Intravitreal steroids for macular edema in diabetes

Rittiphairoj, Thanitsara; Mir, Tahreem A.; Li, Tianjing; Virgili, Gianni

doi:10.1002/14651858.cd005656.pub3

Cited by 26 publications

(29 citation statements)

References 119 publications

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“…Initiation of the inflammatory response that is linked to the early stages of the pathogenesis of DR was demonstrated initially by leukocyte-mediated endothelial cell injury and death in animal models ( Joussen et al, 2001 , 2004 ). Indeed, one of the most compelling arguments for an involvement of inflammation in DR is the well-established potency of corticosteroids in the treatment of DME ( Rittiphairoj et al, 2020 ; Whitcup et al, 2018 ; Wykoff, 2017 ). Interestingly, there is evidence that benefits of steroid treatment are not limited to just edema but may also slow down development of PDR and overall progression of DR ( Pearson et al, 2011 ; Querques et al, 2017 ; Wykoff et al, 2017 ), suggesting that inflammatory mechanisms (such as persistent low-grade inflammation) make a causal contribution to DR ( Kinuthia et al, 2020 ).…”

Section: Role Of Vegfr1 In Retinal Vascular Diseasementioning

confidence: 99%

VEGFR1 signaling in retinal angiogenesis and microinflammation

Uemura

Fruttiger

D’Amore

et al. 2021

Progress in Retinal and Eye Research

168

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Five vascular endothelial growth factor receptor (VEGFR) ligands (VEGF-A, -B, –C, -D, and placental growth factor [PlGF]) constitute the VEGF family. VEGF-A binds VEGF receptors 1 and 2 (VEGFR1/2), whereas VEGF-B and PlGF only bind VEGFR1. Although much research has been conducted on VEGFR2 to elucidate its key role in retinal diseases, recent efforts have shown the importance and involvement of VEGFR1 and its family of ligands in angiogenesis, vascular permeability, and microinflammatory cascades within the retina. Expression of VEGFR1 depends on the microenvironment, is differentially regulated under hypoxic and inflammatory conditions, and it has been detected in retinal and choroidal endothelial cells, pericytes, retinal and choroidal mononuclear phagocytes (including microglia), Müller cells, photoreceptor cells, and the retinal pigment epithelium. Whilst the VEGF-A decoy function of VEGFR1 is well established, consequences of its direct signaling are less clear. VEGFR1 activation can affect vascular permeability and induce macrophage and microglia production of proinflammatory and proangiogenic mediators. However the ability of the VEGFR1 ligands (VEGF-A, PlGF, and VEGF-B) to compete against each other for receptor binding and to heterodimerize complicates our understanding of the relative contribution of VEGFR1 signaling alone toward the pathologic processes seen in diabetic retinopathy, retinal vascular occlusions, retinopathy of prematurity, and age-related macular degeneration. Clinically, anti-VEGF drugs have proven transformational in these pathologies and their impact on modulation of VEGFR1 signaling is still an opportunity-rich field for further research.

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Section: Role Of Vegfr1 In Retinal Vascular Diseasementioning

confidence: 99%

VEGFR1 signaling in retinal angiogenesis and microinflammation

Uemura

Fruttiger

D’Amore

et al. 2021

Progress in Retinal and Eye Research

168

View full text Add to dashboard Cite

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“…The neuropathy occurs early, even before microangiopathy is detected, as shown by recent retinal imaging technologies [ 3 ] or by electrophysiology showing progressive deterioration of electrical retinal responses with loss of electrical signal amplitudes and extended response times, reflecting retinal neuron alterations [ 4 , 5 ]. This could explain the fact that despite long-term repeated intraocular injections of anti-VEGF and glucocorticoids, visual gain remains limited, of around five letters in real world studies [ 6 , 7 ]. To date, there is no available treatment to stop or even slow down retinal neurodegeneration.…”

Section: Introductionmentioning

confidence: 99%

Long-Term Oral Treatment with Non-Hypoglycemic Dose of Glibenclamide Reduces Diabetic Retinopathy Damage in the Goto-KakizakiRat Model

et al. 2021

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Diabetic retinopathy (DR) remains a major cause of vision loss, due to macular edema, retinal ischemia and death of retinal neurons. We previously demonstrated that acute administration of glibenclamide into the vitreous, or given orally at a non-hypoglycemic dose, protected the structure and the function of the retina in three animal models that each mimic aspects of diabetic retinopathy in humans. In this pilot study, we investigated whether one year of chronic oral glibenclamide, in a non-hypoglycemic regimen (Amglidia®, 0.4 mg/kg, Ammtek/Nordic Pharma, 5 d/week), could alleviate the retinopathy that develops in the Goto-Kakizaki (GK) rat. In vivo, retinal function was assessed by electroretinography (ERG), retinal thickness by optical coherence tomography (OCT) and retinal perfusion by fluorescein and indocyanin green angiographies. The integrity of the retinal pigment epithelium (RPE) that constitutes the outer retinal barrier was evaluated by quantitative analysis of the RPE morphology on flat-mounted fundus ex vivo. Oral glibenclamide did not significantly reduce the Hb1Ac levels but still improved retinal function, as witnessed by the reduction in scotopic implicit times, limited diabetes-induced neuroretinal thickening and the extension of ischemic areas, and it improved the capillary coverage. These results indicate that low doses of oral glibenclamide could still be beneficial for the prevention of type 2 diabetic retinopathy. Whether the retinas ofpatients treated specifically with glibenclamideare less at risk of developing diabetic complications remains to be demonstrated.

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“…Increased intraocular pressure (IOP) and cataract formation are common side effects of various types of steroids ( Jonas et al, 2005b ; Yang et al, 2015 ). According to a Cochrane systematic review, cataracts progressed in 5 or 6 out of 10 patients treated with steroids, and IOP increased in roughly 3 out of 10 patients, which is significantly greater than the control group ( Rittiphairoj et al, 2020 ). These possible side effects must be carefully monitored when using steroids to treat macular edema.…”

Section: Discussionmentioning

confidence: 99%

Steroid Treatment in Macular Edema: A Bibliometric Study and Visualization Analysis

2022

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The use of steroids to treat macular edema (ME) is a research hotspot in ophthalmology. We utilized CiteSpace and VOSviewer software to evaluate the Web of Science Core Collection publications and to build visualizing maps to describe the research progress in this topic. There were 3,252 publications for three decades during 1988–2021. The number of studies was low during the first 14 years but has risen consistently in the following two decades. The average publications per year were only 4.8 during 1988–2002, which jumped to 113 per year during 2003–2012, and 227 per year during 2013–2021. These publications came from 83 countries/regions, with the United States, Germany, and Italy leading positions. Most studies were published in Investigative Ophthalmology Visual Science, and Ophthalmology was the most cited journal. We found 9,993 authors, with Bandello F having the most publications and Jonas JB being the most frequently co-cited. According to our research, the most popular keyword is triamcinolone acetonide (TA). Macular edema, diabetic macular edema (DME), retinal vein occlusion (RVO), dexamethasone (DEX), fluocinolone acetonide (FA), and some other keywords were commonly studied in this field. In conclusion, the bibliometric analysis provides a comprehensive overview of steroid hotspots and developmental tendencies in the macular edema study. While anti-VEGF therapy is the first-line treatment for DME and RVO-induced macular edema, steroids implant is a valid option for these DME patients not responding to anti-VEGF therapy and non-DME patients with macular edema. Combined therapy with anti-VEGF and steroid agents is vital for future research.

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Intravitreal steroids for macular edema in diabetes

Cited by 26 publications

References 119 publications

VEGFR1 signaling in retinal angiogenesis and microinflammation

VEGFR1 signaling in retinal angiogenesis and microinflammation

Long-Term Oral Treatment with Non-Hypoglycemic Dose of Glibenclamide Reduces Diabetic Retinopathy Damage in the Goto-KakizakiRat Model

Steroid Treatment in Macular Edema: A Bibliometric Study and Visualization Analysis

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