hypoxia and VEGF. Significant up-regulation of Tie2 mRNA expression was found and this lasted up to 12 h. However, using BAECs, we found that only the Ang2 expression responded to these two angiogenic stimuli. In OLETF rats, the Ang-Tie2 expression patterns were similar with those of the BAECs. Ang2 and VEGF mRNA were increased at 30 and 50 weeks for the OLETF rats, whereas the Ang1 expression was not changed. The up-regulation of Ang2 and VEGF was decreased with the losartan treatment, an AT1 receptor antagonist. Tie2 mRNA expression was increased only at 50 weeks and it did not show any decrement by the losartan treatment. CONCLUSION: Our data suggest that hypoxia and VEGF treatment differentially regulate the angiopoietin-Tie2 system in the two vascular cells. Ang2 and VEGF expressions were predominantly increased in type 2 diabetic rats, and the unopposed action of Ang2 with VEGF might be involved in the development of diabetic retinopathy. The renin-angiotensin system may be a potential mechanism for the up-regulated VEGF-Ang2 system

Diabetes Metab J : Diabetes & Metabolism Journal
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